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Sample records for chloride induced stress

  1. Cadmium Chloride Induces DNA Damage and Apoptosis of Human Liver Carcinoma Cells via Oxidative Stress

    PubMed Central

    Skipper, Anthony; Sims, Jennifer N.; Yedjou, Clement G.; Tchounwou, Paul B.

    2016-01-01

    Cadmium is a heavy metal that has been shown to cause its toxicity in humans and animals. Many documented studies have shown that cadmium produces various genotoxic effects such as DNA damage and chromosomal aberrations. Ailments such as bone disease, renal damage, and several forms of cancer are attributed to overexposure to cadmium.  Although there have been numerous studies examining the effects of cadmium in animal models and a few case studies involving communities where cadmium contamination has occurred, its molecular mechanisms of action are not fully elucidated. In this research, we hypothesized that oxidative stress plays a key role in cadmium chloride-induced toxicity, DNA damage, and apoptosis of human liver carcinoma (HepG2) cells. To test our hypothesis, cell viability was determined by MTT assay. Lipid hydroperoxide content stress was estimated by lipid peroxidation assay. Genotoxic damage was tested by the means of alkaline single cell gel electrophoresis (Comet) assay. Cell apoptosis was measured by flow cytometry assessment (Annexin-V/PI assay). The result of MTT assay indicated that cadmium chloride induces toxicity to HepG2 cells in a concentration-dependent manner, showing a 48 hr-LD50 of 3.6 µg/mL. Data generated from lipid peroxidation assay resulted in a significant (p < 0.05) increase of hydroperoxide production, specifically at the highest concentration tested. Data obtained from the Comet assay indicated that cadmium chloride causes DNA damage in HepG2 cells in a concentration-dependent manner. A strong concentration-response relationship (p < 0.05) was recorded between annexin V positive cells and cadmium chloride exposure. In summary, these in vitro studies provide clear evidence that cadmium chloride induces oxidative stress, DNA damage, and programmed cell death in human liver carcinoma (HepG2) cells. PMID:26729151

  2. Astaxanthin ameliorates aluminum chloride-induced spatial memory impairment and neuronal oxidative stress in mice.

    PubMed

    Al-Amin, Md Mamun; Reza, Hasan Mahmud; Saadi, Hasan Mahmud; Mahmud, Waich; Ibrahim, Abdirahman Adam; Alam, Musrura Mefta; Kabir, Nadia; Saifullah, A R M; Tropa, Sarjana Tarannum; Quddus, A H M Ruhul

    2016-04-15

    Aluminum chloride induces neurodegenerative disease in animal model. Evidence suggests that aluminum intake results in the activation of glial cells and generation of reactive oxygen species. By contrast, astaxanthin is an antioxidant having potential neuroprotective activity. In this study, we investigate the effect of astaxanthin on aluminum chloride-exposed behavioral brain function and neuronal oxidative stress (OS). Male Swiss albino mice (4 months old) were divided into 4 groups: (i) control (distilled water), (ii) aluminum chloride, (iii) astaxanthin+aluminum chloride, and (iv) astaxanthin. Two behavioral tests; radial arm maze and open field test were conducted, and OS markers were assayed from the brain and liver tissues following 42 days of treatment. Aluminum exposed group showed a significant reduction in spatial memory performance and anxiety-like behavior. Moreover, aluminum group exhibited a marked deterioration of oxidative markers; lipid peroxidation (MDA), nitric oxide (NO), glutathione (GSH) and advanced oxidation of protein products (AOPP) in the brain. To the contrary, co-administration of astaxanthin and aluminum has shown improved spatial memory, locomotor activity, and OS. These results indicate that astaxanthin improves aluminum-induced impaired memory performances presumably by the reduction of OS in the distinct brain regions. We suggest a future study to determine the underlying mechanism of astaxanthin in improving aluminum-exposed behavioral deficits.

  3. Chloride Secretion Induced by Rotavirus Is Oxidative Stress-Dependent and Inhibited by Saccharomyces boulardii in Human Enterocytes

    PubMed Central

    Buccigrossi, Vittoria; Laudiero, Gabriella; Russo, Carla; Miele, Erasmo; Sofia, Morena; Monini, Marina; Ruggeri, Franco Maria; Guarino, Alfredo

    2014-01-01

    Rotavirus (RV) infection causes watery diarrhea via multiple mechanisms, primarily chloride secretion in intestinal epithelial cell. The chloride secretion largely depends on non-structural protein 4 (NSP4) enterotoxic activity in human enterocytes through mechanisms that have not been defined. Redox imbalance is a common event in cells infected by viruses, but the role of oxidative stress in RV infection is unknown. RV SA11 induced chloride secretion in association with an increase in reactive oxygen species (ROS) in Caco-2 cells. The ratio between reduced (GSH) and oxidized (GSSG) glutathione was decreased by RV. The same effects were observed when purified NSP4 was added to Caco-2 cells. N-acetylcysteine (NAC), a potent antioxidant, strongly inhibited the increase in ROS and GSH imbalance. These results suggest a link between oxidative stress and RV-induced diarrhea. Because Saccharomyces boulardii (Sb) has been effectively used to treat RV diarrhea, we tested its effects on RV-infected cells. Sb supernatant prevented RV-induced oxidative stress and strongly inhibited chloride secretion in Caco-2 cells. These results were confirmed in an organ culture model using human intestinal biopsies, demonstrating that chloride secretion induced by RV-NSP4 is oxidative stress-dependent and is inhibited by Sb, which produces soluble metabolites that prevent oxidative stress. The results of this study provide novel insights into RV-induced diarrhea and the efficacy of probiotics. PMID:24918938

  4. Pluchea lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity in Swiss albino mice.

    PubMed

    Jahangir, Tamanna; Khan, Tajdar Husain; Prasad, Lakshmi; Sultana, Sarwat

    2005-09-01

    Cadmium intoxication induces lipid peroxidation and causes oxidative damage to various tissues by altering antioxidant defence system enzymes. At 24 h after treatment with a single intraperitoneal dose of cadmium chloride (5 mg kg-1), Swiss albino mice showed a significant increase in the levels of malanodialdehyde and xanthine oxidase (P<0.001), and a concomitant depletion of renal glutathione, catalase (P<0.001) and other antioxidant enzymes. CdCl2 also led to a simultaneous increase in micronuclei formation (P<0.001) and chromosomal aberrations (P<0.05) in mouse bone marrow cells. Oral pre-treatment with Pluchea lanceolata extract at doses of 100 and 200 mg kg-1 for 7 consecutive days before CdCl2 intoxication caused a significant reduction in malanodialdehyde formation and xanthine oxidase activity (P<0.001). A significant restoration of the activity of antioxidant defence system enzymes such as catalase, glutathione peroxidase (P<0.05), glutathione-S-transferase and glutathione reductase (P<0.001) was observed. A significant dose-dependent decrease in chromosomal aberrations and micronuclei formation was also observed (P<0.05). The results indicate that pre-treatment with P. lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity by altering antioxidant enzymes and reducing chromatid breaks and micronuclei formation. PMID:16105241

  5. Sensitivity of Interfibrillar and Subsarcolemmal Mitochondria to Cobalt Chloride-induced Oxidative Stress and Hydrogen Sulfide Treatment.

    PubMed

    Ayswarya, A; Kurian, G A

    2016-01-01

    Oxidative stress plays a significant role not only in cardiovascular disease but also in non-communicable diseases, where it plays a significant role the mortality rate. Hydrogen sulfide, the biological gaseous signaling molecule that preserves mitochondria in its mode of action, is an effective cardioprotective drug. However, cardiac mitochondria comprise of two distinct populations, namely interfibrillar and subsarcolemmal mitochondria, which respond distinctly in cardiovascular disease. This study was designed to determine the direct impact of cobalt chloride-induced oxidative stress in isolated mitochondrial subpopulations with an intention to examine the efficacy of hydrogen sulfide in preserving interfibrillar and subsarcolemmal mitochondria functional activities when they were incubated as pretreated, co-treated and post-treated agent. Mitochondrial subpopulations were isolated from the heart of male Wistar rats and subjected to cobalt chloride treatment (500 μM) for 20 min, followed by incubation with 10 μM sodium hydrosulfide in three different ways (Pre, Co, and Post-cobalt chloride treatment). Mitochondrial oxidative stress was measured by the concentration of thiobarbituric acid reactive species, reduced glutathione and the activities of enzymes like superoxide dismutase, catalase and glutathione peroxidase. Mitochondrial membrane potential, swelling behavior and enzyme activities were measured to assess its function. The increased level of lipid peroxidation and the decreased level of reduced glutathione in cobalt chloride-induced group confirm the induction of oxidative stress and were more predominant in the subsarcolemmal mitochondria. Hydrogen sulfide treatment to interfibrillar and subsarcolemmal mitochondria preserved their functional activities, but the effect was prominent only with co-treated group. In conclusion, the present study demonstrated that subsarcolemmal mitochondria are more prone to oxidative stress and the co-treatment of the

  6. Sensitivity of Interfibrillar and Subsarcolemmal Mitochondria to Cobalt Chloride-induced Oxidative Stress and Hydrogen Sulfide Treatment

    PubMed Central

    Ayswarya, A.; Kurian, G. A.

    2016-01-01

    Oxidative stress plays a significant role not only in cardiovascular disease but also in non-communicable diseases, where it plays a significant role the mortality rate. Hydrogen sulfide, the biological gaseous signaling molecule that preserves mitochondria in its mode of action, is an effective cardioprotective drug. However, cardiac mitochondria comprise of two distinct populations, namely interfibrillar and subsarcolemmal mitochondria, which respond distinctly in cardiovascular disease. This study was designed to determine the direct impact of cobalt chloride-induced oxidative stress in isolated mitochondrial subpopulations with an intention to examine the efficacy of hydrogen sulfide in preserving interfibrillar and subsarcolemmal mitochondria functional activities when they were incubated as pretreated, co-treated and post-treated agent. Mitochondrial subpopulations were isolated from the heart of male Wistar rats and subjected to cobalt chloride treatment (500 μM) for 20 min, followed by incubation with 10 μM sodium hydrosulfide in three different ways (Pre, Co, and Post-cobalt chloride treatment). Mitochondrial oxidative stress was measured by the concentration of thiobarbituric acid reactive species, reduced glutathione and the activities of enzymes like superoxide dismutase, catalase and glutathione peroxidase. Mitochondrial membrane potential, swelling behavior and enzyme activities were measured to assess its function. The increased level of lipid peroxidation and the decreased level of reduced glutathione in cobalt chloride-induced group confirm the induction of oxidative stress and were more predominant in the subsarcolemmal mitochondria. Hydrogen sulfide treatment to interfibrillar and subsarcolemmal mitochondria preserved their functional activities, but the effect was prominent only with co-treated group. In conclusion, the present study demonstrated that subsarcolemmal mitochondria are more prone to oxidative stress and the co-treatment of the

  7. Sensitivity of Interfibrillar and Subsarcolemmal Mitochondria to Cobalt Chloride-induced Oxidative Stress and Hydrogen Sulfide Treatment.

    PubMed

    Ayswarya, A; Kurian, G A

    2016-01-01

    Oxidative stress plays a significant role not only in cardiovascular disease but also in non-communicable diseases, where it plays a significant role the mortality rate. Hydrogen sulfide, the biological gaseous signaling molecule that preserves mitochondria in its mode of action, is an effective cardioprotective drug. However, cardiac mitochondria comprise of two distinct populations, namely interfibrillar and subsarcolemmal mitochondria, which respond distinctly in cardiovascular disease. This study was designed to determine the direct impact of cobalt chloride-induced oxidative stress in isolated mitochondrial subpopulations with an intention to examine the efficacy of hydrogen sulfide in preserving interfibrillar and subsarcolemmal mitochondria functional activities when they were incubated as pretreated, co-treated and post-treated agent. Mitochondrial subpopulations were isolated from the heart of male Wistar rats and subjected to cobalt chloride treatment (500 μM) for 20 min, followed by incubation with 10 μM sodium hydrosulfide in three different ways (Pre, Co, and Post-cobalt chloride treatment). Mitochondrial oxidative stress was measured by the concentration of thiobarbituric acid reactive species, reduced glutathione and the activities of enzymes like superoxide dismutase, catalase and glutathione peroxidase. Mitochondrial membrane potential, swelling behavior and enzyme activities were measured to assess its function. The increased level of lipid peroxidation and the decreased level of reduced glutathione in cobalt chloride-induced group confirm the induction of oxidative stress and were more predominant in the subsarcolemmal mitochondria. Hydrogen sulfide treatment to interfibrillar and subsarcolemmal mitochondria preserved their functional activities, but the effect was prominent only with co-treated group. In conclusion, the present study demonstrated that subsarcolemmal mitochondria are more prone to oxidative stress and the co-treatment of the

  8. Chloride-inducible transient apoplastic alkalinizations induce stomata closure by controlling abscisic acid distribution between leaf apoplast and guard cells in salt-stressed Vicia faba.

    PubMed

    Geilfus, Christoph-Martin; Mithöfer, Axel; Ludwig-Müller, Jutta; Zörb, Christian; Muehling, Karl H

    2015-11-01

    Chloride stress causes the leaf apoplast transiently to alkalize, an event that is presumed to contribute to the ability of plants to adapt to saline conditions. However, the initiation of coordinated processes downstream of the alkalinization is unknown. We hypothesize that chloride-inducible pH dynamics are a key chemical feature modulating the compartmental distribution of abscisic acid (ABA) and, as a consequence, affecting stomata aperture. Apoplastic pH and stomata aperture dynamics in intact Vicia faba leaves were monitored by microscopy-based ratio imaging and porometric measurements of stomatal conductance. ABA concentrations in leaf apoplast and guard cells were compared with pH dynamics by gas-chromatography-mass-spectrometry (GC-MS) and liquid-chromatography-tandem-mass spectrometry (LC-MS/MS). Results demonstrate that, upon chloride addition to roots, an alkalizing factor that initiates the pH dynamic propagates from root to leaf in a way similar to xylem-distributed water. In leaves, it induces a systemic transient apoplastic alkalinization that causes apoplastic ABA concentration to increase, followed by an elevation of endogenous guard cell ABA. We conclude that the transient alkalinization, which is a remote effect of chloride stress, modulates the compartmental distribution of ABA between the leaf apoplast and the guard cells and, in this way, is instrumental in inducing stomata closure during the beginning of salinity. PMID:26096890

  9. Chloride-inducible transient apoplastic alkalinizations induce stomata closure by controlling abscisic acid distribution between leaf apoplast and guard cells in salt-stressed Vicia faba.

    PubMed

    Geilfus, Christoph-Martin; Mithöfer, Axel; Ludwig-Müller, Jutta; Zörb, Christian; Muehling, Karl H

    2015-11-01

    Chloride stress causes the leaf apoplast transiently to alkalize, an event that is presumed to contribute to the ability of plants to adapt to saline conditions. However, the initiation of coordinated processes downstream of the alkalinization is unknown. We hypothesize that chloride-inducible pH dynamics are a key chemical feature modulating the compartmental distribution of abscisic acid (ABA) and, as a consequence, affecting stomata aperture. Apoplastic pH and stomata aperture dynamics in intact Vicia faba leaves were monitored by microscopy-based ratio imaging and porometric measurements of stomatal conductance. ABA concentrations in leaf apoplast and guard cells were compared with pH dynamics by gas-chromatography-mass-spectrometry (GC-MS) and liquid-chromatography-tandem-mass spectrometry (LC-MS/MS). Results demonstrate that, upon chloride addition to roots, an alkalizing factor that initiates the pH dynamic propagates from root to leaf in a way similar to xylem-distributed water. In leaves, it induces a systemic transient apoplastic alkalinization that causes apoplastic ABA concentration to increase, followed by an elevation of endogenous guard cell ABA. We conclude that the transient alkalinization, which is a remote effect of chloride stress, modulates the compartmental distribution of ABA between the leaf apoplast and the guard cells and, in this way, is instrumental in inducing stomata closure during the beginning of salinity.

  10. Methacryloxylethyl Cetyl Ammonium Chloride Induces DNA Damage and Apoptosis in Human Dental Pulp Cells via Generation of Oxidative Stress.

    PubMed

    Jiao, Yang; Ma, Sai; Wang, Yirong; Li, Jing; Shan, Lequn; Sun, Jinlong; Chen, Jihua

    2016-01-01

    The polymerizable antibacterial monomer methacryloxylethyl cetyl ammonium chloride (DMAE-CB) has provided an effective strategy to combat dental caries. However, the application of such material raises the question about the biological safety and the question remains open. The mechanism of this toxic action, however, is not yet clearly understood. The present study aims at providing novel insight into the possible causal link between cellular oxidative stress and DNA damage, as well as apoptosis in human dental pulp cells exposed to DMAE-CB. The enhanced formation of reactive oxygen species and depletion of glutathione, as well as differential changes in activities of superoxide dismutase, glutathione peroxidase, and catalase in DMAE-CB-treated cells indicated oxidative stress. By using substances that can alter GSH synthesis, we found that GSH was the key component in the regulation of cell response towards oxidative stress induced by DMAE-CB. The increase in oxidative stress-sensitive 8-Oxo-2'-deoxyguanosine (8-OHdG) content, formation of γ-H2AX and cell cycle G1 phase arrest indicated that DNA damage occurred as a result of the interaction between DNA base and ROS beyond the capacities of antioxidant mechanisms in cells exposed to DMAE-CB. Such oxidative DNA damage thus triggers the activation of ataxia telangiectasia-mutated (ATM) signaling, the intrinsic apoptotic pathway, and destruction of mitochondrial morphology and function. PMID:27143955

  11. Methacryloxylethyl Cetyl Ammonium Chloride Induces DNA Damage and Apoptosis in Human Dental Pulp Cells via Generation of Oxidative Stress

    PubMed Central

    Jiao, Yang; Ma, Sai; Wang, Yirong; Li, Jing; Shan, Lequn; Sun, Jinlong; Chen, Jihua

    2016-01-01

    The polymerizable antibacterial monomer methacryloxylethyl cetyl ammonium chloride (DMAE-CB) has provided an effective strategy to combat dental caries. However, the application of such material raises the question about the biological safety and the question remains open. The mechanism of this toxic action, however, is not yet clearly understood. The present study aims at providing novel insight into the possible causal link between cellular oxidative stress and DNA damage, as well as apoptosis in human dental pulp cells exposed to DMAE-CB. The enhanced formation of reactive oxygen species and depletion of glutathione, as well as differential changes in activities of superoxide dismutase, glutathione peroxidase, and catalase in DMAE-CB-treated cells indicated oxidative stress. By using substances that can alter GSH synthesis, we found that GSH was the key component in the regulation of cell response towards oxidative stress induced by DMAE-CB. The increase in oxidative stress-sensitive 8-Oxo-2'-deoxyguanosine (8-OHdG) content, formation of γ-H2AX and cell cycle G1 phase arrest indicated that DNA damage occurred as a result of the interaction between DNA base and ROS beyond the capacities of antioxidant mechanisms in cells exposed to DMAE-CB. Such oxidative DNA damage thus triggers the activation of ataxia telangiectasia-mutated (ATM) signaling, the intrinsic apoptotic pathway, and destruction of mitochondrial morphology and function. PMID:27143955

  12. Effect of sodium chloride on the response of the halophyte species Sesuvium portulacastrum grown in mannitol-induced water stress.

    PubMed

    Slama, Inès; Ghnaya, Tahar; Messedi, Dorsaf; Hessini, Kamel; Labidi, Nahla; Savoure, Arnould; Abdelly, Chedly

    2007-03-01

    Sesuvium portulacastrum is a halophytic species well adapted to salinity and drought. In order to evaluate the physiological impact of salt on water deficit-induced stress response, we cultivated seedlings for 12 days, in the presence or absence of 100 mmol l(-1) NaCl, on a nutrient solution containing either 0 mmol l(-1) or 25 mmol l(-1) mannitol. Mannitol-induced water stress reduced growth, increased the root/shoot ratio, and led to a significant decrease in water potential and leaf relative water content, whereas leaf Na(+) and K(+) concentrations remained unchanged. The addition of 100 mmol l(-1) NaCl to 25 mmol l(-1) mannitol-containing medium mitigated the deleterious impact of water stress on growth of S. portulacastrum, improved the relative water content, induced a significant decrease in leaf water potential and, concomitantly, resulted in enhancement of overall plant photosynthetic activity (i.e. CO(2) net assimilation rate, stomatal conductance). Presence of NaCl in the culture medium, together with mannitol, significantly increased the level of Na(+) and proline in the leaves, but it had no effect on leaf soluble sugar content. These findings suggest that the ability of NaCl to improve plant performance under mannitol-induced water stress may be due to its effect on osmotic adjustment through Na(+) and proline accumulation, which is coupled with an improvement in photosynthetic activity. A striking recovery in relative water content and growth of the seedlings was also recorded in the presence of NaCl on release of the water stress induced by mannitol.

  13. Mangiferin ameliorates aluminium chloride-induced cognitive dysfunction via alleviation of hippocampal oxido-nitrosative stress, proinflammatory cytokines and acetylcholinesterase level.

    PubMed

    Kasbe, Prajapati; Jangra, Ashok; Lahkar, Mangala

    2015-01-01

    Mangiferin is a phytochemical primarily present in the stem, leaves and bark of Mangifera indica. It offers neuroprotection mainly through inhibition of oxidative stress, and decreasing proinflammatory cytokines level in the brain. Aluminium has been reported to cause oxidative stress-associated damage in the brain. In the present investigation, protective effect of mangiferin against aluminium chloride (AlCl3)-induced neurotoxicity and cognitive impairment was studied in male Swiss albino mice. AlCl3 (100 mg/kg) was administered once daily through oral gavage for 42 days. Mangiferin (20 and 40 mg/kg, p.o.) was given to mice for last 21 days of the study. We found cognitive dysfunction in AlCl3-treated group, which was assessed by Morris water maze test, and novel object recognition test. AlCl3-treated group showed elevated level of oxidative stress markers, proinflammatory cytokines level and lowered hippocampal brain-derived neurotrophic factor (BDNF) content. Mangiferin (40 mg/kg) prevented the cognitive deficits, hippocampal BDNF depletion, and biochemical anomalies induced by AlCl3-treatment. In conclusion, our data demonstrated that mangiferin offers neuroprotection in AlCl3-induced neurotoxicity and it may be a potential therapeutic approach in the treatment of oxido-nitrosative stress and inflammation-associated neurotoxicity.

  14. Mangiferin ameliorates aluminium chloride-induced cognitive dysfunction via alleviation of hippocampal oxido-nitrosative stress, proinflammatory cytokines and acetylcholinesterase level.

    PubMed

    Kasbe, Prajapati; Jangra, Ashok; Lahkar, Mangala

    2015-01-01

    Mangiferin is a phytochemical primarily present in the stem, leaves and bark of Mangifera indica. It offers neuroprotection mainly through inhibition of oxidative stress, and decreasing proinflammatory cytokines level in the brain. Aluminium has been reported to cause oxidative stress-associated damage in the brain. In the present investigation, protective effect of mangiferin against aluminium chloride (AlCl3)-induced neurotoxicity and cognitive impairment was studied in male Swiss albino mice. AlCl3 (100 mg/kg) was administered once daily through oral gavage for 42 days. Mangiferin (20 and 40 mg/kg, p.o.) was given to mice for last 21 days of the study. We found cognitive dysfunction in AlCl3-treated group, which was assessed by Morris water maze test, and novel object recognition test. AlCl3-treated group showed elevated level of oxidative stress markers, proinflammatory cytokines level and lowered hippocampal brain-derived neurotrophic factor (BDNF) content. Mangiferin (40 mg/kg) prevented the cognitive deficits, hippocampal BDNF depletion, and biochemical anomalies induced by AlCl3-treatment. In conclusion, our data demonstrated that mangiferin offers neuroprotection in AlCl3-induced neurotoxicity and it may be a potential therapeutic approach in the treatment of oxido-nitrosative stress and inflammation-associated neurotoxicity. PMID:26004900

  15. Repeated stress-induced expression pattern alterations of the hippocampal chloride transporters KCC2 and NKCC1 associated with behavioral abnormalities in female mice.

    PubMed

    Tsukahara, Takao; Masuhara, Masaaki; Iwai, Haruki; Sonomura, Takahiro; Sato, Tomoaki

    2015-09-11

    The balance of cation-chloride co-transporters, particularly KCC2 and NKCC1, is critical for GABAergic inhibitory signaling. However, KCC2/NKCC1 balance is disrupted in many neurodegenerative diseases. Moreover, correlations between chronic stress, KCC2 and NKCC1 in the hippocampus remain poorly understood. Despite the fact that emotional disorders in humans are far more prevalent in women, there have been relatively few studies about female subjects. Here we investigated behaviors and expression patterns of KCC2 and NKCC1 in the hippocampi of female mice under chronic stress. Repeated stress (RS) was induced in experimental mice by repeated forced water administration. Then, expression patterns of GABAergic signaling molecules were identified by immunohistochemical analysis and performance was assessed using several behavioral tests. The results of semi-quantitative analysis showed that RS decreased KCC2 expression and increased NKCC1 expression in membranes of granular and pyramidal cells in the hippocampus. The novel object recognition (NOR) test and sociability test revealed that RS induced cognitive and sociability deficits, whereas RS increased the time spent in the open arms of the elevated plus maze test and induced attention deficits in other tests. In summary, RS induced alterations in membrane KCC2/NKCC1 balance in the hippocampus of female mice, which may contribute to GABAergic disinhibition associated with cognitional, sociability and attention deficits. PMID:26239662

  16. Syzyguim guineense Extracts Show Antioxidant Activities and Beneficial Activities on Oxidative Stress Induced by Ferric Chloride in the Liver Homogenate

    PubMed Central

    Pieme, Constant Anatole; Ngoupayo, Joseph; Khou-Kouz Nkoulou, Claude Herve; Moukette Moukette, Bruno; Njinkio Nono, Borgia Legrand; Ama Moor, Vicky Jocelyne; Ze Minkande, Jacqueline; Yonkeu Ngogang, Jeanne

    2014-01-01

    The aim of this study was to determine the in vitro antioxidant activity, free radical scavenging property and the beneficial effects of extracts of various parts of Syzygium guineense in reducing oxidative stress damage in the liver. The effects of extracts on free radicals were determined on radicals DPPH, ABTS, NO and OH followed by the antioxidant properties using Ferric Reducing Antioxidant Power assay (FRAP) and hosphomolybdenum (PPMB). The phytochemical screening of these extracts was performed by determination of the phenolic content. The oxidative damage inhibition in the liver was determined by measuring malondialdehyde (MDA) as well as the activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and peroxidase. Overall, the bark extract of the ethanol/water or methanol showed the highest radical scavenging activities against DPPH, ABTS and OH radicals compared to the other extracts. This extract also contained the highest phenolic content implying the potential contribution of phenolic compounds towards the antioxidant activities. However, the methanol extract of the root demonstrated the highest protective effects of SOD and CAT against ferric chloride while the hydro-ethanol extract of the leaves exhibited the highest inhibitory effects on lipid peroxidation. These findings suggest that antioxidant properties of S. guineense extracts could be attributed to phenolic compounds revealed by phytochemical studies. Thus, the present results indicate clearly that the extracts of S. guineense possess antioxidant properties and could serve as free radical inhibitors or scavengers, acting possibly as primary antioxidants. The antioxidant properties of the bark extract may thus sustain its various biological activities. PMID:26785075

  17. Cobalt chloride decreases fibroblast growth factor-21 expression dependent on oxidative stress but not hypoxia-inducible factor in Caco-2 cells

    SciTech Connect

    Liu, Yanlong; Wang, Chunhong; Wang, Yuhua; Ma, Zhenhua; Xiao, Jian; McClain, Craig; Li, Xiaokun; Feng, Wenke

    2012-10-15

    Fibroblast growth factor-21 (FGF21) is a potential metabolic regulator with multiple beneficial effects on metabolic diseases. FGF21 is mainly expressed in the liver, but is also found in other tissues including the intestine, which expresses β-klotho abundantly. The intestine is a unique organ that operates in a physiologically hypoxic environment, and is responsible for the fat absorption processes including triglyceride breakdown, re-synthesis and absorption into the portal circulation. In the present study, we investigated the effects of hypoxia and the chemical hypoxia inducer, cobalt chloride (CoCl{sub 2}), on FGF21 expression in Caco-2 cells and the consequence of fat accumulation. Physical hypoxia (1% oxygen) and CoCl{sub 2} treatment decreased both FGF21 mRNA and secreted protein levels. Gene silence and inhibition of hypoxia-inducible factor-α (HIFα) did not affect the reduction of FGF21 mRNA and protein levels by hypoxia. However, CoCl{sub 2} administration caused a significant increase in oxidative stress. The addition of n-acetylcysteine (NAC) suppressed CoCl{sub 2}-induced reactive oxygen species (ROS) formation and completely negated CoCl{sub 2}-induced FGF21 loss. mRNA stability analysis demonstrated that the CoCl{sub 2} administration caused a remarkable reduction in FGF21 mRNA stability. Furthermore, CoCl{sub 2} increased intracellular triglyceride (TG) accumulation, along with a reduction in mRNA levels of lipid lipase, hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), and an increase of sterol regulatory element-binding protein-1c (SREBP1c) and stearoyl-coenzyme A (SCD1). Addition of both NAC and recombinant FGF21 significantly attenuated the CoCl{sub 2}-induced TG accumulation. In conclusion, the decrease of FGF21 in Caco-2 cells by chemical hypoxia is independent of HIFα, but dependent on an oxidative stress-mediated mechanism. The regulation of FGF21 by hypoxia may contribute to intestinal lipid metabolism and

  18. Sodium chloride stress induces nitric oxide accumulation in root tips and oil body surface accompanying slower oleosin degradation in sunflower seedlings.

    PubMed

    David, Anisha; Yadav, Sunita; Bhatla, Satish C

    2010-12-01

    Present work highlights the involvement of endogenous nitric oxide (NO) in sodium chloride (NaCl)-induced biochemical regulation of seedling growth in sunflower (Helianthus annuus L., cv. Morden). The growth response is dependent on NaCl concentration to which seedlings are exposed, they being tolerant to 40 mM NaCl and showing a reduction in extension growth at 120 mM NaCl. NaCl sensitivity of sunflower seedlings accompanies a fourfold increase in Na(+) /K(+) ratio in roots (as compared to that in cotyledons) and rapid transport of Na(+) to the cotyledons, thereby enhancing Na(+) /K(+) ratio in cotyledons as well. A transient increase in endogenous NO content, primarily contributed by putative NOS activity in roots of 4-day-old seedlings subjected to NaCl stress and the relative reduction in Na(+) /K(+) ratio after 4 days, indicates that NO regulates Na(+) accumulation, probably by affecting the associated transporter proteins. Root tips exhibit an early and transient enhanced expression of 4,5-diaminofluorescein diacetate (DAF-2DA) positive NO signal in the presence of 120 mM NaCl. Oil bodies from 2-day-old seedling cotyledons exhibit enhanced localization of NO signal in response to 120 mM NaCl treatment, coinciding with a greater retention of the principal oil body membrane proteins, i.e. oleosins. Abolition of DAF positive fluorescence by the application of specific NO scavenger [2-phenyl-4,4,5,5-tetramethyllimidazoline-1-oxyl-3-oxide (PTIO)] authenticates the presence of endogenous NO. These novel findings provide evidence for a possible protective role of NO during proteolytic degradation of oleosins prior to/accompanying lipolysis.

  19. Transcriptional analysis of different stress response genes in Escherichia coli strains subjected to sodium chloride and lactic acid stress.

    PubMed

    Peng, Silvio; Stephan, Roger; Hummerjohann, Jörg; Tasara, Taurai

    2014-12-01

    Survival of Escherichia coli in food depends on its ability to adapt against encountered stress typically involving induction of stress response genes. In this study, the transcriptional induction of selected acid (cadA, speF) and salt (kdpA, proP, proW, otsA, betA) stress response genes was investigated among five E. coli strains, including three Shiga toxin-producing strains, exposed to sodium chloride or lactic acid stress. Transcriptional induction upon lactic acid stress exposure was similar in all but one E. coli strain, which lacked the lysine decarboxylase gene cadA. In response to sodium chloride stress exposure, proW and otsA were similarly induced, while significant differences were observed between the E. coli strains in induction of kdpA, proP and betA. The kdpA and betA genes were significantly induced in four and three strains, respectively, whereas one strain did not induce these genes. The proP gene was only induced in two E. coli strains. Interestingly, transcriptional induction differences in response to sodium chloride stress exposure were associated with survival phenotypes observed for the E. coli strains in cheese as the E. coli strain lacking significant induction in three salt stress response genes investigated also survived poorly compared to the other E. coli strains in cheese.

  20. Vinyl chloride-induced hepatic angiosarcoma.

    PubMed

    Falk, H

    1987-01-01

    In early 1974, an alert plant physician reported the occurrence of several cases of the otherwise rare hepatic angiosarcoma (HAS) at a single polyvinyl chloride (PVC) production facility in Louisville, Kentucky (U.S.A.). Upon further investigation, the relative risk for HAS at this plant appeared to be approximately 5,000, strongly indicating a causal relationship with some factor at the plant. Epidemiologic studies at this and other PVC polymerization plants identified vinyl chloride monomer (VCM) as the causative agent. Experimental studies reported in early 1974 confirmed VCM as a hepatic carcinogen capable of producing HAS and other tumors. Follow-up epidemiologic studies revealed that: 1) HAS is the end stage of a progressive liver disease consisting of hepatocytic and sinusoidal cell hyperplasia, sinusoidal dilatation, and hepatic fibrosis; 2) over 100 cases of VCM-induced HAS have occurred worldwide; and 3) an increased risk of lung cancer has been reported in some cohort studies of PVC polymerization workers, although this outcome may be related to PVC dust or factors other than VCM. A national study of HAS in the United States identified 3 other causes of HAS: Thorotrast, inorganic arsenic, and androgenic-anabolic steroids. Of 168 cases found to occur during 1964 through 1974, 42 cases (25%) were associated with the 4 known etiologic agents, while 126 cases (75%) were of unknown etiology.

  1. Cyclic stress effect on stress corrosion cracking of duplex stainless steel in chloride and caustic solutions

    NASA Astrophysics Data System (ADS)

    Yang, Di

    hardening. Cyclic SSRTs were performed under the conditions that SCC occurs in sodium chloride and WL solutions. Test results show that cyclic stress facilitated crack initiations in DSS 2205. Stress corrosion cracks initiated from the intermetallic precipitates in acidic chloride environment, and the cracks initiated from austenite phase in WL environment. Cold-working has been found to retard the crack initiations induced by cyclic stresses.

  2. Ferric Chloride-induced Murine Thrombosis Models.

    PubMed

    Li, Wei; Nieman, Marvin; Sen Gupta, Anirban

    2016-01-01

    Arterial thrombosis (blood clot) is a common complication of many systemic diseases associated with chronic inflammation, including atherosclerosis, diabetes, obesity, cancer and chronic autoimmune rheumatologic disorders. Thrombi are the cause of most heart attacks, strokes and extremity loss, making thrombosis an extremely important public health problem. Since these thrombi stem from inappropriate platelet activation and subsequent coagulation, targeting these systems therapeutically has important clinical significance for developing safer treatments. Due to the complexities of the hemostatic system, in vitro experiments cannot replicate the blood-to-vessel wall interactions; therefore, in vivo studies are critical to understand pathological mechanisms of thrombus formation. To this end, various thrombosis models have been developed in mice. Among them, ferric chloride (FeCl3) induced vascular injury is a widely used model of occlusive thrombosis that reports platelet activation and aggregation in the context of an aseptic closed vascular system. This model is based on redox-induced endothelial cell injury, which is simple and sensitive to both anticoagulant and anti-platelets drugs. The time required for the development of a thrombus that occludes blood flow gives a quantitative measure of vascular injury, platelet activation and aggregation that is relevant to thrombotic diseases. We have significantly refined this FeCl3-induced vascular thrombosis model, which makes the data highly reproducible with minimal variation. Here we describe the model and present representative data from several experimental set-ups that demonstrate the utility of this model in thrombosis research. PMID:27684194

  3. The association between splenocyte apoptosis and alterations of Bax, Bcl-2 and caspase-3 mRNA expression, and oxidative stress induced by dietary nickel chloride in broilers.

    PubMed

    Huang, Jianying; Cui, Hengmin; Peng, Xi; Fang, Jing; Zuo, Zhicai; Deng, Junliang; Wu, Bangyuan

    2013-12-01

    Two hundred and forty avian broilers were equally divided into four groups, and raised with a corn-soybean basal diet or the same diet supplemented with 300, 600, 900 mg/kg NiCl2 for 42 days. Numbers or percentages of apoptotic splenocytes by flow cytometry (FCM) and TUNEL were higher (p < 0.05 or p < 0.01) in the 300, 600 and 900 mg/kg groups than those in the control group. Results measured by qRT-PCR and ELISA showed that mRNA expression and contents were significantly higher (p < 0.05 or p < 0.01) in Bax and Caspase-3, and were significantly lower (p < 0.05 or p < 0.01) in Bcl-2 of the 300, 600 and 900 mg/kg groups. Also, the SOD, CAT and GSH-Px activities, and the ability to inhibit hydroxyl radical, and GSH contents were significantly decreased (p < 0.05 or p < 0.01), and MDA contents were increased (p < 0.05 or p < 0.01) in all groups. In conclusion, dietary NiCl2 in excess of 300 mg/kg caused apoptosis, altered Bax, Bcl-2 and Caspase-3 mRNA expression levels and contents, and induced oxidative stress in the spleen. Also, splenocyte apoptosis was closely related to the alternations of Bax, Bcl-2 and Caspase-3 mRNA expression, and oxidative damage. The splenic immunity and blood filtration functions were impaired in broilers. PMID:24351749

  4. The chloride stress-corrosion cracking behavior of stainless steels under different test methods

    SciTech Connect

    Jin, L.Z. . Dept. of Materials Science and Engineering)

    1994-12-01

    Chloride-induced stress-corrosion cracking (SCC) is one of the failure modes of stainless steels. Highly alloyed austenitic stainless steels S32654, S31254, and N08028, and duplex grades S32750 and S31803 possess much improved resistance to SCC compared with S30400 and S31600 steels. With the development of a database, SSData, experimental data collected from calcium chloride tests, autoclave tests, and drop evaporation tests were evaluated. Stress-corrosion cracking data generated by autoclave tests agreed well with the practical service conditions and can be used to discriminate alloys for SCC resistance in sodium chloride solution. Drop evaporation test data can be used in situations where evaporation may occur and cyclic loading may be involved. The SCC resistance of alloys under each method increased with increasing molybdenum equivalent Mo + 0.25Cr + 0.1Ni. For a given alloy, the testing result depends on the stress state and environment; different test methods can give different ranking orders concerning SCC resistance. The performance of duplex stainless steels in a chloride-containing environment at higher temperatures was not as good as expected when dynamic loading was involved.

  5. Mild Potassium Chloride Stress Alters the Mineral Composition, Hormone Network, and Phenolic Profile in Artichoke Leaves

    PubMed Central

    Lucini, Luigi; Borgognone, Daniela; Rouphael, Youssef; Cardarelli, Mariateresa; Bernardi, Jamila; Colla, Giuseppe

    2016-01-01

    There is a growing interest among consumers and researchers in the globe artichoke [Cynara cardunculus L. subsp. scolymus (L.) Hegi] leaf extract due to its nutraceutical and therapeutic properties. The application of an abiotic stress such as salinity can activate the stress-signaling pathways, thus enhancing the content of valuable phytochemicals. The aim of this study was to assess the metabolic changes in artichokes by probing the leaf metabolome of artichoke plants grown in a floating system and exposed to a relatively mild (30 mM) potassium chloride (KCl) salt stress. Potassium chloride treatment decreased the leaf dry biomass of artichoke, macro- and microelements in leaves (e.g., Ca, Mg, Mn, Zn, and B) but increased the concentrations of K and Cl. Metabolomics highlighted that the hormonal network of artichokes was strongly imbalanced by KCl. The indole-3-acetic acid conjugates, the brassinosteroids hormone 6-deoxocastasterone, and even more the cytokinin precursor N6-(Delta-2-isopentenyl)-adenosine-5′-triphosphate, strongly increased in leaves of KCl-treated plants. Moreover, KCl saline treatment induced accumulation of GA4, a bioactive form additional to the already known GA3. Another specific response to salinity was changes in the phenolic compounds profile, with flavones and isoflavones being decreased by KCl treatment, whereas flavonoid glycosides increased. The osmotic/oxidative stress that salinity generates also induced some expected changes at the biochemical level (e.g., ascorbate degradation, membrane lipid peroxidation, and accumulation of mannitol phosphate). These latter results help explain the molecular/physiological mechanisms that the plant uses to cope with potassium chloride stress exposure. PMID:27446175

  6. Mild Potassium Chloride Stress Alters the Mineral Composition, Hormone Network, and Phenolic Profile in Artichoke Leaves.

    PubMed

    Lucini, Luigi; Borgognone, Daniela; Rouphael, Youssef; Cardarelli, Mariateresa; Bernardi, Jamila; Colla, Giuseppe

    2016-01-01

    There is a growing interest among consumers and researchers in the globe artichoke [Cynara cardunculus L. subsp. scolymus (L.) Hegi] leaf extract due to its nutraceutical and therapeutic properties. The application of an abiotic stress such as salinity can activate the stress-signaling pathways, thus enhancing the content of valuable phytochemicals. The aim of this study was to assess the metabolic changes in artichokes by probing the leaf metabolome of artichoke plants grown in a floating system and exposed to a relatively mild (30 mM) potassium chloride (KCl) salt stress. Potassium chloride treatment decreased the leaf dry biomass of artichoke, macro- and microelements in leaves (e.g., Ca, Mg, Mn, Zn, and B) but increased the concentrations of K and Cl. Metabolomics highlighted that the hormonal network of artichokes was strongly imbalanced by KCl. The indole-3-acetic acid conjugates, the brassinosteroids hormone 6-deoxocastasterone, and even more the cytokinin precursor N(6)-(Delta-2-isopentenyl)-adenosine-5'-triphosphate, strongly increased in leaves of KCl-treated plants. Moreover, KCl saline treatment induced accumulation of GA4, a bioactive form additional to the already known GA3. Another specific response to salinity was changes in the phenolic compounds profile, with flavones and isoflavones being decreased by KCl treatment, whereas flavonoid glycosides increased. The osmotic/oxidative stress that salinity generates also induced some expected changes at the biochemical level (e.g., ascorbate degradation, membrane lipid peroxidation, and accumulation of mannitol phosphate). These latter results help explain the molecular/physiological mechanisms that the plant uses to cope with potassium chloride stress exposure. PMID:27446175

  7. Gadolinium chloride pretreatment ameliorates acute cadmium-induced hepatotoxicity.

    PubMed

    Kyriakou, Loukas G; Tzirogiannis, Konstantinos N; Demonakou, Maria D; Kourentzi, Kalliopi T; Mykoniatis, Michael G; Panoutsopoulos, Georgios I

    2013-08-01

    Cadmium is a known industrial and environmental pollutant. It causes hepatotoxicity upon acute administration. Features of cadmium-induced acute hepatoxicity encompass necrosis, apoptosis, peliosis and inflammatory infiltration. Gadolinium chloride (GdCl3) may prevent cadmium-induced hepatotoxicity by suppressing Kupffer cells. The effect of GdCl3 pretreatment on a model of acute cadmium-induced liver injury was investigated. Male Wistar rats 4-5 months old were injected intraperitoneally with normal saline followed by cadmium chloride (CdCl2; 6.5 mg/kg) or GdCl3 (10 mg/kg) followed by CdCl2 (6.5 mg/kg; groups I and II, respectively). Rats of both the groups were killed at 9, 12, 16, 24, 48 and 60 h after cadmium intoxication. Liver sections were analyzed for necrosis, apoptosis, peliosis and mitoses. Liver regeneration was also evaluated by tritiated thymidine incorporation into hepatic DNA. Serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were also determined. Hepatic necrosis, hepatocyte and nonparenchymal cell apoptosis and macroscopic and microscopic types of peliosis hepatis were minimized by gadolinium pretreatment. Serum levels of AST and ALT were also greatly diminished in rats of group II. Tritiated thymidine incorporation into hepatic DNA was increased in gadolinium pretreatment rats. Kupffer cell activation was minimal in both the groups of rats. Gadolinium pretreatment attenuates acute cadmium-induced liver injury in young Wistar rats, with mechanisms other than Kupffer cell elimination.

  8. Quantitative effects of magnesium chloride stress on aggregation of Sup35p in [psi-] yeast cells.

    PubMed

    Song, Yao; Lan, Wanjun; Wu, Xianyuan; He, Jianwei; Li, Hui; Ben, Songbin; Song, Youtao

    2010-12-01

    [PSI(+)] phenotype can be transiently induced when Magnesium chloride (MgCl(2)) was the selective pressure in SUP35 repeat-expansion mutant [psi(-)] yeast strains. We further investigated [PSI(+)] phenotype change under different MgCl(2) conditions with native Sup35p and quantified the Sup35p status changes with fluorescence recovery after photobleaching (FRAP) and semi-denaturing detergent-agarose gel electrophoresis (SDD-AGE) analysis. It was found that the [PSI(+)] phenotype presented a dose-dependent relationship with the concentrations of MgCl(2). Furthermore, Sup35p aggregated in MgCl(2) treated cells but did not form large aggregates as it does in [PSI(+)] cells, and the size of Sup35p aggregates showed a time-dependent relationship with the MgCl(2) application. The aggregation of Sup35p strictly depended on the presence of MgCl(2) stress in our strains.

  9. Beryllium chloride-induced oxidative DNA damage and alteration in the expression patterns of DNA repair-related genes.

    PubMed

    Attia, Sabry M; Harisa, Gamaleldin I; Hassan, Memy H; Bakheet, Saleh A

    2013-09-01

    Beryllium metal has physical properties that make its use essential for very specific applications, such as medical diagnostics, nuclear/fusion reactors and aerospace applications. Because of the widespread human exposure to beryllium metals and the discrepancy of the genotoxic results in the reported literature, detail assessments of the genetic damage of beryllium are warranted. Mice exposed to beryllium chloride at an oral dose of 23mg/kg for seven consecutive days exhibited a significant increase in the level of DNA-strand breaking and micronuclei formation as detected by a bone marrow standard comet assay and micronucleus test. Whereas slight beryllium chloride-induced oxidative DNA damage was detected following formamidopyrimidine DNA glycosylase digestion, digestion with endonuclease III resulted in considerable increases in oxidative DNA damage after the 11.5 and 23mg/kg/day treatment as detected by enzyme-modified comet assays. Increased 8-hydroxydeoxyguanosine was also directly correlated with increased bone marrow micronuclei formation and DNA strand breaks, which further confirm the involvement of oxidative stress in the induction of bone marrow genetic damage after exposure to beryllium chloride. Gene expression analysis on the bone marrow cells from beryllium chloride-exposed mice showed significant alterations in genes associated with DNA damage repair. Therefore, beryllium chloride may cause genetic damage to bone marrow cells due to the oxidative stress and the induced unrepaired DNA damage is probably due to the down-regulation in the expression of DNA repair genes, which may lead to genotoxicity and eventually cause carcinogenicity.

  10. Inhibition of nitrite-induced toxicity in channel catfish by calcium chloride and sodium chloride

    USGS Publications Warehouse

    Tommasso J.R., Wright; Simco, B.A.; Davis, K.B.

    1980-01-01

    Environmental chloride has been shown to inhibit methemoglobin formation in fish, thereby offering a protective effect against nitrite toxicity. Channel catfish (Ictalurus punctatus) were simultaneously exposed to various environmental nitrite and chloride levels (as either CaCl2 or NaCl) in dechlorinated tap water (40 mg/L total hardness, 47 mg/L alkalinity, 4 mg/L chloride, pH = 6.9-7.1, and temperature 21-24°C). Methemoglobin levels in fish simultaneously exposed to 2.5 mg/L nitrite and up to 30 mg/L chloride as either CaCl2 or NaCl were similar but significantly lower than in unprotected fish. Exposure to 10 mg/L nitrite and 60 mg/L chloride resulted in methemoglobin levels similar to those of the controls; most unprotected fish died. Fish exposed to 10 mg/L nitrite had significantly lower methemoglobin levels when protected with 15.0 mg/L chloride as CaCl2 than with NaCl. Fish exposed to nitrite in the presence of 60 mg/L chloride (as either CaCl2 or NaCl) had similar 24-h LC50 values that were significantly elevated above those obtained in the absence of chloride. Calcium had little effect on tolerance to nitrite toxicity in channel catfish in contrast to its large effect reported in steelhead trout (Salmo gairdneri).

  11. Nanoscale Periodic Modulations on Sodium Chloride Induced by Surface Charges

    SciTech Connect

    Clark, Kendal W; Qin, Shengyong; Zhang, Xiaoguang; Li, An-Ping

    2012-01-01

    The sodium chloride surface is one of the most common platforms for the study of catalysts, thin film growth, and atmospheric aerosols. Here we report a nanoscale periodic modulation pattern on the surface of a cleaved NaCl single crystal, revealed by non-contact atomic force microscopy with a tuning fork sensor. The surface pattern shows two orthogonal domains, extending over the entire cleavage surface. The spatial modulations exhibit a characteristic period of 5.4 nm, along 110 crystallographic directions of the NaCl. The modulations are robust in vacuum, not affected by the tip-induced electric field or gentle annealing (<300 C); however, they are eliminated after exposure to water and an atomically flat surface can be recovered by subsequent thermal annealing after water exposure. A strong electrostatic charging is revealed on the cleavage surface which may facilitate the formation of the observed metastable surface reconstruction.

  12. Hydrogen chloride-induced surface disordering on ice.

    PubMed

    McNeill, V Faye; Loerting, Thomas; Geiger, Franz M; Trout, Bernhardt L; Molina, Mario J

    2006-06-20

    Characterizing the interaction of hydrogen chloride (HCl) with polar stratospheric cloud ice particles is essential for understanding the processes responsible for ozone depletion. We studied the interaction of gas-phase HCl with ice between 243 and 186 K by using (i) ellipsometry to monitor the ice surface and (ii) coated-wall flow tube experiments, both with chemical ionization mass spectrometry detection of the gas phase. We show that trace amounts of HCl induce formation of a disordered region, or quasi-liquid layer, at the ice surface at stratospheric temperatures. We also show that surface disordering enhances the chlorine activation reaction of HCl with chlorine nitrate (ClONO(2)) and also enhances acetic acid (CH(3)COOH) adsorption. These results impact our understanding of the chemistry and physics of ice particles in the atmosphere.

  13. Hibiscus sabdariffa Affects Ammonium Chloride-Induced Hyperammonemic Rats

    PubMed Central

    Essa, M. Mohamed

    2007-01-01

    Hibiscus sabdariffa (HS) is an edible medicinal plant, indigenous to India, China and Thailand and is used in Ayurveda and traditional medicine. Alcoholic extract of HS leaves (HSEt) was studied for its anti-hyperammonemic and antioxidant effects in brain tissues of ammonium chloride-induced hyperammonemic rats. Oral administration of HSEt (250 mg kg−1 body weight) significantly normalizes the levels of ammonia, urea, uric acid, creatinine and non-protein nitrogen in the blood. HSEt significantly reduced brain levels of lipid peroxidation products such as thiobarbituric acid and reactive substances (TBARS) and hydroperoxides (HP). However, the administered extract significantly increased the levels of antioxidants such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) in brain tissues of hyperammonemic rats. This investigation demonstrates significant anti-hyperammonemic and antioxidant activity of HS. PMID:17965762

  14. Neuroprotective effect of Allium cepa L. in aluminium chloride induced neurotoxicity.

    PubMed

    Singh, Tanveer; Goel, Rajesh Kumar

    2015-07-01

    The present study was envisaged to investigate the neuroprotective potential of Allium cepa (A. cepa) in aluminium chloride induced neurotoxicity. Aluminium chloride (50 mg/kg/day) was administered orally in mice supplemented with different doses of A. cepa hydroethanolic extract for a period of 60 days. Various behavioural, biochemical and histopathological parameters were estimated in aluminium exposed animals. Chronic aluminium administration resulted in significant motor incoordination and memory deficits, which were also endorsed biochemically as there was increased oxidative stress as well as elevated acetylcholinesterase (AChE) and aluminium levels in the brain. Supplementation with A. cepa in aluminium exposed animals significantly improved muscle coordination and memory deficits as well as reduced oxidative stress, AChE and decreased abnormal aluminium deposition in the brain. Histopathologically, there was marked deterioration visualized as decreased vacuolated cytoplasm as well as decreased pyramidal cells in the hippocampal area of mice brain which were found to be reversed with A. cepa supplementation. Administration of BADGE (PPARγ antagonist) in aluminium exposed animals reversed the neuroprotective potential of A. cepa as assessed with various behavioural, biochemical, neurochemical and histopathological estimations. In conclusion, finding of this study suggested significant neuroprotective potential of A. cepa in aluminium induced neurotoxicity. Further, the role of PPARγ receptor agonism has also been suggested as a putative neuroprotective mechanism of A. cepa, which needs further studies for confirmation.

  15. Chloride stress triggers maturation and negatively affects the postharvest quality of persimmon fruit. Involvement of calyx ethylene production.

    PubMed

    Besada, Cristina; Gil, Rebeca; Bonet, Luis; Quiñones, Ana; Intrigliolo, Diego; Salvador, Alejandra

    2016-03-01

    In recent years many hectares planted with persimmon trees in E Spain have been diagnosed with chloride toxicity. An effect of this abiotic stress on fruit quality has been reported in different crops. However, the impact of chloride stress on persimmon fruit quality is unknown. The harvest and postharvest quality of persimmons harvested from trees that manifest different intensities of chloride toxicity foliar symptoms was evaluated herein. Our results revealed that fruits from trees under chloride stress conditions underwent chloride accumulation in the calyx, which was more marked the greater the salt stress intensity trees were exposed to. Increased chloride concentrations in the calyx stimulated ethylene production in this tissue. In the fruits affected by slight and moderate chloride stress, calyx ethylene production accelerated the maturity process, as reflected by increased fruit colour and diminished fruit firmness. In the fruits under severe chloride stress, the high ethylene levels in the calyx triggered autocatalytic ethylene production in other fruit tissues, which led fruit maturity to drastically advance. In these fruits effectiveness of CO2 deastringency treatment was not complete and fruit softening enhanced during the postharvest period. Moreover, chloride stress conditions had a marked effect on reducing fruit weight, even in slightly stressed trees. PMID:26807935

  16. Chloride stress triggers maturation and negatively affects the postharvest quality of persimmon fruit. Involvement of calyx ethylene production.

    PubMed

    Besada, Cristina; Gil, Rebeca; Bonet, Luis; Quiñones, Ana; Intrigliolo, Diego; Salvador, Alejandra

    2016-03-01

    In recent years many hectares planted with persimmon trees in E Spain have been diagnosed with chloride toxicity. An effect of this abiotic stress on fruit quality has been reported in different crops. However, the impact of chloride stress on persimmon fruit quality is unknown. The harvest and postharvest quality of persimmons harvested from trees that manifest different intensities of chloride toxicity foliar symptoms was evaluated herein. Our results revealed that fruits from trees under chloride stress conditions underwent chloride accumulation in the calyx, which was more marked the greater the salt stress intensity trees were exposed to. Increased chloride concentrations in the calyx stimulated ethylene production in this tissue. In the fruits affected by slight and moderate chloride stress, calyx ethylene production accelerated the maturity process, as reflected by increased fruit colour and diminished fruit firmness. In the fruits under severe chloride stress, the high ethylene levels in the calyx triggered autocatalytic ethylene production in other fruit tissues, which led fruit maturity to drastically advance. In these fruits effectiveness of CO2 deastringency treatment was not complete and fruit softening enhanced during the postharvest period. Moreover, chloride stress conditions had a marked effect on reducing fruit weight, even in slightly stressed trees.

  17. Comparison of Sodium Chloride Tablets-Induced, Sodium Chloride Solution-Induced, and Glycerol-Induced Hyperhydration on Fluid Balance Responses in Healthy Men.

    PubMed

    Savoie, Félix A; Asselin, Audrey; Goulet, Eric D B

    2016-10-01

    Savoie, FA, Asselin, A, and Goulet, EDB. Comparison of sodium chloride tablets-induced, sodium chloride solution-induced, and glycerol-induced hyperhydration on fluid balance responses in healthy men. J Strength Cond Res 30(10): 2880-2891, 2016-Sodium chloride solution-induced hyperhydration (NaCl-SolIH) is a powerful strategy to increase body water before exercise. However, NaCl-SolIH is associated with an unpleasant salty taste, potentially dissuading some athletes from using it and coaches from recommending it. Therefore, we evaluated the hyperhydrating potential of sodium chloride tablets-induced hyperhydration (NaCl-TabIH), which bypasses the palatability issue of NaCl-SolIH without sacrificing sodium chloride content, and compared it to NaCl-SolIH and glycerol-induced hyperhydration (GIH). Sixteen healthy males (age: 21 ± 2 years; fat-free mass (FFM): 65 ± 6 kg) underwent three, 3-hour long passive hyperhydration protocols during which they drank, over the first 60 minutes, 30-ml·kg FFM of an artificially sweetened solution. During NaCl-TabIH, participants swallowed 7.5, 1 g each, sodium chloride tablets with every liter of solution. During NaCl-SolIH, an equal quantity of sodium chloride tablets was dissolved in each liter of solution. With GIH, the glycerol concentration was 46.7 g·L. Urine production, fluid retention, hemoglobin, hematocrit, plasma volume, and perceptual variables were monitored throughout the trials. Total fluid intake was 1948 ± 182 ml. After 3 hour, there were no significant differences among treatments for hemoglobin, hematocrit, and plasma volume changes. Fluid retention was significantly greater with NaCl-SolIH (1150 ± 287 ml) than NaCl-TabIH (905 ± 340 ml) or GIH (800 ± 211 ml), with no difference between NaCl-TabIH and GIH. No differences were found among treatments for perceptual variables. NaCl-TabIH and GIH are equally effective, but inferior than NaCl-SolIH. NaCl-TabIH represents an alternative to hyperhydration induced

  18. Comparison of Sodium Chloride Tablets-Induced, Sodium Chloride Solution-Induced, and Glycerol-Induced Hyperhydration on Fluid Balance Responses in Healthy Men.

    PubMed

    Savoie, Félix A; Asselin, Audrey; Goulet, Eric D B

    2016-10-01

    Savoie, FA, Asselin, A, and Goulet, EDB. Comparison of sodium chloride tablets-induced, sodium chloride solution-induced, and glycerol-induced hyperhydration on fluid balance responses in healthy men. J Strength Cond Res 30(10): 2880-2891, 2016-Sodium chloride solution-induced hyperhydration (NaCl-SolIH) is a powerful strategy to increase body water before exercise. However, NaCl-SolIH is associated with an unpleasant salty taste, potentially dissuading some athletes from using it and coaches from recommending it. Therefore, we evaluated the hyperhydrating potential of sodium chloride tablets-induced hyperhydration (NaCl-TabIH), which bypasses the palatability issue of NaCl-SolIH without sacrificing sodium chloride content, and compared it to NaCl-SolIH and glycerol-induced hyperhydration (GIH). Sixteen healthy males (age: 21 ± 2 years; fat-free mass (FFM): 65 ± 6 kg) underwent three, 3-hour long passive hyperhydration protocols during which they drank, over the first 60 minutes, 30-ml·kg FFM of an artificially sweetened solution. During NaCl-TabIH, participants swallowed 7.5, 1 g each, sodium chloride tablets with every liter of solution. During NaCl-SolIH, an equal quantity of sodium chloride tablets was dissolved in each liter of solution. With GIH, the glycerol concentration was 46.7 g·L. Urine production, fluid retention, hemoglobin, hematocrit, plasma volume, and perceptual variables were monitored throughout the trials. Total fluid intake was 1948 ± 182 ml. After 3 hour, there were no significant differences among treatments for hemoglobin, hematocrit, and plasma volume changes. Fluid retention was significantly greater with NaCl-SolIH (1150 ± 287 ml) than NaCl-TabIH (905 ± 340 ml) or GIH (800 ± 211 ml), with no difference between NaCl-TabIH and GIH. No differences were found among treatments for perceptual variables. NaCl-TabIH and GIH are equally effective, but inferior than NaCl-SolIH. NaCl-TabIH represents an alternative to hyperhydration induced

  19. Aqueous chloride stress corrosion cracking of titanium - A comparison with environmental hydrogen embrittlement

    NASA Technical Reports Server (NTRS)

    Nelson, H. G.

    1974-01-01

    The physical characteristics of stress corrosion cracking of titanium in an aqueous chloride environment are compared with those of embrittlement of titanium by a gaseous hydrogen environment in an effort to help contribute to the understanding of the possible role of hydrogen in the complex stress corrosion cracking process. Based on previous studies, the two forms of embrittlement are shown to be similar at low hydrogen pressures (100 N/sq m) but dissimilar at higher hydrogen pressures. In an effort to quantify this comparison, tests were conducted in an aqueous chloride solution using the same material and test techniques as had previously been employed in a gaseous hydrogen environment. The results of these tests strongly support models based on hydrogen as the embrittling species in an aqueous chloride environment.

  20. Effect of lysozyme chloride on betel quid chewing aggravated gastric oxidative stress and hemorrhagic ulcer in diabetic rats

    PubMed Central

    Hung, Chen-Road

    2005-01-01

    AIM: To evaluate the protective effect of lysozyme chloride on betel quid chewing (BQC) aggravated gastric oxidative stress and hemorrhagic ulcer in rats with diabetes mellitus (DM). METHODS: Male Wistar rats were challenged intravenously with streptozotocin (65 mg/kg) to induce DM. Rats were fed with regular pellet food or BQC-containing diets. After 90 d, rats were deprived of food for 24 h. Rat stomachs were irrigated for 3 h with normal saline or simulated gastric juice. Rats were killed and gastric specimens were harvested. RESULTS: An enhancement of various gastric ulcerogenic parameters, including acid back-diffusion, mucosal lipid peroxide generation, as well as decreased glutathione levels and mucus content, were observed in DM rats. After feeding DM rats with BQC, an exacerbation of these ulcero-genic parameters was achieved. Gastric juice caused a further aggravation of these ulcerogenic parameters. Daily intragastric lysozyme chloride dose-dependently inhibited exacerbation of various ulcerogenic parameters in those BQC-fed DM rats. CONCLUSION: (1) Gastric juice could aggravate both DM and BQC-fed DM rat hemorrhagic ulcer; (2) BQC exacerbated gastric hemorrhagic ulcer in DM rats via enhancing oxidative stress and reducing defensive factors; (3) lysozyme chloride effectively protected BQC aggravated gastric damage in DM rats. PMID:16270397

  1. Dietary nickel chloride induces oxidative intestinal damage in broilers.

    PubMed

    Wu, Bangyuan; Cui, Hengmin; Peng, Xi; Fang, Jing; Zuo, Zhicai; Deng, Junliang; Huang, Jianying

    2013-06-01

    The purpose of this study was to investigate the oxidative damage induced by dietary nickel chloride (NiCl2) in the intestinal mucosa of different parts of the intestine of broilers, including duodenum, jejunum and ileum. A total of 240 one-day-old broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600 or 900 mg/kg NiCl2 during a 42-day experimental period. The results showed that the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (p < 0.05 or p < 0.01) decreased in the 300, 600 and 900 mg/kg groups in comparison with those of the control group. In contrast, malondialdehyde (MDA) content was significantly (p < 0.05 or p < 0.01) higher in the 300, 600 and 900 mg/kg groups than that in the control group. It was concluded that dietary NiCl2 in excess of 300 mg/kg could cause oxidative damage in the intestinal mucosa in broilers, which finally impaired the intestinal functions including absorptive function and mucosal immune function. The oxidative damage might be a main mechanism on the effects of NiCl2 on the intestinal health of broilers. PMID:23702803

  2. Stress anisotropy and concentration effects in high pressure measurements. [sodium chloride

    NASA Technical Reports Server (NTRS)

    Nelson, D. A., Jr.; Ruoff, A. L.

    1974-01-01

    Sodium chloride is used as an internal pressure standard in high pressure research. Possible corrections are discussed which are needed in the calibration of this standard due to the independent effects of stress anisotropy and stress concentration in pressure vessels. The first is due to the lack of a truly hydrostatic state of stress in solid state pressure vessels. The second is due to the difference in the compressibilities between the pressure transmitting substances (sodium chloride) and a stiffer test specimen. These two corrections are then combined and a total correction, as a function of measured pressure, is discussed for two systems presently in use. The predicted value of the combined effect is about 5-10% of the pressure at 30 GPa.

  3. Chloride channels involve in hydrogen peroxide-induced apoptosis of PC12 cells.

    PubMed

    Zuo, Wanhong; Zhu, Linyan; Bai, Zhiquan; Zhang, Haifeng; Mao, Jianwen; Chen, Lixin; Wang, Liwei

    2009-10-01

    Chloride channel activity is one of the critical factors responsible for cell apoptotic volume decrease (AVD). However, the roles of chloride channels in apoptosis have not been fully understood. In the current study, we assessed the role of chloride channels in hydrogen peroxide (H(2)O(2))-induced apoptosis of pheochromocytoma cells (PC12). Extracellular application of H(2)O(2) activated a chloride current and induced cell volume decrease in a few minutes. Incubation of cells with H(2)O(2) elevated significantly the membrane permeability to the DNA dye Hoechst 33258 in 1h and induced apoptosis of most PC12 cells tested in 24h. The chloride channel blocker NPPB (5-nitro-2-(3-phenylpropylamino)-benzoate) prevented appearance of H(2)O(2)-induced high membrane permeability and cell shrinkage, suppressed H(2)O(2)-activated chloride currents and protected PC12 cells from apoptosis induced by H(2)O(2). The results suggest that chloride channels may contribute to H(2)O(2)-induced apoptosis by ways of elevation of membrane permeability and AVD in PC12 cells.

  4. Sodium selenite and vitamin E in preventing mercuric chloride induced renal toxicity in rats.

    PubMed

    Aslanturk, Ayse; Uzunhisarcikli, Meltem; Kalender, Suna; Demir, Filiz

    2014-08-01

    This study aims to investigate improving effects of sodium selenite and/or vitamin E on mercuric chloride-induced kidney impairments in rats. Wistar male rats were exposed either to sodium selenite (0.25mg/kgday), vitamin E (100mg/kgday), sodium selenite+vitamin E, mercuric chloride (1mg/kgday), sodium selenite+mercuric chloride, vitamin E+mercuric chloride and sodium selenite+vitamin E+mercuric chloride for 4weeks. Mercuric chloride exposure resulted in an increase in the uric acid, creatinine, blood urea nitrogen and malondialdehyde (MDA) levels and a decrease in the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Histopathological changes were detected in kidney tissues in mercuric chloride-treated groups. A significant decrease in the uric acid, creatinine, blood urea nitrogen and MDA levels and a significant increase in the SOD, CAT and GPx activities were observed in the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated groups. Conclusively, sodium selenite, vitamin E and vitamin E+sodium selenite significantly reduce mercuric chloride induced nephrotoxicity in rats, but not protect completely.

  5. Stress-induced cervical lesions.

    PubMed

    Braem, M; Lambrechts, P; Vanherle, G

    1992-05-01

    The increasing occurrence of dental lesions at the cervical surfaces requires more knowledge of the causes of the process. Acidic and abrasive mechanisms have clearly been documented as causes but the stress theory by Lee and Eakle is still controversial. This report describes several incidences of possible stress-induced lesions according to the characteristics described by Lee and Eakle. The occurrences of subgingival lesions lend credence to the stress-induction theory by exclusion of other superimposing etiologic factors. With the current concepts, a perceptive approach to the treatment of cervical lesions can be executed. PMID:1527763

  6. Aqueous chloride stress corrosion cracking of titanium: A comparison with environmental hydrogen embrittlement

    NASA Technical Reports Server (NTRS)

    Nelson, H. G.

    1973-01-01

    The physical characteristics of stress corrosion cracking of titanium in an aqueous chloride environment are compared with those of embrittlement of titanium by a gaseous hydrogen environment in an effort to help contribute to the understanding of the possible role of hydrogen in the complex stress corrosion cracking process. Based on previous studies, the two forms of embrittlement are shown to be similar at low hydrogen pressures (100 N/sqm) but dissimilar at higher hydrogen pressures. In an effort to quantify this comparison, tests were conducted in an aqueous chloride solution using the same material and test techniques as had previously been employed in a gaseous hydrogen environment. The results of these tests strongly support models based on hydrogen as the embrittling species in an aqueous chloride environment. Further, it is shown that if hydrogen is the causal species, the effective hydrogen fugacity at the surface of titanium exposed to an aqueous chloride environment is equivalent to a molecular hydrogen pressure of approximately 10 N/sqm.

  7. Antioxidant-Induced Stress

    PubMed Central

    Villanueva, Cleva; Kross, Robert D.

    2012-01-01

    Antioxidants are among the most popular health-protecting products, sold worldwide without prescription. Indeed, there are many reports showing the benefits of antioxidants but only a few questioning the possible harmful effects of these “drugs”. The normal balance between antioxidants and free radicals in the body is offset when either of these forces prevails. The available evidence on the harmful effects of antioxidants is analyzed in this review. In summary, a hypothesis is presented that “antioxidant-induced stress” results when antioxidants overwhelm the body’s free radicals. PMID:22408440

  8. Protective effect of a calcium channel blocker "diltiazem" on aluminum chloride-induced dementia in mice.

    PubMed

    Rani, Anu; Neha; Sodhi, Rupinder K; Kaur, Amanpreet

    2015-11-01

    Many studies report that heavy metals such as aluminum are involved in amyloid beta aggregation and neurotoxicity. Further, high concentration of aluminum in the brain deregulates calcium signaling which contributes to synaptic dysfunction and halts neuronal communication which ultimately leads to the development of Alzheimer's disease. Recently, diltiazem, a calcium channel blocker clinically used in angina, is reported to decrease amyloid beta production by inhibiting calcium influx, decreasing inflammation and oxidative stress. However, the probable role of this drug in aluminum chloride (AlCl3)-induced experimental dementia is yet to be explored. Therefore, the present study is designed to investigate the effect of AlCl3-induced dementia in mice. Morris water maze test and elevated plus maze were utilized to evaluate learning and memory. Various biochemical estimations including brain acetylcholinesterase activity (AChE), brain total protein, thiobarbituric acid-reactive species (TBARS) level, reduced glutathione (GSH) level, nitrate/nitrite, and superoxide dismutase (SOD) were measured. AlCl3 significantly impaired learning and memory and increased brain AChE, brain total protein, TBARS, and nitrate/nitrite and decreased brain GSH or SOD. On the other hand, treatment with diltiazem significantly reversed AlCl3-induced behavioral and biochemical deficits. The present study indicates the beneficial role of diltiazem in AlCl3-induced dementia.

  9. Stress proteins induced by arsenic.

    PubMed

    Del Razo, L M; Quintanilla-Vega, B; Brambila-Colombres, E; Calderón-Aranda, E S; Manno, M; Albores, A

    2001-12-01

    The elevated expression of stress proteins is considered to be a universal response to adverse conditions, representing a potential mechanism of cellular defense against disease and a potential target for novel therapeutics. Exposure to arsenicals either in vitro or in vivo in a variety of model systems has been shown to cause the induction of a number of the major stress protein families such as heat shock proteins (Hsp). Among them are members with low molecular weight, such as metallotionein and ubiquitin, as well as ones with masses of 27, 32, 60, 70, 90, and 110 kDa. In most of the cases, the induction of stress proteins depends on the capacity of the arsenical to reach the target, its valence, and the type of exposure, arsenite being the biggest inducer of most Hsp in several organs and systems. Hsp induction is a rapid dose-dependent response (1-8 h) to the acute exposure to arsenite. Thus, the stress response appears to be useful to monitor the sublethal toxicity resulting from a single exposure to arsenite. The present paper offers a critical review of the capacity of arsenicals to modulate the expression and/or accumulation of stress proteins. The physiological consequences of the arsenic-induced stress and its usefulness in monitoring effects resulting from arsenic exposure in humans and other organisms are discussed.

  10. Protective effect of resveratrol against aluminum chloride induced nephrotoxicity in rats

    PubMed Central

    Dera, Hussain S. Al

    2016-01-01

    Objectives: To investigate the potential protective effect of resveratrol (RES) on aluminum chloride (AlCl3)-induced nephrotoxicity in rats. Methods: This experimental study was conducted from April to June 2015 at the Medical College of King Khalid University, Abha, Kingdom of Saudi Arabia. The experiments were performed on 24 male Wistar rats. The rats were randomly allocated into 4 groups; 1) group A: control rats received only normal saline, 2) group B: received RES dissolved in normal saline, 3) group C: model group and received AlCl3 dissolved in normal saline and 4) group D: RES treated group and received concomitant doses of RES+AlCl3. All treatments were administered for consecutive 40 days. After 40 days of treatments, kidney function tests, oxidative stress parameters and histopathological assay were evaluated. Results: all findings clearly showed significant deteriorations in kidney function and architectures after AlCl3 exposure. This was accompanied by increased renal oxidative stress and inflammation suggesting strong pro-oxidant activity of AlCl3 in spite of its non-redox status. Resveratrol co-treatment with AlCl3 to the rats showed significant improvement in all biochemical and histological parameters related to kidney function and structure. Conclusion: The findings of the current study showed that RES pre-administration to rats ameliorates renal damage and improves renal function in AlCl3 intoxicated rats in a mechanism related to its antioxidant potential. PMID:27052279

  11. Antagonistic effect of magnesium chloride on the nickel chloride-induced inhibition of DNA replication in Chinese hamster ovary cells.

    PubMed

    Conway, K; Sen, P; Costa, M

    1986-06-01

    The degree of inhibition of semiconservative DNA replication induced by nickel chloride (NiCl2) was analyzed by radiolabeled-thymidine incorporation alone or with cesium chloride (CsCl) density gradient centrifugation. The onset and duration of this Ni2+-induced inhibition was time- and concentration-dependent, but the degree of inhibition was not. A maximal reduction in the rate of DNA synthesis was observed within the first hour of treatment with 2.5 mM NiCl2, which was the highest noncytotoxic concentration utilized. After six hours, 500 microM and 1 mM as well as 2.5 mM NiCl2 all produced the same 50% to 60% reduction in [3H]-thymidine incorporation into DNA. The inhibitory effect of nickel ions on DNA synthesis was reversible. The rate of DNA synthesis following a 500 microM or 1 mM NiCl2 treatment began to increase after washout of nickel, but a six-hour exposure of cells to 2.5 mM NiCl2 produced a sustained 50% to 60% suppression of DNA synthetic activity for at least 36 hours. At all concentrations of NiCl2 used in this study, some inhibition of DNA synthesis persisted for at least 48 hours, but by 72 hours after treatment, the rate of [3H]-thymidine incorporation was actually 10% above the control. Examination of autoradiographic slides of cells treated with 2.5 mM NiCl2 for six hours demonstrated a 60% reduction of silver grains, but there was no preferential reduction in the quantity of grains in the nucleolus or any other region. Cesium chloride density gradient analysis of the replication of nucleolar DNA in cells treated with 2.5 mM nickel supported the autoradiographic findings. The inhibitory effect of NiCl2 on DNA replication was prevented by the addition of magnesium chloride (MgCl2) to cells maintained in a simple salts/glucose medium (SGM). This effect did not appear to be due to an antagonism of the cellular uptake of nickel by Mg2+, since the maximally effective dose of Mg2+ reduced 63Ni2+ uptake by no more than 25% while the inhibition of

  12. Inhibition of Chloride Induced Crevice Corrosion in Alloy 22 by Fluoride Ions

    SciTech Connect

    Carranza, R M; Rodr?guez, M A; Rebak, R B

    2005-10-09

    Alloy 22 (N06022) is highly resistant to localized corrosion. Alloy 22 may be susceptible to crevice corrosion in pure chloride (Cl{sup -}) solutions under aggressive environmental conditions. The effect of the fluoride (F{sup -}) over the crevice corrosion induced by chloride ions is still not well established. The objective of the present work was to explore the crevice corrosion resistance of this alloy to different mixtures of fluorides and chlorides. Cyclic potentiodynamic polarization (CPP) tests were conducted in deaerated aqueous solutions of pure halide ions and also in different mixtures of chloride and fluoride at 90 C and pH 6. The range of chloride concentration [Cl{sup -}] was 0.001 M {le} [Cl{sup -}] {le} 1 M and the range of molar fluoride to chloride ratio [F{sup -}]/[Cl{sup -}] was 0.1 {le} [F{sup -}]/[Cl{sup -}] {le} 10. Results showed that Alloy 22 was susceptible to crevice corrosion in all the pure chloride solutions but not in the pure fluoride solutions. Fluoride ions showed an inhibitor behavior only in mixtures with a molar ratio [F{sup -}]/[Cl{sup -}] > 2. For mixtures with a molar ratio [F{sup -}]/[Cl{sup -}] of 7 and 10 the inhibition of crevice corrosion was complete.

  13. Electron microscopic observations of hepatic and subcutaneous hemangiosarcomas induced in mice exposed to vinyl chloride monomer.

    PubMed

    Suzuki, Y

    1981-01-01

    Both subcutaneous and hepatic hemangiosarcomas were induced in mice exposed to vinyl chloride monomer, and for the first time, the ultrastructure of hemangiosarcomas related to vinyl chloride exposure has been described. The subcutaneous hemangiosarcoma developed in a mouse's ear 29 weeks after exposure to 10 ppm vinyl chloride for 4 weeks, and the hepatic hemangiosarcoma was found in a mouse's liver at necropsy 56 weeks after exposure to 600 ppm vinyl chloride for 4 weeks. Both tumors showed a localized, cystic nodular appearance with a dark red tone. Histologically, an angiomatous architecture, the presence of neoplastic mesenchymal cell aggregates, focal necrosis, and hemorrhagic foci were common. Ultrastructurally, two neoplastic cell types, a mesenchymal and a well-differentiated endothelial cell type, were identified in both tumors. In addition, in the hepatic tumor, a pericyte-like neoplastic cell was also present. The incidence of hemangiosarcoma was much lower than that of lung tumors (alveologenic tumor) in mice exposed to vinyl chloride at the same concentrations for the same duration. This study suggests that there is no basic difference in ultrastructure between the vinyl chloride-induced hemangiosarcomas and hemangiosarcomas not related to this chemical exposure.

  14. Ameliorative Effect of Green Tea Catechin Against Cadmium Chloride-Induced Testicular Toxicity in Mice.

    PubMed

    Sharma, Priyanka; Goyal, Pradeep Kumar

    2015-01-01

    The present study was designed to evaluate the effect of green tea catechin (7500 µg/kg/animal/day) against cadmium-induced testicular dysfunctions and oxidative stress in the testes of mice. For this purpose, Swiss albino mice were divided into six groups: group I, negative control; group II, catechin-treated control; group III, cadmium chloride (CdCl2)-treated control; group IV, experimental group I; group V, experimental group II; and group VI, experimental group III. Animals from all of these groups were necropsied at various post-treatment intervals between 12 hours and 30 days for various biochemical alterations in the testes. CdCl2 intoxication resulted in a significant decline in testicular total proteins, cholesterol, and alkaline phosphatase, whereas acid phosphatase and lipid peroxidation exhibited a noticeable augmentation as compared to negative control. Catechin treatment effectively protected CdCl2-induced alterations in all such parameters throughout the experiment. Catechin was effective in reducing the CdCl2-induced augmentation of phase I (P450 and CYPB5) as well as phase II (DT-diaphorase and glutathione-S-transferase) enzymes in testes. Furthermore, CdCl2 intoxication was found to attenuate the antioxidant potential of testes, which was however augmented when supplemented with green tea extract. Compared to CdCl2-treated control mice, superoxide dismutase, glutathione peroxidase, glutathione, and catalase levels were significantly decreased in testes. Indeed, green tea catechin significantly increased testicular antioxidant enzymatic activities compared to those given CdCl2 alone. In conclusion, the use of green tea extract appeared to be beneficial to a great extent in inhibiting and restoring the testicular injuries induced by CdCl2 intoxication in mammals. PMID:26756426

  15. Ameliorative Effect of Green Tea Catechin Against Cadmium Chloride-Induced Testicular Toxicity in Mice.

    PubMed

    Sharma, Priyanka; Goyal, Pradeep Kumar

    2015-01-01

    The present study was designed to evaluate the effect of green tea catechin (7500 µg/kg/animal/day) against cadmium-induced testicular dysfunctions and oxidative stress in the testes of mice. For this purpose, Swiss albino mice were divided into six groups: group I, negative control; group II, catechin-treated control; group III, cadmium chloride (CdCl2)-treated control; group IV, experimental group I; group V, experimental group II; and group VI, experimental group III. Animals from all of these groups were necropsied at various post-treatment intervals between 12 hours and 30 days for various biochemical alterations in the testes. CdCl2 intoxication resulted in a significant decline in testicular total proteins, cholesterol, and alkaline phosphatase, whereas acid phosphatase and lipid peroxidation exhibited a noticeable augmentation as compared to negative control. Catechin treatment effectively protected CdCl2-induced alterations in all such parameters throughout the experiment. Catechin was effective in reducing the CdCl2-induced augmentation of phase I (P450 and CYPB5) as well as phase II (DT-diaphorase and glutathione-S-transferase) enzymes in testes. Furthermore, CdCl2 intoxication was found to attenuate the antioxidant potential of testes, which was however augmented when supplemented with green tea extract. Compared to CdCl2-treated control mice, superoxide dismutase, glutathione peroxidase, glutathione, and catalase levels were significantly decreased in testes. Indeed, green tea catechin significantly increased testicular antioxidant enzymatic activities compared to those given CdCl2 alone. In conclusion, the use of green tea extract appeared to be beneficial to a great extent in inhibiting and restoring the testicular injuries induced by CdCl2 intoxication in mammals.

  16. The calcium chloride-induced rodent model of abdominal aortic aneurysm.

    PubMed

    Wang, Yutang; Krishna, Smriti; Golledge, Jonathan

    2013-01-01

    Abdominal aortic aneurysm (AAA) affects ∼5% men aged over 65 years and is an important cause of death in this population. Research into AAA pathogenesis has been fuelled by the need to identify new diagnostic biomarkers and therapeutic targets for this disease. One animal model of AAA involves peri-vascular application of calcium chloride (CaCl(2)) onto the infra-renal aorta of mice and rats to induce extracellular matrix remodelling. Twenty-three studies assessing CaCl(2)-induced AAA and six studies assessing AAA induced by a modified CaCl(2) method were identified. In the current report the preparation and pathological features of this AAA model are discussed. We also compared this animal model to human AAA. CaCl(2)-induced AAA shows the following pathological characteristics typically found in human AAA: calcification, inflammatory cell infiltration, oxidative stress, neovascularisation, elastin degradation and vascular smooth muscle cell apoptosis. A number of mechanisms involved in CaCl(2)-induced AAA have been identified which may be relevant to the pathogenesis of human AAA. Key molecules include c-Jun N-terminal kinase, peroxisome proliferator-activated receptor-γ, chemokine (C-C motif) receptor 2, group x secretory phospholipase A2 and plasminogen. CaCl(2)-induced AAA does not display aortic thrombus, atherosclerosis and rupture which are classical features of human AAA. Advantages of the CaCl(2)-induced AAA technique include (1) it can be applied to wild type mice making assessment of transgenic rodent models more straight forward and rapid; and (2) CaCl(2)-induced AAAs are usually developed in the infra-renal abdominal aorta, which is the most common location of human AAA. Currently findings obtained from the CaCl(2)-induced AAA model or other animal models of AAA have not been translated into the human situation. It is hoped that this deficiency will be corrected over the next decade with a number of clinical trials currently examining novel

  17. Effects of heavy particle irradiation and diet on amphetamine- and lithium chloride-induced taste avoidance learning in rats

    NASA Technical Reports Server (NTRS)

    Rabin, Bernard M.; Shukitt-Hale, Barbara; Szprengiel, Aleksandra; Joseph, James A.

    2002-01-01

    Rats were maintained on diets containing either 2% blueberry or strawberry extract or a control diet for 8 weeks prior to being exposed to 1.5 Gy of 56Fe particles in the Alternating Gradient Synchrotron at Brookhaven National Laboratory. Three days following irradiation, the rats were tested for the effects of irradiation on the acquisition of an amphetamine- or lithium chloride-induced (LiCl) conditioned taste avoidance (CTA). The rats maintained on the control diet failed to show the acquisition of a CTA following injection of amphetamine. In contrast, the rats maintained on antioxidant diets (strawberry or blueberry extract) continued to show the development of an amphetamine-induced CTA following exposure to 56Fe particles. Neither irradiation nor diet had an effect on the acquisition of a LiCl-induced CTA. The results are interpreted as indicating that oxidative stress following exposure to 56Fe particles may be responsible for the disruption of the dopamine-mediated amphetamine-induced CTA in rats fed control diets; and that a reduction in oxidative stress produced by the antioxidant diets functions to reinstate the dopamine-mediated CTA. The failure of either irradiation or diet to influence LiCl-induced responding suggests that oxidative stress may not be involved in CTA learning following injection of LiCl.

  18. Chloride inhibition of nitrite-induced methemoglobinemia in channel catfish (Ictalurus punctatus)

    USGS Publications Warehouse

    Tomasso, J.R.; Simco, B.A.; Davis, K.B.

    1979-01-01

    Exposure of channel catfish (Ictalurus punctatus) fingerlings for 24?h to 1.0, 2.5, and 5.0?mg/L nitrite (pH?=?7; hardness?=?40?mg/L; temperature?=?22–25 °C) produced methemoglobin levels of 20.7?±?1.9%, 59.8?±?1.9%, and 77.4?±?1.4% (SE), respectively. However, methemoglobin levels were not elevated when fish were simultaneously exposed to 1.0, 2.5, and 5.0?mg/L nitrite and 25, 50, and 100?mg/L sodium chloride, respectively. Acclimation to sodium chloride for 24?h before exposure to nitrite did not enhance the inhibitory action of sodium chloride. Fish exposed to 5?mg/L nitrite for 5?h developed 42.5?±?3.8% methemoglobin. When transferred to water containing 5?mg/L nitrite and 250?mg/L sodium chloride, methemoglobin levels returned to normal within 24?h. Environmental chloride probably inhibits methemoglobin formation by competing with nitrite for entrance into the gills of the fish. An ionic ratio of 16 Cl- to 1 NO2- is capable of complete suppression of nitrite-induced methemoglobin formation. Bicarbonate ion present in the test water (1?meq/L) may also have contributed to the inhibitive action of chloride.

  19. Effect of the CYP2E1 genotype on vinyl chloride monomer-induced liver fibrosis among polyvinyl chloride workers.

    PubMed

    Hsieh, Hui-I; Chen, Pau-Chung; Wong, Ruey-Hong; Wang, Jung-Der; Yang, Pei-Ming; Cheng, Tsun-Jen

    2007-09-24

    Although a relationship between vinyl chloride monomer (VCM) and liver cirrhosis has been reported, the underlying mechanisms are not clear. Cytochrome P450 2E1 (CYP2E1), aldehyde dehydrogenase 2 (ALDH2) and glutathione S-transferase theta 1 (GSTT1) enzymes are involved in activation and detoxification of VCM, and thus may be important determinants of interindividual susceptibility to VCM-induced liver damage, including liver cirrhosis. The objective of this study was to evaluate if metabolizing genetic polymorphisms could modify individual susceptibility to liver fibrosis of the VCM exposure. CYP2E1, ALDH2, and GSTT1 polymorphisms were determined by the PCR-RFLP method among 320 workers who were employed in five polyvinyl chloride manufacturing plants. Cumulative VCM exposure levels for study subjects were calculated using a job exposure matrix model. Thirteen workers were diagnosed as having liver fibrosis by using ultrasonography. We observed a dose-response trend between VCM exposure and liver fibrosis. Regarding the results on genetic polymorphisms, CYP2E1 c2c2 genotype showed a significant increase in the risk of liver fibrosis as compared to those with CYP2E1 c1c1 or c1c2 genotypes. No differences were observed between GSTT1 and ALDH2 genotypes and liver fibrosis. In summary, our result suggests that genetic polymorphism in CYP2E1 may be responsible for individual differences in susceptibility to liver fibrosis with regard to chronic VCM exposure. Thus, polymorphism analysis of metabolizing enzymes might be useful in the risk assessment of liver damage in workers with VCM exposure.

  20. Biochemical alterations during swimming induced stress.

    PubMed

    Aruj, N; Sharafatullah, T; Najam, R; Ahmed, S P; Ahmad, S I

    1994-07-01

    Stress can be defined as any stimulus that creates an imbalance in the internal environment. Hypothalamus has sensors that detect changes produced in the body. Stress can cause diseases by altering immune system, cardiovascular System neurotransmitter and neuroendocrine functions. Present study is designed to evaluate the effect of stress on few biochemical parameters during swimming induced stress. Significant changes have been observed especially in lipid profile. Corticosterone was also evaluated as reliable stress marker.

  1. Effects of antiemetics on the acquisition and recall of radiation- and lithium chloride-induced conditioned taste aversions

    SciTech Connect

    Rabin, B.M.; Hunt, W.A.

    1983-04-01

    A series of experiments were run to evaluate the effect of antiemetics on the acquisition and recall of a conditioned taste aversion induced by exposure to ionizing radiation or by injection of lithium chloride. Groups of male rats were exposed to 100 rad gamma radiation or 3 mEq/kg lithium chloride following consumption of a 10% sucrose solution. They were then injected with saline or with one of three antiemetics (prochlorperazine, trimethobenzamide, or cyclizine) at dose levels that have been reported to be effective in attenuating a previously acquired lithium chloride-induced taste aversion. The pretreatments with antiemetics had no effect on the acquisition or recall of either the lithium chloride- or radiation-induced taste aversion. The data suggest that antiemetics do not disrupt lithium chloride-induced taste aversions as previously reported, nor do they effect radiation-induced taste aversion learning.

  2. Chloride-Inducible Expression Vector for Delivery of Antimicrobial Peptides Targeting Antibiotic-Resistant Enterococcus faecium

    PubMed Central

    Geldart, Kathryn; Borrero, Juan

    2015-01-01

    Antibiotic-resistant enterococcal infections are a major concern in hospitals where patients with compromised immunity are readily infected. Enterococcus faecium bacteria are of particular interest as these pathogens account for over 80% of vancomycin-resistant enterococcal infections. Antimicrobial peptides (AMPs) produced at the site of infection by engineered bacteria may offer a potential alternative to traditional antibiotics for the treatment of resistant bacteria such as E. faecium. For this mode of delivery to be effective, it is essential to identify a suitable protein expression system that can be used in the desired delivery bacterium. In this study, we describe a promising chloride-inducible promoter and its application in the bacterial delivery of AMPs from Lactococcus lactis to reduce counts of E. faecium bacteria in vitro. Reporter gene studies show that at chloride concentrations found within the human intestines, the chloride-inducible promoter exhibits high levels of protein expression compared to those of the commonly used nisin-inducible promoter. These results indicate that this system is powerful and would not require the exogenous administration of an inducer molecule. In its application for AMP production against E. faecium in vitro, L. lactis producing AMPs under the chloride promoter rapidly decreased E. faecium counts by nearly 10,000-fold. As an extension of this application, we also demonstrate the potential in using this type of delivery system in combination with traditional antibiotics to slow the development of resistance. Collectively, this study shows the promise of using a chloride-inducible promoter for the bacterial delivery of AMPs in the body for the treatment of vancomycin-resistant enterococci (VRE) and other antibiotic-resistant bacteria. PMID:25841002

  3. Chloride-Inducible Expression Vector for Delivery of Antimicrobial Peptides Targeting Antibiotic-Resistant Enterococcus faecium.

    PubMed

    Geldart, Kathryn; Borrero, Juan; Kaznessis, Yiannis N

    2015-06-01

    Antibiotic-resistant enterococcal infections are a major concern in hospitals where patients with compromised immunity are readily infected. Enterococcus faecium bacteria are of particular interest as these pathogens account for over 80% of vancomycin-resistant enterococcal infections. Antimicrobial peptides (AMPs) produced at the site of infection by engineered bacteria may offer a potential alternative to traditional antibiotics for the treatment of resistant bacteria such as E. faecium. For this mode of delivery to be effective, it is essential to identify a suitable protein expression system that can be used in the desired delivery bacterium. In this study, we describe a promising chloride-inducible promoter and its application in the bacterial delivery of AMPs from Lactococcus lactis to reduce counts of E. faecium bacteria in vitro. Reporter gene studies show that at chloride concentrations found within the human intestines, the chloride-inducible promoter exhibits high levels of protein expression compared to those of the commonly used nisin-inducible promoter. These results indicate that this system is powerful and would not require the exogenous administration of an inducer molecule. In its application for AMP production against E. faecium in vitro, L. lactis producing AMPs under the chloride promoter rapidly decreased E. faecium counts by nearly 10,000-fold. As an extension of this application, we also demonstrate the potential in using this type of delivery system in combination with traditional antibiotics to slow the development of resistance. Collectively, this study shows the promise of using a chloride-inducible promoter for the bacterial delivery of AMPs in the body for the treatment of vancomycin-resistant enterococci (VRE) and other antibiotic-resistant bacteria. PMID:25841002

  4. Maternal restraint stress delays maturation of cation-chloride cotransporters and GABAA receptor subunits in the hippocampus of rat pups at puberty.

    PubMed

    Veerawatananan, Bovorn; Surakul, Pornprom; Chutabhakdikul, Nuanchan

    2016-06-01

    The GABAergic synapse undergoes structural and functional maturation during early brain development. Maternal stress alters GABAergic synapses in the pup's brain that are associated with the pathophysiology of neuropsychiatric disorders in adults; however, the mechanism for this is still unclear. In this study, we examined the effects of maternal restraint stress on the development of Cation-Chloride Cotransporters (CCCs) and the GABAA receptor α1 and α5 subunits in the hippocampus of rat pups at different postnatal ages. Our results demonstrate that maternal restraint stress induces a transient but significant increase in the level of NKCC1 (Sodium-Potassium Chloride Cotransporter 1) only at P14, followed by a brief, yet significant increase in the level of KCC2 (Potassium-Chloride Cotransporter 2) at P21, which then decreases from P28 until P40. Thus, maternal stress alters NKCC1 and KCC2 ratio in the hippocampus of rat pups, especially during P14 to P28. Maternal restraint stress also caused biphasic changes in the level of GABAA receptor subunits in the pup's hippocampus. GABAA receptor α1 subunit gradually increased at P14 then decreased thereafter. On the contrary, GABAA receptor α5 subunit showed a transient decrease followed by a long-term increase from P21 until P40. Altogether, our study suggested that the maternal restraint stress might delay maturation of the GABAergic system by altering the expression of NKCC1, KCC2 and GABAA receptor α1 and α5 subunits in the hippocampus of rat pups. These changes demonstrate the dysregulation of inhibitory neurotransmission during early life, which may underlie the pathogenesis of psychiatric diseases at adolescence. PMID:26844244

  5. Maternal restraint stress delays maturation of cation-chloride cotransporters and GABAA receptor subunits in the hippocampus of rat pups at puberty

    PubMed Central

    Veerawatananan, Bovorn; Surakul, Pornprom; Chutabhakdikul, Nuanchan

    2015-01-01

    The GABAergic synapse undergoes structural and functional maturation during early brain development. Maternal stress alters GABAergic synapses in the pup's brain that are associated with the pathophysiology of neuropsychiatric disorders in adults; however, the mechanism for this is still unclear. In this study, we examined the effects of maternal restraint stress on the development of Cation-Chloride Cotransporters (CCCs) and the GABAA receptor α1 and α5 subunits in the hippocampus of rat pups at different postnatal ages. Our results demonstrate that maternal restraint stress induces a transient but significant increase in the level of NKCC1 (Sodium–Potassium Chloride Cotransporter 1) only at P14, followed by a brief, yet significant increase in the level of KCC2 (Potassium-Chloride Cotransporter 2) at P21, which then decreases from P28 until P40. Thus, maternal stress alters NKCC1 and KCC2 ratio in the hippocampus of rat pups, especially during P14 to P28. Maternal restraint stress also caused biphasic changes in the level of GABAA receptor subunits in the pup's hippocampus. GABAA receptor α1 subunit gradually increased at P14 then decreased thereafter. On the contrary, GABAA receptor α5 subunit showed a transient decrease followed by a long-term increase from P21 until P40. Altogether, our study suggested that the maternal restraint stress might delay maturation of the GABAergic system by altering the expression of NKCC1, KCC2 and GABAA receptor α1 and α5 subunits in the hippocampus of rat pups. These changes demonstrate the dysregulation of inhibitory neurotransmission during early life, which may underlie the pathogenesis of psychiatric diseases at adolescence. PMID:26844244

  6. Effect of sodium chloride and cadmium on the growth, oxidative stress and antioxidant enzyme activities of Zygosaccharomyces rouxii

    NASA Astrophysics Data System (ADS)

    Li, Chunsheng; Xu, Ying; Jiang, Wei; Lv, Xin; Dong, Xiaoyan

    2014-06-01

    Zygosaccharomyces rouxii is a salt-tolerant yeast species capable of removing cadmium (Cd) pollutant from aqueous solution. Presently, the physiological characteristics of Z. rouxii under the stress of sodium chloride (NaCl) and Cd are poorly understood. This study investigated the effects of NaCl and Cd on the growth, oxidative stress and antioxidant enzyme activities of Z. rouxii after stress treatment for 24 h. Results showed that NaCl or Cd alone negatively affected the growth of Z. rouxii, but the growth-inhibiting effect of Cd on Z. rouxii was reduced in the presence of NaCl. Flow cytometry assay showed that under Cd stress, NaCl significantly reduced the production of reactive oxygen species (ROS) and cell death of Z. rouxii compared with those in the absence of NaCl. The activities of superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) of Z. rouxii were significantly enhanced by 2%-6% NaCl, which likely contributed to the high salt tolerance of Z. rouxii. The POD activity was inhibited by 20 mg L-1 Cd while the SOD and CAT activities were enhanced by 8 mg L-1 Cd and inhibited by 20 mg L-1 or 50 mg L-1 Cd. The inhibitory effect of high-level Cd on the antioxidant enzyme activities of Z. rouxii was counteracted by the combined use of NaCl, especially at 6%. This probably accounted for the decrease in Cd-induced ROS production and cell death of Z. rouxii after incubation with NaCl and Cd. Our work provided physiological clues as to the use of Z. rouxii as a biosorbent for Cd removal from seawater and liquid highly salty food.

  7. Stress corrosion cracking and life prediction evaluation of austenitic stainless steels in calcium chloride solution

    SciTech Connect

    Leinonen, H.

    1996-05-01

    The stress corrosion cracking (SCC) susceptibility of austenitic stainless steels (SS) in calcium chloride solutions was studied using a constant-load method. Initiation and propagation of stress corrosion cracks were examined using fractography. The distribution of cracks was classified. A physical cracking was introduced, and creep deformation measurements were performed. The steady-state strain rate obtained from the corrosion elongation curve (elongation-vs-time curve) showed a linear function of time to failure (t{sub f}). This implied that {var_epsilon}{sub ss} can be applied as a parameter for prediction of t{sub f}. Furthermore, {var_epsilon}{sub ss} below which no failure occurs within a laboratory time scale was estimated. Based on results obtained, the critical values of stress below which no SCC occurred were evaluated. Based upon creep measurements in a noncorrosive environment, the influence of environment on {var_epsilon}{sub ss} was more than fivefold. Cracking characteristics were divided into three categories according to the crack initiation distribution. Transgranular cracking predominated at relatively low {sigma} and {var_epsilon}{sub ss}.

  8. On the stress corrosion cracking of lean duplex steel in chloride environment

    NASA Astrophysics Data System (ADS)

    Tayyaba, Qanita; Farooq, Hina; Shahid, Muhammad; Jadoon, Ammer Khan; Shahzad, M.; Qureshi, A. H.

    2014-06-01

    Duplex stainless steel having attractive combination of austenitic and ferritic properties is being used in industry such as petrochemical, pulp and paper mills. In this study, the corrosion and stress corrosion behavior of duplex stainless steel in 3.5% sodium chloride environment was investigated by weight loss measurements, electrochemical DC testing and slow strain rate test (SSRT). Weight loss data showed no significant corrosion after 1700 hours. Electrochemical polarization test in 3.5% NaCl solution exhibited a uniform corrosion rate of 0.008 mpy (calculated using Tafel analysis) showing passivity in the range of 735-950 mV. A comparison of the slow strain rate test in 3.5% NaCl solution with air shows almost a similar stress strain curve for duplex stainless steel. In comparison, the stress strain curves for 0.15% carbon steel show a loss of about 25% tensile elongation for the same comparison. The excellent corrosion and especially resistance to localized corrosion (pitting) is responsible for no loss of ductility in duplex stainless steel.

  9. Genetic susceptibility to scleroderma-like syndrome induced by vinyl chloride.

    PubMed

    Black, C M; Welsh, K I; Walker, A E; Bernstein, R M; Catoggio, L J; McGregor, A R; Jones, J K

    1983-01-01

    Vinyl chloride (VC) monomer can induce a scleroderma-like syndrome in a proportion of workers exposed to it during production of polyvinyl chloride. As part of a 5-year follow-up study HLA A, B, and DR antigens and anti-centromere and anti-scleroderma-70 antibodies were determined in 44 such workers. 21 of these had severe and 23 mild forms of vinyl-chloride disease. 50 patients with "classical" scleroderma and 148 healthy hospital workers acted as controls. 11 of the 21 patients classified as having severe VC disease were DR3 positive, and 8 of these had both B8 and DR3 antigens. None of the 23 patients with mild disease carried either antigen. The HLA-antigen frequencies in VC disease mirrored those found in scleroderma (raised DR5 frequency and increased linkage disequilibrium between B8 and DR3). There were, however, significant differences in the frequency of autoantibodies in the two conditions.

  10. Sodium chloride-induced self-assembly of microfibers from nanofiber components.

    PubMed

    Iwaura, Rika; Minamikawa, Hiroyuki; Shimizu, Toshimi

    2004-09-15

    Self-assembly of a nucleotide bolaamphiphile, terminated with two nucleotide moieties including thymine, deoxyribose, and phosphodiester at both ends of the C20 oligomethylene chain, in sodium chloride aqueous solutions has been studied by SEM, LSM, FE-SEM, micro-FTIR, and zeta-potential measurement. The self-assembly behavior of the nucleotide bolaamphiphile was strongly dependent on the concentration of sodium chloride added. The nucleotide bolaamphiphile was found to hierarchically self-assemble to form micrometer-sized fibers (microfibers) consisting of bundles of entangled nanometer-sized fibers (nanofibers) under certain conditions of sodium chloride concentration (approximately 44 mM). The zeta-potential measurement suggested that the surface-charge tuning of the nanofibers induce the hierarchical self-assembly of the microfibers.

  11. Chloride-induced shape transformation of silver nanoparticles in a water environment.

    PubMed

    Zhang, Lan; Li, Xin; He, Rong; Wu, Lijun; Zhang, Liyun; Zeng, Jie

    2015-09-01

    The effects of chloride on dissolution and toxicity of silver nanoparticles (AgNPs) have been well studied. However, their intermediate shapes during the transition have not been illustrated to-date. Herein, the chloride-induced shape transformation process of AgNPs under long-term, low-concentration conditions is explored. A unique triangular Ag-AgCl heterostructure is observed. The structure then evolves into a symmetric hexapod and finally into a smaller AgNP. This transformation process could be affected by other environmental conditions, such as 0.4 mg/mL humic acid, 5% surfactants and 1 mg/mL bovine serum albumin protein. Our results offer new knowledge regarding the shape transformation process of AgNPs in the presence of chloride, which can be valuable in relevant studies concerning the effect of water chemistry on the behavior of AgNPs. PMID:25965964

  12. Coagulation of β-conglycinin, glycinin and isoflavones induced by calcium chloride in soymilk.

    PubMed

    Hsiao, Yu-Hsuan; Yu, Chia-Jung; Li, Wen-Tai; Hsieh, Jung-Feng

    2015-08-11

    The coagulation of β-conglycinin (7S), glycinin (11S) and isoflavones induced by calcium chloride was investigated. Approximately 92.6% of the soymilk proteins were coagulated into the soymilk pellet fraction (SPF) after the addition of 5 mM calcium chloride. SDS-PAGE and two-dimensional electrophoresis analysis indicated that most of the 7S (α', α and β), 11S acidic (A1a, A1b, A2, A3 and A4) and 11S basic (B1a) proteins in the SSF were coagulated into the SPF after treatment with 5 mM calcium chloride. Isoflavones, including daidzein and genistein, were also coagulated into the SPF after the addition of 5 mM calcium chloride. The amounts of daidzein and genistein in the SSF decreased to 39.4 ± 1.6 and 11.8 ± 7.0%, respectively. HPLC analysis suggested that daidzein and genistein were bound with 7S and 11S proteins and then were coprecipitated into the SPF by 5 mM calcium chloride.

  13. Coagulation of β-conglycinin, glycinin and isoflavones induced by calcium chloride in soymilk

    NASA Astrophysics Data System (ADS)

    Hsiao, Yu-Hsuan; Yu, Chia-Jung; Li, Wen-Tai; Hsieh, Jung-Feng

    2015-08-01

    The coagulation of β-conglycinin (7S), glycinin (11S) and isoflavones induced by calcium chloride was investigated. Approximately 92.6% of the soymilk proteins were coagulated into the soymilk pellet fraction (SPF) after the addition of 5 mM calcium chloride. SDS-PAGE and two-dimensional electrophoresis analysis indicated that most of the 7S (α’, α and β), 11S acidic (A1a, A1b, A2, A3 and A4) and 11S basic (B1a) proteins in the SSF were coagulated into the SPF after treatment with 5 mM calcium chloride. Isoflavones, including daidzein and genistein, were also coagulated into the SPF after the addition of 5 mM calcium chloride. The amounts of daidzein and genistein in the SSF decreased to 39.4 ± 1.6 and 11.8 ± 7.0%, respectively. HPLC analysis suggested that daidzein and genistein were bound with 7S and 11S proteins and then were coprecipitated into the SPF by 5 mM calcium chloride.

  14. Interactive role of nitric oxide and calcium chloride in enhancing tolerance to salt stress.

    PubMed

    Khan, M Nasir; Siddiqui, Manzer H; Mohammad, Firoz; Naeem, M

    2012-12-01

    Nitric oxide (NO), a small diffusible, ubiquitous bioactive molecule, acts as prooxidant as well as antioxidant, and also regulates remarkable spectrum of plant cellular mechanisms. The present work was undertaken to investigate the role of nitric oxide donor sodium nitroprusside (SNP) and/or calcium chloride (CaCl(2)) in the tolerance of excised mustard leaves to salt stress. After 24h, salt stressed leaves treated with SNP and/or CaCl(2), showed an improvement in the activities of carbonic anhydrase (CA) and nitrate reductase (NR), and leaf chlorophyll (Chl) content, leaf relative water content (LRWC) and leaf ion concentration as compared with the leaves treated with NaCl only. Salinity stress caused a significant increase in H(2)O(2) content and membrane damage which is witnessed by enhanced levels of thiobarbituric acid reactive substances (TBARS) and electrolyte leakage. By contrast, such increases were blocked by the application of 0.2mM SNP and 10mM CaCl(2) to salt stressed leaves. Application of SNP and/or CaCl(2) alleviated NaCl stress by enhancing the activities of antioxidative enzymes viz. superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX) and glutathione reductase (GR) and by enhancing proline (Pro) and glycinebetaine (GB) accumulation with a concomitant decrease in H(2)O(2) content, TBARS and electrolyte leakage, which is manifested in the tolerance of plants to salinity stress. Moreover, application of SNP with CaCl(2) was more effective to reduce the detrimental effects of NaCl stress on excised mustard leaves. In addition to this, ameliorating effect of SNP was not effective in presence of NO scavenger cPTIO [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide]. To put all these in a nut shell, the results advocate that SNP in association with CaCl(2) plays a role in enhancing the tolerance of plants to salt stress by improving antioxidative defence system, osmolyte accumulation and ionic

  15. Corrosion Product Film-Induced Stress Facilitates Stress Corrosion Cracking

    PubMed Central

    Wang, Wenwen; Zhang, Zhiliang; Ren, Xuechong; Guan, Yongjun; Su, Yanjing

    2015-01-01

    Finite element analyses were conducted to clarify the role of corrosion product films (CPFs) in stress corrosion cracking (SCC). Flat and U-shaped edge-notched specimens were investigated in terms of the CPF-induced stress in the metallic substrate and the stress in the CPF. For a U-shaped edge-notched specimen, the stress field in front of the notch tip is affected by the Young’s modulus of the CPF and the CPF thickness and notch geometry. The CPF-induced tensile stress in the metallic substrate is superimposed on the applied load to increase the crack tip strain and facilitate localized plasticity deformation. In addition, the stress in the CPF surface contributes to the rupture of the CPFs. The results provide physical insights into the role of CPFs in SCC. PMID:26066367

  16. Effect of cadmium chloride exposure during the induction of collagen induced arthritis.

    PubMed

    Ansari, Md Meraj; Neha; Khan, Haider A

    2015-08-01

    The precise cause of autoimmune diseases such as rheumatoid arthritis remains uncertain. Collagen induced arthritis (CIA) in animals is the most commonly used model of human rheumatoid arthritis (RA). Exposure of humans and animals to toxic metals is widespread. Cadmium is one of the most prevalent nephrotoxic heavy metal, but it may cause other systemic toxicity as well. Cadmium may cause adverse health effects by impairment of the immune systems and induction of reactive oxygen species. Since rheumatoid arthritis pathogenesis involve immune system disorder and chronic inflammation, the present study has been designed to find out the effect of cadmium chloride exposure on clinical manifestation of development of collagen induced rheumatoid arthritis. Arthritis was induced in rats by intradermal injection of emulsion of type II collagen in Complete Freund's Adjuvant. Rats were treated with cadmium chloride dissolved in drinking water at concentrations of 5ppm and 50ppm for 21 days from day of immunization. The effects of cadmium in the rats were assessed by biochemical parameters (articular elastase, articular nitrite, lipid peroxidation, reduced glutathione, catalase and superoxide dismutase) histopathological analysis and immunohistochemical expression of pro-inflammatory cytokines in rat joint tissue. Histopathological changes further confirmed the biochemical and immunohistochemical results. Our results suggest that exposure to cadmium chloride during the induction phase of collagen induced arthritis abrogate disease development at lower dose whereas exacerbates at higher dose in Wistar rats. PMID:26070417

  17. A small synthetic molecule functions as a chloride-bicarbonate dual-transporter and induces chloride secretion in cells.

    PubMed

    Liu, Peng-Yun; Li, Shing-To; Shen, Fang-Fang; Ko, Wing-Hung; Yao, Xiao-Qiang; Yang, Dan

    2016-05-31

    A C2 symmetric small molecule composed of l-phenylalanine and isophthalamide was found to function as a Cl(-)/HCO3(-) dual transporter and self-assemble into chloride channels. In Ussing-chamber based short-circuit current measurements, this molecule elicited chloride-dependent short-circuit current (Isc) increase in both Calu-3 cell and CFBE41o-cell (with F508del mutant CFTR) monolayers. PMID:27188496

  18. A possible role of Aspergillus niger mitochondrial cytochrome c in malachite green reduction under calcium chloride stress.

    PubMed

    Gomaa, Ola M; Selim, Nabila S; Linz, John E

    2013-01-01

    In previous work, decolorization of malachite green (MG) was studied in Aspergillus niger in the presence and absence of calcium chloride stress. Decolorization took place within 24 h, and a signal transduction process that initiated MG decolorization was suggested to be involved. In the present study, further investigation of the relationship between calcium chloride stress and enhanced MG biodegradation was conducted at the sub-cellular level. MG-NADH reductase activity, a key enzyme in MG decolorization, was produced as decolorization commenced, and enzyme activity increased threefold upon exposure to calcium chloride. Inhibitors of cytochrome p450, Ca(2+) channel activity as well as activity of the signaling protein phosphoinositide 3-kinase were tested. All three activities were inhibited to different extents resulting in reduced MG decolorization. Spectral analysis of the mitochondrial fraction showed a heme signal at 405 nm and A405/A280 ratio that is characteristic of the porphoryin ring of cytochromes. There were no peaks detected for cytochromes a or b, but a shoulder appearing at 550 nm was observed, which suggested that cytochrome c is involved; the absorbance for cytochrome c doubled after calcium chloride stress supporting this idea. MG decolorization took place via a series of demethylation steps, and cytotoxicity analysis revealed a decrease in the toxicity associated with generation of leucomalachite green.

  19. Genoprotective effect of hyaluronic acid against benzalkonium chloride-induced DNA damage in human corneal epithelial cells

    PubMed Central

    Wu, Han; Zhang, Huina; Wang, Changjun; Wu, Yihua; Xie, Jiajun; Jin, Xiuming; Yang, Jun

    2011-01-01

    Purpose The aim of this study was to investigate hyaluronic acid (HA) protection on cultured human corneal epithelial cells (HCEs) against benzalkonium chloride (BAC)-induced DNA damage and intracellular reactive oxygen species (ROS) increase. Methods Cells were incubated with different concentrations of BAC with or without the presence of 0.2% HA for 30 min. DNA damage to HCEs was examined by alkaline comet assay and by immunofluorescence microscopic detection of the phosphorylated form of histone variant H2AX (γH2AX) foci. ROS production was assessed by the fluorescent probe, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). Cell apoptosis was determined with annexin V staining by flow cytometry. Results HA significantly reduced BAC-induced DNA damage as indicated by the tail length (TL) and tail moment (TM) of alkaline comet assay and by γH2AX foci formation, respectively. Moreover, HA significantly decreased BAC-induced ROS increase and cell apoptosis. However, exposure to HA alone did not produce any significant change in DNA damage, ROS generation, or cell apoptosis. Conclusions BAC could induce DNA damage and cell apoptosis in HCEs, probably through increasing oxidative stress. Furthermore, HA was an effective protective agent that had antioxidant properties and could decrease DNA damage and cell apoptosis induced by BAC. PMID:22219631

  20. Selective Inducible Nitric Oxide Synthase Inhibitor Reversed Zinc Chloride-Induced Spatial Memory Impairment via Increasing Cholinergic Marker Expression.

    PubMed

    Tabrizian, Kaveh; Azami, Kian; Belaran, Maryam; Soodi, Maliheh; Abdi, Khosrou; Fanoudi, Sahar; Sanati, Mehdi; Mottaghi Dastjerdi, Negar; Soltany Rezaee-Rad, Mohammad; Sharifzadeh, Mohammad

    2016-10-01

    Zinc, an essential micronutrient and biochemical element of the human body, plays structural, catalytic, and regulatory roles in numerous physiological functions. In the current study, the effects of a pretraining oral administration of zinc chloride (10, 25, and 50 mg/kg) for 14 consecutive days and post-training bilateral intra-hippocampal infusion of 1400W as a selective inducible nitric oxide synthase (iNOS) inhibitor (10, 50, and 100 μM/side), alone and in combination, on the spatial memory retention in Morris water maze (MWM) were investigated. Animals were trained for 4 days and tested 48 h after completion of training. Also, the molecular effects of these compounds on the expression of choline acetyltransferase (ChAT), as a cholinergic marker in the CA1 region of the hippocampus and medial septal area (MSA), were evaluated. Behavioral and molecular findings of this study showed that a 2-week oral administration of zinc chloride (50 mg/kg) impaired spatial memory retention in MWM and decreased ChAT expression. Immunohistochemical analysis of post-training bilateral intra-hippocampal infusion of 1400W revealed a significant increase in ChAT immunoreactivity. Furthermore, post-training bilateral intra-hippocampal infusion of 1400W into the CA1 region of the hippocampus reversed zinc chloride-induced spatial memory impairment in MWM and significantly increased ChAT expression in comparison with zinc chloride-treated animals. Taken together, these results emphasize the role of selective iNOS inhibitors in reversing zinc chloride-induced spatial memory deficits via modulation of cholinergic marker expression.

  1. The Trier Social Stress Test protocol for inducing psychological stress.

    PubMed

    Birkett, Melissa A

    2011-10-19

    This article demonstrates a psychological stress protocol for use in a laboratory setting. Protocols that allow researchers to study the biological pathways of the stress response in health and disease are fundamental to the progress of research in stress and anxiety. Although numerous protocols exist for inducing stress response in the laboratory, many neglect to provide a naturalistic context or to incorporate aspects of social and psychological stress. Of psychological stress protocols, meta-analysis suggests that the Trier Social Stress Test (TSST) is the most useful and appropriate standardized protocol for studies of stress hormone reactivity. In the original description of the TSST, researchers sought to design and evaluate a procedure capable of inducing a reliable stress response in the majority of healthy volunteers. These researchers found elevations in heart rate, blood pressure and several endocrine stress markers in response to the TSST (a psychological stressor) compared to a saline injection (a physical stressor). Although the TSST has been modified to meet the needs of various research groups, it generally consists of a waiting period upon arrival, anticipatory speech preparation, speech performance, and verbal arithmetic performance periods, followed by one or more recovery periods. The TSST requires participants to prepare and deliver a speech, and verbally respond to a challenging arithmetic problem in the presence of a socially evaluative audience. Social evaluation and uncontrollability have been identified as key components of stress induction by the TSST. In use for over a decade, the goal of the TSST is to systematically induce a stress response in order to measure differences in reactivity, anxiety and activation of the hypothalamic-pituitary-adrenal (HPA) or sympathetic-adrenal-medullary (SAM) axis during the task. Researchers generally assess changes in self-reported anxiety, physiological measures (e.g. heart rate), and

  2. Stress induced obesity: lessons from rodent models of stress

    PubMed Central

    Patterson, Zachary R.; Abizaid, Alfonso

    2013-01-01

    Stress was once defined as the non-specific result of the body to any demand or challenge to homeostasis. A more current view of stress is the behavioral and physiological responses generated in the face of, or in anticipation of, a perceived threat. The stress response involves activation of the sympathetic nervous system and recruitment of the hypothalamic-pituitary-adrenal (HPA) axis. When an organism encounters a stressor (social, physical, etc.), these endogenous stress systems are stimulated in order to generate a fight-or-flight response, and manage the stressful situation. As such, an organism is forced to liberate energy resources in attempt to meet the energetic demands posed by the stressor. A change in the energy homeostatic balance is thus required to exploit an appropriate resource and deliver useable energy to the target muscles and tissues involved in the stress response. Acutely, this change in energy homeostasis and the liberation of energy is considered advantageous, as it is required for the survival of the organism. However, when an organism is subjected to a prolonged stressor, as is the case during chronic stress, a continuous irregularity in energy homeostasis is considered detrimental and may lead to the development of metabolic disturbances such as cardiovascular disease, type II diabetes mellitus and obesity. This concept has been studied extensively using animal models, and the neurobiological underpinnings of stress induced metabolic disorders are beginning to surface. However, different animal models of stress continue to produce divergent metabolic phenotypes wherein some animals become anorexic and lose body mass while others increase food intake and body mass and become vulnerable to the development of metabolic disturbances. It remains unclear exactly what factors associated with stress models can be used to predict the metabolic outcome of the organism. This review will explore a variety of rodent stress models and discuss the

  3. Chemical Leucoderma Induced by Ear-ring Stoppers Made of Polyvinyl Chloride

    PubMed Central

    Sharma, Reena; Singal, Archana; Verma, Prashant; Grover, Chander

    2012-01-01

    We report a case of chemical leucoderma (CL) in a 15-year-old girl, who developed patterned depigmentation at the back of both ear lobules after contact with plastic ear-ring stoppers made of polyvinyl chloride (PVC) after continuous use for 6–7 months. Patch test with Indian standard series and cosmetic series was negative after 48 h, but she refused patch testing for extended duration as the possibility of induced depigmentation at the test site was unacceptable to her. To the best of our knowledge, this is the first report of plastic ear-ring stopper induced CL. PMID:23060712

  4. Nigella sativa oil reduces aluminium chloride-induced oxidative injury in liver and erythrocytes of rats.

    PubMed

    Bouasla, Ihcene; Bouasla, Asma; Boumendjel, Amel; Messarah, Mahfoud; Abdennour, Cherif; Boulakoud, Mohamed Salah; El Feki, Abdelfattah

    2014-12-01

    The present study was planned to investigate the protective effects of Nigella sativa oil (NSO) supplementation against aluminium chloride (AlCl3)-induced oxidative damage in liver and erythrocytes of rats. Simultaneously, a preliminary phytochemical study was affected in order to characterize the bioactive components containing in the NSO using chemical assays. The antioxidant capacities of NSO were evaluated by DPPH assay. The results showed that NSO was found to contain large amounts of total phenolics, flavonoids and tannins. Twenty-four rats were equally divided into two groups, in which group A received standard diet, whereas group B treated daily with an oral gavage dose of 2 ml NSO/kg body weight. After 5 weeks pretreatment, both groups were divided again into two subgroups (A and B) of six animals each and treated for other 3 weeks. Therefore, subgroup A1 was served as a control which received standard diet, but subgroup A2 received AlCl3 (34 mg/kg bw mixed with food). Subgroup B1 received both AlCl3 and NSO; however, subgroup B2 received NSO only. Results showed that AlCl3 exhibited an increase in white blood cell counts and a marked decrease in erythrocyte counts and haemoglobin content. Plasma aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase activities and total bilirubin concentration were higher in AlCl3 group than those of the control, while albumin and total protein concentration were significantly lower. Compared to the control, a significant raise of hepatic and erythrocyte malondialdehyde level associated with a decrease in reduced glutathione content, glutathione peroxidase, superoxide dismutase and catalase, activities of AlCl3 treated rats. However, the administration of NSO alone or combined with AlCl3 has improved the status of all parameters studied. It can be concluded that AlCl3 has induced the oxidative stress, altered the biochemical parameters and the hepatic histological profile, but the

  5. Determination of chloride in brazilian crude oils by ion chromatography after extraction induced by emulsion breaking.

    PubMed

    Robaina, Nicolle F; Feiteira, Fernanda N; Cassella, Alessandra R; Cassella, Ricardo J

    2016-08-01

    The present paper reports on the development of a novel extraction induced by emulsion breaking (EIEB) method for the determination of chloride in crude oils. The proposed method was based on the formation and breaking of oil-in-water emulsions with the samples and the consequential transference of the highly water-soluble chloride to the aqueous phase during emulsion breaking, which was achieved by centrifugation. The determination of chloride in the extracts was performed by ion chromatography (IC) with conductivity detection. Several parameters (oil phase:aqueous phase ratio, crude oil:mineral oil ratio, shaking time and type and concentration of surfactant) that could affect the performance of the method were evaluated. Total extraction of chloride from samples could be achieved when 1.0g of oil phase (0.5g of sample+0.5g of mineral oil) was emulsified in 5mL of a 2.5% (m/v) solution of Triton X-114. The obtained emulsion was shaken for 60min and broken by centrifugation for 5min at 5000rpm. The separated aqueous phase was collected, filtered and diluted before analysis by IC. Under these conditions, the limit of detection was 0.5μgg(-1) NaCl and the limit of quantification was 1.6μgg(-1) NaCl. We applied the method to the determination of chloride in six Brazilian crude oils and the results did not differ statistically from those obtained by the ASTM D6470 method when the paired Student-t-test, at 95% confidence level, was applied.

  6. Determination of chloride in brazilian crude oils by ion chromatography after extraction induced by emulsion breaking.

    PubMed

    Robaina, Nicolle F; Feiteira, Fernanda N; Cassella, Alessandra R; Cassella, Ricardo J

    2016-08-01

    The present paper reports on the development of a novel extraction induced by emulsion breaking (EIEB) method for the determination of chloride in crude oils. The proposed method was based on the formation and breaking of oil-in-water emulsions with the samples and the consequential transference of the highly water-soluble chloride to the aqueous phase during emulsion breaking, which was achieved by centrifugation. The determination of chloride in the extracts was performed by ion chromatography (IC) with conductivity detection. Several parameters (oil phase:aqueous phase ratio, crude oil:mineral oil ratio, shaking time and type and concentration of surfactant) that could affect the performance of the method were evaluated. Total extraction of chloride from samples could be achieved when 1.0g of oil phase (0.5g of sample+0.5g of mineral oil) was emulsified in 5mL of a 2.5% (m/v) solution of Triton X-114. The obtained emulsion was shaken for 60min and broken by centrifugation for 5min at 5000rpm. The separated aqueous phase was collected, filtered and diluted before analysis by IC. Under these conditions, the limit of detection was 0.5μgg(-1) NaCl and the limit of quantification was 1.6μgg(-1) NaCl. We applied the method to the determination of chloride in six Brazilian crude oils and the results did not differ statistically from those obtained by the ASTM D6470 method when the paired Student-t-test, at 95% confidence level, was applied. PMID:27388656

  7. Physiological effects of potassium chloride, formalin and handling stress on bonytail

    USGS Publications Warehouse

    Sykes, Catherine L.; Caldwell, Colleen A.; Gould, William R.

    2011-01-01

    We characterized the sublethal physiological changes in bonytail Gila elegans subjected to consecutive 750-mg/L potassium chloride (KCl) and 25-mg/L formalin treatments for the removal of zebra mussel Dreissena polymorpha and quagga mussel D. bugensis veligers. Plasma cortisol, glucose, and osmolality were measured over 24 h and at 14 d posthandling after exposing bonytail to KCl and one net stressor (capture with a net), KCl plus formalin and two net stressors, and one or two net stressors without chemicals. Elevated plasma cortisol (322–440 ng/mL) and glucose (254–399 mg/dL) concentrations were observed in all treatments compared with the concentrations in control fish (plasma cortisol, 56 ng/mL; glucose, 43 mg/dL). While there were no detectable differences in plasma osmolality among the treatment and control fish, a difference was observed between fish that were handled once versus twice. Chemical effects of stress were not observed in any of the physiological responses when the KCl treatment was compared with the one-net stressor treatment or when the KCl plus formalin treatment was compared with the two-net stressor treatment. Cumulative responses, however, were observed between one net stressor and two net stressors for plasma glucose and osmolality but not for plasma cortisol. Plasma cortisol and glucose levels remained elevated at 24 h posthandling, indicating that bonytail had not completely recovered from the handling stressors and would benefit from a recovery period in protected refugia before being released.

  8. Acquisition of lithium chloride- and radiation-induced taste aversions in hypophysectomized rats

    SciTech Connect

    Rabin, B.M.; Hunt, W.A.; Lee, J.

    1983-03-01

    The effects of hypophysectomy on the acquisition of conditioned taste aversions following injection of lithium chloride and following exposure to ionizing radiation were studied using a two-bottle preference test. Hypophysectomy did not disrupt the acquisition of a taste aversion following either treatment. The results are interpreted as: (a) suggesting that pituitary/adrenal hormones do not mediate the acquisition of a conditioned taste aversion following injections of lithium chloride or following exposure to ionizing radiation in a two-bottle preference test, and (b) consistent with other research suggesting that the involvement of pituitary/adrenal hormones in taste aversion learning may be related to the conflict induced by using a one-bottle test and not to the learning itself.

  9. In Vitro and in Vivo Experimental Studies on Trabecular Meshwork Degeneration Induced by Benzalkonium Chloride (An American Ophthalmological Society Thesis)

    PubMed Central

    Baudouin, Christophe; Denoyer, Alexandre; Desbenoit, Nicolas; Hamm, Gregory; Grise, Alice

    2012-01-01

    Purpose: Long-term antiglaucomatous drug administration may cause irritation, dry eye, allergy, subconjunctival fibrosis, or increased risk of glaucoma surgery failure, potentially due to the preservative benzalkonium chloride (BAK), whose toxic, proinflammatory, and detergent effects have extensively been shown experimentally. We hypothesize that BAK also influences trabecular meshwork (TM) degeneration. Methods: Trabecular specimens were examined using immunohistology and reverse transcriptase–polymerase chain reaction. A trabecular cell line was stimulated by BAK and examined for apoptosis, oxidative stress, fractalkine and SDF-1 expression, and modulation of their receptors. An experimental model was developed with BAK subconjunctival injections to induce TM degeneration. Mass spectrometry (MS) imaging assessed BAK penetration after repeated instillations in rabbit eyes. Results: Trabecular specimens showed extremely low densities of trabecular cells and presence of cells expressing fractalkine and fractalkine receptor and their respective mRNAs. Benzalkonium in vitro induced apoptosis, oxidative stress, and fractalkine expression and inhibited the protective chemokine SDF-1 and Bcl2, also inducing a sustained intraocular pressure (IOP) increase, with dramatic apoptosis of trabecular cells and reduction of aqueous outflow. MS imaging showed that BAK could access the TM at measurable levels after repeated instillations. Conclusion: BAK enhances all characteristics of TM degeneration typical of glaucoma—trabecular apoptosis, oxidative stress, induction of inflammatory chemokines—and causes degeneration in acute experimental conditions, potentially mimicking long-term accumulation. BAK was also shown to access the TM after repeated instillations. These findings support the hypothesis that antiglaucoma medications, through toxicity of their preservative, may cause further long-term trabecular degeneration and therefore enhance outflow resistance, reducing the

  10. Chloride channel protein 2 prevents glutamate-induced apoptosis in retinal ganglion cells

    PubMed Central

    Bi, Miao-Miao; Hong, Sen; Ma, Ling-Jun; Zhou, Hong-Yan; Lu, Jia; Zhao, Jing; Zheng, Ya-Juan

    2016-01-01

    Objective(s): The purpose of this study was to investigate the role of chloride channel protein 2 (ClC-2) in glutamate-induced apoptosis in the retinal ganglion cell line (RGC-5). Materials and Methods: RGC-5 cells were treated with 1 mM glutamate for 24 hr. The expression of ClC-2, Bax, and Bcl-2 was detected by western blot analysis. Cell survival and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Caspase-3 and -9 activities were determined by a colorimetric assay. The roles of ClC-2 in glutamate-induced apoptosis were examined by using ClC-2 complementary deoxyribonucleic acid (cDNA) and small inference ribonucleic acid (RNA) transfection technology. Results: Overexpression of ClC-2 in RGC-5 cells significantly decreased glutamate-induced apoptosis and increased cell viability, whereas silencing of ClC-2 with short hairpin (sh) RNA produced opposite effects. ClC-2 overexpression increased the expression of Bcl-2, decreased the expression of Bax, and decreased caspase-3 and -9 activation in RGC-5 cells treated with glutamate, but silencing of ClC-2 produced opposite effects. Conclusion: Our data suggest that ClC-2 chloride channels might play a protective role in glutamate-induced apoptosis in retinal ganglion cells via the mitochondria-dependent apoptosis pathway.

  11. Chloride channel protein 2 prevents glutamate-induced apoptosis in retinal ganglion cells

    PubMed Central

    Bi, Miao-Miao; Hong, Sen; Ma, Ling-Jun; Zhou, Hong-Yan; Lu, Jia; Zhao, Jing; Zheng, Ya-Juan

    2016-01-01

    Objective(s): The purpose of this study was to investigate the role of chloride channel protein 2 (ClC-2) in glutamate-induced apoptosis in the retinal ganglion cell line (RGC-5). Materials and Methods: RGC-5 cells were treated with 1 mM glutamate for 24 hr. The expression of ClC-2, Bax, and Bcl-2 was detected by western blot analysis. Cell survival and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Caspase-3 and -9 activities were determined by a colorimetric assay. The roles of ClC-2 in glutamate-induced apoptosis were examined by using ClC-2 complementary deoxyribonucleic acid (cDNA) and small inference ribonucleic acid (RNA) transfection technology. Results: Overexpression of ClC-2 in RGC-5 cells significantly decreased glutamate-induced apoptosis and increased cell viability, whereas silencing of ClC-2 with short hairpin (sh) RNA produced opposite effects. ClC-2 overexpression increased the expression of Bcl-2, decreased the expression of Bax, and decreased caspase-3 and -9 activation in RGC-5 cells treated with glutamate, but silencing of ClC-2 produced opposite effects. Conclusion: Our data suggest that ClC-2 chloride channels might play a protective role in glutamate-induced apoptosis in retinal ganglion cells via the mitochondria-dependent apoptosis pathway. PMID:27635193

  12. Aqueous sodium chloride induced intergranular corrosion of Al-Li-Cu alloys

    NASA Technical Reports Server (NTRS)

    Pizzo, P. P.; Daeschner, D. L.

    1986-01-01

    Two methods have been explored to assess the susceptibility of Al-Li-Cu alloys to intergranular corrosion in aqueous sodium chloride solution. They are: (1) constant extension rate testing with and without alternate-immersion preexposure and (2) metallographic examination after exposure to a NaCl-H2O2 corrosive solution per Mil-H-6088F. Intergranular corrosion was found to occur in both powder and ingot metallurgy alloys of similar composition, using both methods. Underaging rendered the alloys most susceptible. The results correlate to stress-corrosion data generated in conventional time-to-failure and crack growth-rate tests. Alternate-immersion preexposure may be a reliable means to assess stress corrosion susceptibility of Al-Li-Cu alloys.

  13. Gadolinium Chloride Inhibits the Spontaneous Resolution of Fibrosis in CCL(4)-Induced Cirrhosis.

    PubMed

    Chávez, Enrique; Alcantar, Lidia K; Moreno, Mario G; Muriel, Pablo

    2006-01-01

    Current evidence indicates that liver fibrosis is dynamic and can be bidirectional, involving phases of progression and regression, and that in addition to increased matrix synthesis, this pathological process involves major changes in the regulation of matrix degradation. There is also evidence that Kupffer cells participate in both fibrogenesis and fibrolysis. Therefore, the aim of the present work was to study the participation of Kupffer cells on the spontaneous resolution of hepatic fibrosis. Cirrhosis was produced by 3 months of chronic CCl(4) intoxication in male Wistar rats, and then CCl(4) was discontinued and two groups were formed: One group received gadolinium chloride (10 mg/kg, IP, daily) and the other received the vehicle (water) only for 2 months. Serum enzyme activities of alkaline phosphatase and alanine aminotransferase and liver lipid peroxidation increased by CCl(4) treatment but returned to normal by discontinuation of CCl(4). GSH, GSH/GSSG, and GSH+GSSG decreased significantly by CCl(4), but withdrawal of CCl(4) restored normal glutathione parameters. Fibrosis increased five-fold and glycogen decreased significantly by CCl(4) treatment, while discontinuation of CCl(4) reversed completely glycogen depletion and partially fibrosis. Gadolinium chloride showed effects only in the content of glycogen and collagen; the former was decreased further and the latter remained elevated despite discontinuation of the toxic agent. Persistent fibrosis induced by gadolinium chloride, a selective inhibitor of Kupffer cells, indicates that these cells play a pivotal role in fibrolysis. PMID:20020993

  14. Rapid analysis of liquid formulations containing sodium chloride using laser-induced breakdown spectroscopy.

    PubMed

    St-Onge, Louis; Kwong, Elizabeth; Sabsabi, Mohamad; Vadas, Elizabeth B

    2004-10-29

    The purpose of this work was to demonstrate the possibilities offered by laser-induced breakdown spectroscopy (LIBS) for the direct and rapid analysis of pharmaceutical liquid formulations. Sodium chloride in solution was chosen as a model compound. A pulsed Nd:YAG laser (1064 nm) was used to produce a gaseous plasma from the liquid sample. The ensuing plasma emission was spectrally analysed, and the intensity of an atomic line from sodium was used to quantitate the sodium chloride. Using surface analysis of a flowing solution, the precision (%R.S.D.) of a measurement lasting 50 s (average of 50 laser shots at 1 shot/s) was approximately 0.5% for isotonic solutions. On a non-flowing solution, a 50 s measurement had an R.S.D. of 1.8%. Direct analysis in closed (transparent) bottles was possible but more complex, requiring the superimposition of two sequential laser sparks. Using a surface procedure, common commercial isotonic products (including injectable, bacteriostatic injectable, and nasal solutions) were analysed. Their sodium content (corresponding to 0.9% sodium chloride) was accurately determined in all cases, demonstrating the capabilities of LIBS for the rapid analysis of liquid pharmaceutical products.

  15. Indium chloride-induced micronuclei via reactive oxygen species in Chinese hamster lung fibroblast V79 cells.

    PubMed

    Lin, Ruey-Hseng; Yang, Ming-Ling; Li, Yi-Ching; Chang, Hui-Min; Kuan, Yu-Hsiang

    2013-10-01

    We study the cytotoxicity of indium chloride (InCl₃) in Chinese hamster lung fibroblasts, the V79 cells, using MTT assay. The results showed that InCl₃ did not induce significant cytotoxicity at various concentrations tested. In addition, the frequency of micronuclei (MN) was assayed to evaluate the genotoxic effects of InCl₃ in V79 cells. InCl₃ at concentrations ranged 0.1-1 μM significantly increased MN frequency in a concentration-dependent manner. Both catalase and superoxide dismutase at concentrations of 75 and 150 μg/mL significantly inhibited InCl₃-induced MN. Similarly, Germanium oxide (GeO₂) and dimercaprol expressed antigenotoxic effects. From these findings, it is concluded that InCl₃ is a potent genotoxic chemical, which may be mediated partly by inducing oxidative stress. The significance of this study shows that the workers in the semiconductor factories should be cautious in exposing to the hazardous genotoxic InCl₃.

  16. Barium chloride induces redox status unbalance, upregulates cytokine genes expression and confers hepatotoxicity in rats-alleviation by pomegranate peel.

    PubMed

    Elwej, Awatef; Grojja, Yousri; Ghorbel, Imen; Boudawara, Ons; Jarraya, Raoudha; Boudawara, Tahia; Zeghal, Najiba

    2016-04-01

    The present study was performed to establish the therapeutic efficacy of pomegranate peel against barium chloride induced liver injury. Adult rats were divided into four groups of six animals each: group I, serving as controls, received distilled water; group II received by their drinking water 67 ppm of BaCl2; group III received both 67 ppm of BaCl2 by the same way than group II and 5 % of pomegranate peel (PP) via diet; group IV received 5 % of PP. Analysis by HPLC/MS of PP showed its rich composition in flavonoids such as gallic acid, castalin, hyperin, quercitrin, syringic acid, and quercetin. The protective effects of pomegranate peel against hepatotoxicity induced by barium chloride were assessed using biochemical parameters and histological studies. Exposure of rats to barium caused oxidative stress in the liver as evidenced by an increase in malondialdehyde (MDA), lipid hydroperoxides (LOOHs), H2O2 and advanced oxidation protein product (AOPP) levels, and lactate dehydrogenase (LDH), gamma glutamyl transpeptidase (GGT), alanine aminotransferase (AST) and aspartate aminotransferase (ALT) activities, a decrease in catalase (CAT) and glutathione peroxidase (GPx) activities, glutathion (GSH), non-protein thiol (NPSH), vitamin C levels, and Mn-SOD gene expression. Liver total MT levels, MT-1, and MT-2 and pro-inflammatory cytokine genes expression like TNF-α, IL-1β and IL-6 were increased. Pomegranate peel, supplemented in the diet of barium-treated rats, showed an improvement of all the parameters indicated above.The present work provided ethnopharmacological relevance of pomegranate peel against the toxic effects of barium, suggesting its beneficial role as a potential antioxidant.

  17. Annexin A4 induces platinum resistance in a chloride-and calcium-dependent manner.

    PubMed

    Morimoto, Akiko; Serada, Satoshi; Enomoto, Takayuki; Kim, Ayako; Matsuzaki, Shinya; Takahashi, Tsuyoshi; Ueda, Yutaka; Yoshino, Kiyoshi; Fujita, Masami; Fujimoto, Minoru; Kimura, Tadashi; Naka, Tetsuji

    2014-09-15

    Platinum resistance has long been a major issue in the treatment of various cancers. We previously reported that enhanced annexin A4 (ANXA4) expression, a Ca2+-regulated phospholipid-binding protein, induces chemoresistance to platinum-based drugs. In this study, we investigated the role of annexin repeats, a conserved structure of all the annexin family, responsible for platinum-resistance as well as the effect of knockdown of ANXA4. ANXA4 knockdown increased sensitivity to platinum-based drugs both in vitro and in vivo. To identify the domain responsible for chemoresistance, ANXA4 deletion mutants were constructed by deleting annexin repeats one by one from the C terminus. Platinum resistance was induced both in vitro and in vivo in cells expressing either full-length ANXA4 or the deletion mutants, containing at least one intact annexin repeat. However, cells expressing the mutant without any calcium-binding sites in the annexin repeated sequence, which is essential for ANXA4 translocation from the cytosol to plasma membrane, failed to acquire platinum resistance. After cisplatin treatment, the intracellular chloride ion concentration, whose channel is partly regulated by ANXA4, significantly increased in the platinum-resistant cells. These findings indicate that the calcium-binding site in the annexin repeat induces chemoresistance to the platinum-based drug by elevating the intracellular chloride concentration.

  18. Apical leptin induces chloride secretion by intestinal epithelial cells and in a rat model of acute chemotherapy-induced colitis

    PubMed Central

    Hoda, Raschid M.; Scharl, Michael; Keely, Stephen J.; McCole, Declan F.

    2010-01-01

    The purpose of this study was to investigate whether luminal leptin alters ion transport properties of the intestinal epithelium under acute inflammatory conditions. Monolayers of human intestinal T84 epithelial cells and a rat model of chemotherapy-induced enterocolitis were used. Cells were treated with leptin and mounted in Ussing chambers to measure basal and secretagogue-induced changes in transepithelial short-circuit current (Isc). Furthermore, the role of MAPK and phosphatidylinositol 3-kinase (PI3K) signaling pathways in mediating responses to leptin was investigated. Acute colitis in Sprague-Dawley rats was induced by intraperitoneal injection of 40 mg/kg methotrexate. Leptin (100 ng/ml) induced a time-dependent increase in basal Isc in T84 intestinal epithelial cells (P < 0.01). Moreover, pretreatment of T84 cells with leptin for up to 1 h significantly potentiated carbachol- and forskolin-induced increases in Isc. Pretreatment with an inhibitor of MAPK abolished the effect of leptin on basal, carbachol- and forskolin-induced chloride secretion (P < 0.05). However, the PI3K inhibitor, wortmannin, only blunted the effect of leptin on forskolin-induced increases in Isc. Furthermore, leptin treatment evoked both ERK1/2 and Akt1 phosphorylation in T84 cells. In the rat model, luminal leptin induced significant increases in Isc across segments of proximal and, to a lesser extent, distal colon (P < 0.05). We conclude that luminal leptin is likely an intestinal chloride secretagogue, particularly when present at elevated concentrations and/or in the setting of inflammation. Our findings may provide a mechanistic explanation, at least in part, for the clinical condition of secretory diarrhea both in hyperleptinemic obese patients and in patients with chemotherapy-induced intestinal inflammation. PMID:20203064

  19. [Stress-induced Takotsubo cardiomyopathy].

    PubMed

    Høst, Ulla; Søgaard, Peter; Hansen, Peter Riis

    2009-09-14

    A case of Takotsubo cardiomyopathy is described in a postmenopausal woman admitted for suspected recent myocardial infarction, triggered by significant social stress during a family Christmas dinner. Coronary angiography showed no significant lesions. Acute echocardiography demonstrated apical ballooning and an ejection fraction of 30%. The clinical course was uneventful and after one month, echocardiography showed complete resolution of the apical ballooning and recovery of left ventricular systolic function.

  20. Cobalt chloride induces metaphase when topically applied to larvae and pupae of the stingless bee Melipona scutellaris (Hymenoptera, Apidae, Meliponini).

    PubMed

    Ueira-Vieira, C; Tavares, R R; Morelli, S; Pereira, B B; Silva, R P; Torres-Mariano, A R; Kerr, W E; Bonetti, A M

    2013-06-20

    In order to optimize preparations of bee metaphases, we tested cobalt chloride, which has been used as a metaphase inducer in other organisms, such as hamsters and fish. Four microliters of 65 mM cobalt chloride aqueous solution was topically applied to larval and pupal stages of the stingless bee Melipona scutellaris. The cerebral ganglion was removed after treatment and prepared for cytogenetic analysis. Identically manipulated untreated individuals were used as controls. The number of metaphases was increased 3-fold in treated individuals compared to controls. The micronucleus test showed no mutagenic effects of cobalt chloride on M. scutellaris cells. We concluded that cobalt chloride is a metaphase-inducing agent in M. scutellaris, thus being useful for cytogenetic analyses.

  1. Cobalt chloride induces metaphase when topically applied to larvae and pupae of the stingless bee Melipona scutellaris (Hymenoptera, Apidae, Meliponini).

    PubMed

    Ueira-Vieira, C; Tavares, R R; Morelli, S; Pereira, B B; Silva, R P; Torres-Mariano, A R; Kerr, W E; Bonetti, A M

    2013-01-01

    In order to optimize preparations of bee metaphases, we tested cobalt chloride, which has been used as a metaphase inducer in other organisms, such as hamsters and fish. Four microliters of 65 mM cobalt chloride aqueous solution was topically applied to larval and pupal stages of the stingless bee Melipona scutellaris. The cerebral ganglion was removed after treatment and prepared for cytogenetic analysis. Identically manipulated untreated individuals were used as controls. The number of metaphases was increased 3-fold in treated individuals compared to controls. The micronucleus test showed no mutagenic effects of cobalt chloride on M. scutellaris cells. We concluded that cobalt chloride is a metaphase-inducing agent in M. scutellaris, thus being useful for cytogenetic analyses. PMID:23420403

  2. Gravity-induced stresses in finite slopes

    USGS Publications Warehouse

    Savage, W.Z.

    1994-01-01

    An exact solution for gravity-induced stresses in finite elastic slopes is presented. This solution, which is applied for gravity-induced stresses in 15, 30, 45 and 90?? finite slopes, has application in pit-slope design, compares favorably with published finite element results for this problem and satisfies the conditions that shear and normal stresses vanish on the ground surface. The solution predicts that horizontal stresses are compressive along the top of the slopes (zero in the case of the 90?? slope) and tensile away from the bottom of the slopes, effects which are caused by downward movement and near-surface horizontal extension in front of the slope in response to gravity loading caused by the additional material associated with the finite slope. ?? 1994.

  3. Role of chloride ions in the promotion of auxin-induced growth of maize coleoptile segments

    PubMed Central

    Burdach, Zbigniew; Kurtyka, Renata; Siemieniuk, Agnieszka; Karcz, Waldemar

    2014-01-01

    Background and Aims The mechanism of auxin action on ion transport in growing cells has not been determined in detail. In particular, little is known about the role of chloride in the auxin-induced growth of coleoptile cells. Moreover, the data that do exist in the literature are controversial. This study describes experiments that were carried out with maize (Zea mays) coleoptile segments, this being a classical model system for studies of plant cell elongation growth. Methods Growth kinetics or growth and pH changes were recorded in maize coleoptiles using two independent measuring systems. The growth rate of the segments was measured simultaneously with medium pH changes. Membrane potential changes in parenchymal cells of the segments were also determined for chosen variants. The question of whether anion transport is involved in auxin-induced growth of maize coleoptile segments was primarily studied using anion channel blockers [anthracene-9-carboxylic acid (A-9-C) and 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS)]. In addition, experiments in which KCl was replaced by KNO3 were also performed. Key Results Both anion channel blockers, added at 0·1 mm, diminished indole-3-acetic acid (IAA)-induced elongation growth by ∼30 %. Medium pH changes measured simultaneously with growth indicated that while DIDS stopped IAA-induced proton extrusion, A-9-C diminished it by only 50 %. Addition of A-9-C to medium containing 1 mm KCl did not affect the characteristic kinetics of IAA-induced membrane potential changes, while in the presence of 10 mm KCl the channel blocker stopped IAA-induced membrane hyperpolarization. Replacement of KCl with KNO3 significantly decreased IAA-induced growth and inhibited proton extrusion. In contrast to the KCl concentration, the concentration of KNO3 did not affect the growth-stimulatory effect of IAA. For comparison, the effects of the cation channel blocker tetraethylammonium chloride (TEA-Cl) on IAA-induced growth and

  4. Stress Drops for Potentially Induced Earthquake Sequences

    NASA Astrophysics Data System (ADS)

    Huang, Y.; Beroza, G. C.; Ellsworth, W. L.

    2015-12-01

    Stress drop, the difference between shear stress acting across a fault before and after an earthquake, is a fundamental parameter of the earthquake source process and the generation of strong ground motions. Higher stress drops usually lead to more high-frequency ground motions. Hough [2014 and 2015] observed low intensities in "Did You Feel It?" data for injection-induced earthquakes, and interpreted them to be a result of low stress drops. It is also possible that the low recorded intensities could be a result of propagation effects. Atkinson et al. [2015] show that the shallow depth of injection-induced earthquakes can lead to a lack of high-frequency ground motion as well. We apply the spectral ratio method of Imanishi and Ellsworth [2006] to analyze stress drops of injection-induced earthquakes, using smaller earthquakes with similar waveforms as empirical Green's functions (eGfs). Both the effects of path and linear site response should be cancelled out through the spectral ratio analysis. We apply this technique to the Guy-Greenbrier earthquake sequence in central Arkansas. The earthquakes migrated along the Guy-Greenbrier Fault while nearby injection wells were operating in 2010-2011. Huang and Beroza [GRL, 2015] improved the magnitude of completeness to about -1 using template matching and found that the earthquakes deviated from Gutenberg-Richter statistics during the operation of nearby injection wells. We identify 49 clusters of highly similar events in the Huang and Beroza [2015] catalog and calculate stress drops using the source model described in Imanishi and Ellsworth [2006]. Our results suggest that stress drops of the Guy-Greenbrier sequence are similar to tectonic earthquakes at Parkfield, California (the attached figure). We will also present stress drop analysis of other suspected induced earthquake sequences using the same method.

  5. Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E.

    PubMed

    Kalender, Suna; Uzun, Fatma Gokce; Demir, Filiz; Uzunhisarcıklı, Meltem; Aslanturk, Ayse

    2013-05-01

    Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300-320g and each group six animals) were given mercuric chloride (1mg/kg bw) and/or sodium selenite (0.25mg/kg bw)+vitamin E (100mg/kg) daily via gavage for 4weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.

  6. Preserved frontal lobe oxygenation following calcium chloride for treatment of anesthesia-induced hypotension.

    PubMed

    Kitchen, Carl-Christian; Nissen, Peter; Secher, Niels H; Nielsen, Henning B

    2014-01-01

    Vasopressor agents may affect cerebral oxygenation (rScO2) as determined by near-infrared spectroscopy on the forehead. This case series evaluated the effect of calcium chloride vs. α and β-adrenergic receptor agonists on rScO2 in patients (n = 47) undergoing surgery during i.v. anesthesia. Mean arterial pressure (MAP) and cardiac output (CO) were assessed by Model-flow(®) and ephedrine (55 ± 3 vs. 74 ± 9 mmHg; 10 mg, n = 9), phenylephrine (51 ± 5 vs. 78 ± 9 mmHg, 0.1 mg, n = 11), adrenaline (53 ± 3 vs. 72 ± 11 mmHg; 1-2 μg, n = 6), noradrenaline (53 ± 5 vs. 72 ± 12 mmHg; 2-4 μg, n = 11), and calcium chloride (49 ± 7 vs. 57 ± 16 mmHg; 5 mmol, n = 10) increased MAP (all P < 0.05). CO increased with ephedrine (4.3 ± 0.9 vs. 5.3 ± 1.2, P < 0.05) and adrenaline (4.7 ± 1.2 vs. 5.9 ± 1.1 l/min; P = 0.07) but was not significantly affected by phenylephrine (3.9 ± 0.7 vs. 3.6 ± 1.0 l/min), noradrenaline (3.8 ± 1.2 vs. 3.7 ± 0.7 l/min), or calcium chloride (4.0 ± 1.4 vs. 4.1 ± 1.5 l/min). Following administration of β-adrenergic agents and calcium chloride rScO2 was preserved while after administration of α-adrenergic drugs rScO2 was reduced by app. 2% (P < 0.05). Following α-adrenergic drugs to treat anesthesia-induced hypotension tissue oxygenation is reduced while the use of β-adrenergic agonists and calcium chloride preserve tissue oxygenation.

  7. Diabetic Cardiovascular Disease Induced by Oxidative Stress.

    PubMed

    Kayama, Yosuke; Raaz, Uwe; Jagger, Ann; Adam, Matti; Schellinger, Isabel N; Sakamoto, Masaya; Suzuki, Hirofumi; Toyama, Kensuke; Spin, Joshua M; Tsao, Philip S

    2015-10-23

    Cardiovascular disease (CVD) is the leading cause of morbidity and mortality among patients with diabetes mellitus (DM). DM can lead to multiple cardiovascular complications, including coronary artery disease (CAD), cardiac hypertrophy, and heart failure (HF). HF represents one of the most common causes of death in patients with DM and results from DM-induced CAD and diabetic cardiomyopathy. Oxidative stress is closely associated with the pathogenesis of DM and results from overproduction of reactive oxygen species (ROS). ROS overproduction is associated with hyperglycemia and metabolic disorders, such as impaired antioxidant function in conjunction with impaired antioxidant activity. Long-term exposure to oxidative stress in DM induces chronic inflammation and fibrosis in a range of tissues, leading to formation and progression of disease states in these tissues. Indeed, markers for oxidative stress are overexpressed in patients with DM, suggesting that increased ROS may be primarily responsible for the development of diabetic complications. Therefore, an understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of diabetes-induced CVD. The current review focuses on the relationship between diabetes-induced CVD and oxidative stress, while highlighting the latest insights into this relationship from findings on diabetic heart and vascular disease.

  8. Lead induced testicular hypersensitivity in stressed rats.

    PubMed

    Saxena, D K; Lal, B; Srivastava, R S; Chandra, S V

    1990-01-01

    Rats were immobilized for 2 h and treated i.p. with lead Pb2+ (8 mg/kg/day) for 45 d to investigate the testicular effects of lead on rats kept under immobilization stress. Marked alteration in SDH. G6PDH activity, cholesterol and ascorbic acid contents and reduced sperm counts associated with marked pathological changes in the testis of rats were observed after combined treatment with lead and immobilization stress in comparison to either alone. An increase in the disturbances of testicular androgen synthesis seems to be responsible for enhanced testicular injury in lead induced stressed rats. PMID:2401350

  9. Lead induced testicular hypersensitivity in stressed rats.

    PubMed

    Saxena, D K; Lal, B; Srivastava, R S; Chandra, S V

    1990-01-01

    Rats were immobilized for 2 h and treated i.p. with lead Pb2+ (8 mg/kg/day) for 45 d to investigate the testicular effects of lead on rats kept under immobilization stress. Marked alteration in SDH. G6PDH activity, cholesterol and ascorbic acid contents and reduced sperm counts associated with marked pathological changes in the testis of rats were observed after combined treatment with lead and immobilization stress in comparison to either alone. An increase in the disturbances of testicular androgen synthesis seems to be responsible for enhanced testicular injury in lead induced stressed rats.

  10. Quantitative estimation of carbonation and chloride penetration in reinforced concrete by laser-induced breakdown spectroscopy

    NASA Astrophysics Data System (ADS)

    Eto, Shuzo; Matsuo, Toyofumi; Matsumura, Takuro; Fujii, Takashi; Tanaka, Masayoshi Y.

    2014-11-01

    The penetration profile of chlorine in a reinforced concrete (RC) specimen was determined by laser-induced breakdown spectroscopy (LIBS). The concrete core was prepared from RC beams with cracking damage induced by bending load and salt water spraying. LIBS was performed using a specimen that was obtained by splitting the concrete core, and the line scan of laser pulses gave the two-dimensional emission intensity profiles of 100 × 80 mm2 within one hour. The two-dimensional profile of the emission intensity suggests that the presence of the crack had less effect on the emission intensity when the measurement interval was larger than the crack width. The chlorine emission spectrum was measured without using the buffer gas, which is usually used for chlorine measurement, by collinear double-pulse LIBS. The apparent diffusion coefficient, which is one of the most important parameters for chloride penetration in concrete, was estimated using the depth profile of chlorine emission intensity and Fick's law. The carbonation depth was estimated on the basis of the relationship between carbon and calcium emission intensities. When the carbon emission intensity was statistically higher than the calcium emission intensity at the measurement point, we determined that the point was carbonated. The estimation results were consistent with the spraying test results using phenolphthalein solution. These results suggest that the quantitative estimation by LIBS of carbonation depth and chloride penetration can be performed simultaneously.

  11. Effects of temperature and pressure on stress corrosion cracking behavior of 310S stainless steel in chloride solution

    NASA Astrophysics Data System (ADS)

    Zhong, Yunpan; Zhou, Cheng; Chen, Songying; Wang, Ruiyan

    2016-06-01

    310S is an austenitic stainless steel for high temperature applications, having strong resistance of oxidation, hydrogen embrittlement and corrosion. Stress corrosion cracking(SCC) is the main corrosion failure mode for 310S stainless steel. Past researched about SCC of 310S primarily focus on the corrosion mechanism and influence of temperature and corrosive media, but few studies concern the combined influence of temperature, pressure and chloride. For a better understanding of temperature and pressure's effects on SCC of 310S stainless steel, prepared samples are investigated via slow strain rate tensile test(SSRT) in different temperature and pressure in NACE A solution. The result shows that the SCC sensibility indexes of 310S stainless steel increase with the rise of temperature and reach maximum at 10MPa and 160°C, increasing by 22.3% compared with that at 10 MPa and 80 °C. Instead, the sensibility decreases with the pressure up. Besides, the fractures begin to transform from the ductile fracture to the brittle fracture with the increase of temperature. 310S stainless steel has an obvious tendency of stress corrosion at 10MPa and 160°C and the fracture surface exists cleavage steps, river patterns and some local secondary cracks, having obvious brittle fracture characteristics. The SCC cracks initiate from inclusions and tiny pits in the matrix and propagate into the matrix along the cross section gradually until rupture. In particular, the oxygen and chloride play an important role on the SCC of 310S stainless steel in NACE A solution. The chloride damages passivating film, causing pitting corrosion, concentrating in the cracks and accelerated SSC ultimately. The research reveals the combined influence of temperature, pressure and chloride on the SCC of 310S, which can be a guide to the application of 310S stainless steel in super-heater tube.

  12. Confinement and water quality-induced stress in largemouth bass

    SciTech Connect

    Carmichael, G.J.; Tomasso, J.R.; Simco, B.A.; Davis, K.B.

    1984-11-01

    Plasma values of corticosteroids, glucose, chloride, and osmolality were determined in largemouth bass Micropterus salmoides under various environmental conditions. No differences were observed in quiescent fish due to sex, size, time of day, or the types of holding facilities tested (tanks, raceways, ponds). Differences were observed in plasma glucose, chloride, and osmolality values among fish acclimated to 10, 16, and 23 C. Abrupt temperature changes caused elevations in plasma corticosteroid and glucose concentrations and reduced plasma chloride and osmolality. Confinement in a net, for up to 48 hours, caused elevated glucose and corticosteroids and reduced chloride and osmolality values. After 48 hours of confinement, fish required up to 14 days to recover normal plasma characters. Generally, short-term exposure to poor water quality (high concentrations of CO/sub 2/ and NH/sub 3/, and low concentrations of dissolved oxygen) altered plasma corticosteroids and glucose but had little effect on plasma chloride or osmolality. Net confinement plus poor water quality caused additional stress. Plasma glucose and corticosteroid values were good indicators of stress during application of acute stressors whereas chloride and osmolality were useful indicators of long-term stress and patterns of recovery after stressors were removed.

  13. The ClC-7 Chloride Channel Is Downregulated by Hypoosmotic Stress in Human Chondrocytes.

    PubMed

    Kurita, Takashi; Yamamura, Hisao; Suzuki, Yoshiaki; Giles, Wayne R; Imaizumi, Yuji

    2015-07-01

    Articular chondrocytes in osteoarthritis (OA) patients are exposed to hypoosmotic stress because the osmolality of this synovial fluid is significantly decreased. Hypoosmotic stress can cause an efflux of Cl(-) and an associated decrease of cell volume. We have previously reported that a Cl(-) conductance contributes to the regulation of resting membrane potential and thus can alter intracellular Ca(2+) concentration ([Ca(2+)]i) in human chondrocytes. The molecular identity and pathologic function of these Cl(-) channels, however, remained to be determined. Here, we show that the ClC-7 Cl(-) channel is strongly expressed in a human chondrocyte cell line (OUMS-27) and that it is responsible for Cl(-) currents that are activated by extracellular acidification (pH 5.0). These acid-sensitive currents are inhibited by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS; IC50 = 13 μM) and are markedly reduced by small-interfering RNA-induced knockdown of ClC-7. DIDS hyperpolarized these chondrocytes, and this was followed by an increase in [Ca(2+)]i. ClC-7 knockdown caused a similar hyperpolarization of the membrane potential. Short-term culture (48 hours) in hypoosmotic medium (270 mOsm) reduced the expression of ClC-7 and decreased the acid-sensitive currents. Interestingly, these hypoosmotic culture conditions, or ClC-7 knockdown, resulted in enhanced cell death. Taken together, our results show that the significant hyperpolarization due to ClC-7 impairment in chondrocytes can significantly increase [Ca(2+)]i and cell death. Thus, downregulation of ClC-7 channels during the hypoosmotic stress that accompanies OA progression is one important concept of the complex etiology of OA. These findings suggest novel targets for therapeutic intervention(s) and drug development for OA.

  14. Stress-Induced Mutagenesis in Bacteria

    PubMed Central

    Foster, Patricia L.

    2009-01-01

    Bacteria spend their lives buffeted by changing environmental conditions. To adapt to and survive these stresses, bacteria have global response systems that result in sweeping changes in gene expression and cellular metabolism. These responses are controlled by master regulators, which include: alternative sigma factors, such as RpoS and RpoH; small molecule effectors, such as ppGpp; gene repressors such as LexA; and, inorganic molecules, such as polyphosphate. The response pathways extensively overlap and are induced to various extents by the same environmental stresses. These stresses include nutritional deprivation, DNA damage, temperature shift, and exposure to antibiotics. All of these global stress responses include functions that can increase genetic variability. In particular, up-regulation and activation of error-prone DNA polymerases, down-regulation of error-correcting enzymes, and movement of mobile genetic elements are common features of several stress responses. The result is that under a variety of stressful conditions, bacteria are induced for genetic change. This transient mutator state may be important for adaptive evolution. PMID:17917873

  15. IL-17A Induces Pendrin Expression and Chloride-Bicarbonate Exchange in Human Bronchial Epithelial Cells

    PubMed Central

    Adams, Kelly M.; Abraham, Valsamma; Spielman, Daniel; Kolls, Jay K.; Rubenstein, Ronald C.; Conner, Gregory E.; Cohen, Noam A.; Kreindler, James L.

    2014-01-01

    The epithelium plays an active role in the response to inhaled pathogens in part by responding to signals from the immune system. Epithelial responses may include changes in chemokine expression, increased mucin production and antimicrobial peptide secretion, and changes in ion transport. We previously demonstrated that interleukin-17A (IL-17A), which is critical for lung host defense against extracellular bacteria, significantly raised airway surface pH in vitro, a finding that is common to a number of inflammatory diseases. Using microarray analysis of normal human bronchial epithelial (HBE) cells treated with IL-17A, we identified the electroneutral chloride-bicarbonate exchanger Pendrin (SLC26A4) as a potential mediator of this effect. These data were verified by real-time, quantitative PCR that demonstrated a time-dependent increase in Pendrin mRNA expression in HBE cells treated with IL-17A up to 48 h. Using immunoblotting and immunofluorescence, we confirmed that Pendrin protein expression is increased in IL-17 treated HBE cells and that it is primarily localized to the mucosal surface of the cells. Functional studies using live-cell fluorescence to measure intracellular pH demonstrated that IL-17A induced chloride-bicarbonate exchange in HBE cells that was not present in the absence of IL-17A. Furthermore, HBE cells treated with short interfering RNA against Pendrin showed substantially reduced chloride-bicarbonate exchange. These data suggest that Pendrin is part of IL-17A-dependent epithelial changes and that Pendrin may therefore be a therapeutic target in IL-17A-dependent lung disease. PMID:25141009

  16. Salt stress-induced protein phosphorylation

    SciTech Connect

    Godoy, J.A.; Torres-Schumann, S.; Llobell, A.; Pintor-Toro, J.A.

    1989-04-01

    Protein phosphorylation induced by salt stress in tomato germinating seeds were investigated by two-dimensional polyacrilamide gel electrophoresis of proteins labeled in vivo with ({sup 32}P)-Phosphate. NaCl induced the phosphorylation of a 14 Kd polypeptide. Pulse-chase experiments revealed that the phosphorylated molecules of this polypeptide are only stable while the stress is present. Phosphorylated 14 Kd polypeptides could be detected in radicles of salt-shocked seedlings after 6 hours stress period. 14 Kd polypeptide phosphorylation was also observed in seeds germinating in the presence of abscisic acid (ABA). The amount of phosphorylated 14 Kd polypeptide was significantly increased in seeds treated simultaneously with NaCl and ABA.

  17. Mercuric chloride-induced protein-losing enteropathy (PLE) in brown Norway (BN) rats

    SciTech Connect

    Knoflach, P.; Weiser, M.M.; Albini, B.

    1986-03-05

    Prolonged exposure to low doses of mercuric chloride (MC) may induce immunologically mediated kidney disease in man and animals. Mercury compounds are of growing importance as environmental pollutants. Twenty female BN rats were gavaged with 150 microgram MC/100 gm body weight 3x/wk for up to 39 wks. Starting with wk 2, rat intestines demonstrated linear IgG and IgA deposits along the vascular and intestinal basement membranes (VBM and IBM). Serum antibodies to IBM were observed during the first 4 wks of gavage. At wk 11, first granular deposits of IgG and C3 were observed along VBM. Only after wk 35 were granular deposits also seen along the IBM. Using radioactive chromium chloride, 50% of rats with granular deposits along BM showed significantly increased protein loss into the intestines. Thus, granular deposits of IgG and C3 along the IBM, probably representing immune complexes, may lead to PLE. This animal model may contribute to the understanding of the pathogenesis of PLE in man described in graft-vrs-host reactions following bone marrow grafts, allergic enteritides, inflammatory bowel disease, and arsenic intoxication, as well as the assessment of biological effects of environmental pollutants.

  18. Stress induced changes in testis function.

    PubMed

    López-Calderón, A; Ariznavarreta, C; González-Quijano, M I; Tresguerres, J A; Calderón, M D

    1991-01-01

    The mechanism through which chronic stress inhibits the hypothalamic-pituitary-testicular axis has been investigated. Chronic restraint stress decreases testosterone secretion, an effect that is associated with a decrease in plasma gonadotropin levels. In chronically stressed rats there was a decrease in hypothalamic luteinizing hormone-releasing hormone (LHRH) content and the response on plasma gonadotropins to LHRH administration was enhanced. Thus the inhibitory effect of chronic stress on plasma LH and FSH levels seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a modification in LHRH secretion. It has been suggested that beta-endorphin might interfere with hypothalamic LHRH secretion during stress. Chronic immobilization did not modify hypothalamic beta-endorphin, while an increase in pituitary beta-endorphin secretion was observed. Since we cannot exclude that changes in beta-endorphin secreted by the pituitary or other opioids may play some role in the stress-induced decrease in LHRH secretion, the effect of naltrexone administration on plasma gonadotropin was studied in chronically stressed rats. Naltrexone treatment did not modify the decrease in plasma concentrations of LH or FSH. These findings suggest that the inhibitory effect of restraint on the testicular axis is exerted at hypothalamic level by some mechanism other than opioids.

  19. Stress induced changes in testis function.

    PubMed

    López-Calderón, A; Ariznavarreta, C; González-Quijano, M I; Tresguerres, J A; Calderón, M D

    1991-01-01

    The mechanism through which chronic stress inhibits the hypothalamic-pituitary-testicular axis has been investigated. Chronic restraint stress decreases testosterone secretion, an effect that is associated with a decrease in plasma gonadotropin levels. In chronically stressed rats there was a decrease in hypothalamic luteinizing hormone-releasing hormone (LHRH) content and the response on plasma gonadotropins to LHRH administration was enhanced. Thus the inhibitory effect of chronic stress on plasma LH and FSH levels seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a modification in LHRH secretion. It has been suggested that beta-endorphin might interfere with hypothalamic LHRH secretion during stress. Chronic immobilization did not modify hypothalamic beta-endorphin, while an increase in pituitary beta-endorphin secretion was observed. Since we cannot exclude that changes in beta-endorphin secreted by the pituitary or other opioids may play some role in the stress-induced decrease in LHRH secretion, the effect of naltrexone administration on plasma gonadotropin was studied in chronically stressed rats. Naltrexone treatment did not modify the decrease in plasma concentrations of LH or FSH. These findings suggest that the inhibitory effect of restraint on the testicular axis is exerted at hypothalamic level by some mechanism other than opioids. PMID:1958548

  20. Inactivation of Kupffer Cells by Gadolinium Chloride Protects Murine Liver From Radiation-Induced Apoptosis

    SciTech Connect

    Du Shisuo; Qiang Min; Zeng Zhaochong; Ke Aiwu; Ji Yuan; Zhang Zhengyu; Zeng Haiying; Liu Zhongshan

    2010-03-15

    Purpose: To determine whether the inhibition of Kupffer cells before radiotherapy (RT) would protect hepatocytes from radiation-induced apoptosis. Materials and Methods: A single 30-Gy fraction was administered to the upper abdomen of Sprague-Dawley rats. The Kupffer cell inhibitor gadolinium chloride (GdCl3; 10 mg/kg body weight) was intravenously injected 24 h before RT. The rats were divided into four groups: group 1, sham RT plus saline (control group); group 2, sham RT plus GdCl3; group 3, RT plus saline; and group 4, RT plus GdCl3. Liver tissue was collected for measurement of apoptotic cytokine expression and evaluation of radiation-induced liver toxicity by analysis of liver enzyme activities, hepatocyte micronucleus formation, apoptosis, and histologic staining. Results: The expression of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha was significantly attenuated in group 4 compared with group 3 at 2, 6, 24, and 48 h after injection (p <0.05). At early points after RT, the rats in group 4 exhibited significantly lower levels of liver enzyme activity, apoptotic response, and hepatocyte micronucleus formation compared with those in group 3. Conclusion: Selective inactivation of Kupffer cells with GdCl3 reduced radiation-induced cytokine production and protected the liver against acute radiation-induced damage.

  1. Improvement of Mercuric Chloride-Induced Testis Injuries and Sperm Quality Deteriorations by Spirulina platensis in Rats

    PubMed Central

    El-Desoky, Gaber E.; Bashandy, Samir A.; Alhazza, Ibrahim M.; Al-Othman, Zeid A.; Aboul-Soud, Mourad A. M.; Yusuf, Kareem

    2013-01-01

    The present study was undertaken to investigate the protective effect of the filamentous cyanobacterium Spirulina platensis (S. platensis) on mercury (II) chloride (HgCl2)-induced oxidative damages and histopathological alterations in the testis of Wistar albino rats. The animals were divided into four equal groups, i) control, ii) HgCl2, iii) S. platensis and iv) combination of HgCl2+S. platensis. Oxidative stress, induced by a single dose of HgCl2 (5 mg/kg, bw; subcutaneously, s.c.), substantially decreased (P<0.01) the activity level of testicular key enzymatic antioxidant biomarkers (superoxide dismutase, SOD; catalase, CAT and glutathione peroxidase, GPx), oxidative stress makers (blood hydroperoxide; testicular reduced glutathione, GSH and malondialdehyde, MDA), and testicular mercury levels. Moreover, HgCl2 administration resulted in a significant (P<0.01) increase in the number of sperms with abnormal morphology and decrease in epididymal sperm count, motility, plasma testosterone level and testicular cholesterol. Furthermore, HgCl2 exposure induced histopathological changes to the testis including morphological alterations of the seminiferous tubules, and degeneration and dissociation of spermatogenic cells. Notably, oral pretreatment of animals with Spirulina (300 mg/kg, bw) lowered the extent of the observed HgCl2-mediated toxicity, whereby significantly reducing the resulting lipid peroxidation products, mercury accumulation in the testis, histopathological changes of the testes and spermatozoal abnormalities. In parallel, the pretreatment with Spirulina also completely reverted the observed Hg-Cl2-induced inhibition in enzymatic activities of antioxidant biomarkers (SOD, CAT and GPx) back to control levels. The pretreatment of rats with S. platensis significantly recovered the observed HgCl2-mediated decrease in the weight of accessory sex organs. Taken together, our findings clearly highlight the role of S. platensis as a protective modulator of HgCl2

  2. Chloride determination by ion chromatography in petroleum coke after digestion by microwave-induced combustion.

    PubMed

    Pereira, Juliana S F; Diehl, Liange O; Duarte, Fábio A; Santos, Maria F P; Guimarães, Regina C L; Dressler, Valderi L; Flores, Erico M M

    2008-12-12

    Microwave-induced combustion was applied to petroleum coke digestion in closed vessels for further chloride determination by ion chromatography. Samples were pressed as pellets and placed on a quartz holder. Combustion was performed using oxygen pressure of 2 MPa and 50 microl of 6 moll(-1) NH(4)NO(3) as aid for ignition. Recoveries from 97 to 102% were obtained for all studied absorbing solutions (water, H(2)O(2), Na(2)CO(3) or (NH(4))(2)CO(3)). Accuracy was evaluated using certified reference materials with agreement better than 98% using water as absorbing solution with reflux step. The limit of quantification was 3.8 microg g(-1). PMID:18996537

  3. Efficient micropropagation and chlorocholine chloride induced stevioside production of Stevia rebaudiana Bertoni.

    PubMed

    Dey, Avishek; Kundu, Sayanti; Bandyopadhyay, Abhijit; Bhattacharjee, Aloke

    2013-01-01

    A promising method of micropropagation of Stevia rebaudiana Bertoni has been developed with an aim to increase the biomass, survivability of the plantlets and stevioside production, using chlorocholine chloride (CCC). Microshoots transferred to the MS medium containing different combinations CCC and IBA were found to be most effective in terms of growth pattern, hardening ability of the plantlets and stevioside content, compared to MS medium containing either IBA or CCC. Among other combinations tested, MS medium supplemented with 3 mg/l CCC and 3 mg/l IBA was found most effective in inducing significant changes like reduced shoot length, increased number of roots, higher leaf size, increased biomass and chlorophyll retaining capacity, higher survival percentage and most importantly the elevated stevioside content. Collectively, the major observations of this research indicate that application of CCC in micropropagation of S. rebaudiana Bertoni is a promising approach and has commercial prospects.

  4. Efficient micropropagation and chlorocholine chloride induced stevioside production of Stevia rebaudiana Bertoni.

    PubMed

    Dey, Avishek; Kundu, Sayanti; Bandyopadhyay, Abhijit; Bhattacharjee, Aloke

    2013-01-01

    A promising method of micropropagation of Stevia rebaudiana Bertoni has been developed with an aim to increase the biomass, survivability of the plantlets and stevioside production, using chlorocholine chloride (CCC). Microshoots transferred to the MS medium containing different combinations CCC and IBA were found to be most effective in terms of growth pattern, hardening ability of the plantlets and stevioside content, compared to MS medium containing either IBA or CCC. Among other combinations tested, MS medium supplemented with 3 mg/l CCC and 3 mg/l IBA was found most effective in inducing significant changes like reduced shoot length, increased number of roots, higher leaf size, increased biomass and chlorophyll retaining capacity, higher survival percentage and most importantly the elevated stevioside content. Collectively, the major observations of this research indicate that application of CCC in micropropagation of S. rebaudiana Bertoni is a promising approach and has commercial prospects. PMID:23537766

  5. Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

    PubMed Central

    Sheng, Lei; Zhu, Liyuan; Guan, Ning; Gui, Suxin; Sang, Xuezi; Zhao, Xiaoyang; Sun, Qingqing; Wang, Ling; Cheng, Jie; Hu, Renping; Hong, Fashui

    2013-01-01

    Cerium is widely used in many aspects of modern society, including agriculture, industry and medicine. It has been demonstrated to enter the ecological environment, is then transferred to humans through food chains, and causes toxic actions in several organs including the brain of animals. However, the neurotoxic molecular mechanisms are not clearly understood. In this study, mice were exposed to 0.5, 1, and 2 mg/kg BW cerium chloride (CeCl3) for 90 consecutive days, and their learning and memory ability as well as hippocampal gene expression profile were investigated. Our findings suggested that exposure to CeCl3 led to hippocampal lesions, apoptosis, oxidative stress and impairment of spatial recognition memory. Furthermore, microarray data showed marked alterations in the expression of 154 genes involved in learning and memory, immunity and inflammation, signal transduction, apoptosis and response to stress in the 2 mg/kg CeCl3 exposed hippocampi. Specifically, the significant up-regulation of Axud1, Cdc37, and Ube2v1 caused severe apoptosis, and great suppression of Adcy8, Fos, and Slc5a7 expression led to impairment of mouse cognitive ability. Therefore, Axud1, Cdc37, Ube2v1, Adcy8, Fos, and Slc5a7 may be potential biomarkers of hippocampal toxicity caused by CeCl3 exposure. PMID:23573234

  6. Tributyltin-induced endoplasmic reticulum stress and its Ca{sup 2+}-mediated mechanism

    SciTech Connect

    Isomura, Midori; Kotake, Yaichiro Masuda, Kyoichi; Miyara, Masatsugu; Okuda, Katsuhiro; Samizo, Shigeyoshi; Sanoh, Seigo; Hosoi, Toru; Ozawa, Koichiro; Ohta, Shigeru

    2013-10-01

    Organotin compounds, especially tributyltin chloride (TBT), have been widely used in antifouling paints for marine vessels, but exhibit various toxicities in mammals. The endoplasmic reticulum (ER) is a multifunctional organelle that controls post-translational modification and intracellular Ca{sup 2+} signaling. When the capacity of the quality control system of ER is exceeded under stress including ER Ca{sup 2+} homeostasis disruption, ER functions are impaired and unfolded proteins are accumulated in ER lumen, which is called ER stress. Here, we examined whether TBT causes ER stress in human neuroblastoma SH-SY5Y cells. We found that 700 nM TBT induced ER stress markers such as CHOP, GRP78, spliced XBP1 mRNA and phosphorylated eIF2α. TBT also decreased the cell viability both concentration- and time-dependently. Dibutyltin and monobutyltin did not induce ER stress markers. We hypothesized that TBT induces ER stress via Ca{sup 2+} depletion, and to test this idea, we examined the effect of TBT on intracellular Ca{sup 2+} concentration using fura-2 AM, a Ca{sup 2+} fluorescent probe. TBT increased intracellular Ca{sup 2+} concentration in a TBT-concentration-dependent manner, and Ca{sup 2+} increase in 700 nM TBT was mainly blocked by 50 μM dantrolene, a ryanodine receptor antagonist (about 70% inhibition). Dantrolene also partially but significantly inhibited TBT-induced GRP78 expression and cell death. These results suggest that TBT increases intracellular Ca{sup 2+} concentration by releasing Ca{sup 2+} from ER, thereby causing ER stress. - Highlights: • We established that tributyltin induces endoplasmic reticulum (ER) stress. • Tributyltin induces ER stress markers in a concentration-dependent manner. • Tributyltin increases Ca{sup 2+} release from ER, thereby causing ER stress. • Dibutyltin and monobutyltin did not increase GRP78 or intracellular Ca{sup 2+}.

  7. Temperature-induced lipocalin (TIL) is translocated under salt stress and protects chloroplasts from ion toxicity.

    PubMed

    Abo-Ogiala, Atef; Carsjens, Caroline; Diekmann, Heike; Fayyaz, Payam; Herrfurth, Cornelia; Feussner, Ivo; Polle, Andrea

    2014-02-15

    Temperature-induced lipocalins (TIL) have been invoked in the defense from heat, cold and oxidative stress. Here we document a function of TIL for basal protection from salinity stress. Heterologous expression of TIL from the salt resistant poplar Populus euphratica did not rescue growth but prevented chlorophyll b destruction in salt-exposed Arabidopsis thaliana. The protein was localized to the plasma membrane but was re-translocated to the symplast under salt stress. The A. thaliana knock out and knock down lines Attil1-1 and Attil1-2 showed stronger stress symptoms and stronger chlorophyll b degradation than the wildtype (WT) under excess salinity. They accumulated more chloride and sodium in chloroplasts than the WT. Chloroplast chloride accumulation was found even in the absence of salt stress. Since lipocalins are known to bind regulatory fatty acids of channel proteins as well as iron, we suggest that the salt-induced trafficking of TIL may be required for protection of chloroplasts by affecting ion homeostasis.

  8. Cobalt chloride attenuates hypobaric hypoxia induced vascular leakage in rat brain: Molecular mechanisms of action of cobalt chloride

    SciTech Connect

    Kalpana, S.; Dhananjay, S.; Anju, B. Lilly, G.; Sai Ram, M.

    2008-09-15

    This study reports the efficacy of cobalt preconditioning in preventing hypobaric hypoxia induced vascular leakage (an indicator of cerebral edema) using male Sprague-Dawley rats as model system. Exposure of animals to hypobaric hypoxia led to a significant increase in vascular leakage, reactive oxygen species (ROS), nitric oxide (NO), and vascular endothelial growth factor (VEGF) levels. There was a marked increase in Nuclear Factor {kappa}B (NF{kappa}B) DNA binding activity and levels of pro-inflammatory cytokines such as Monocyte chemoattractant protein (MCP-1), Interferon-{gamma} (IFN-{gamma}), Interleukin-1 (IL-1), and Tumor Necrosis Factor-{alpha} (TNF-{alpha}) and cell adhesion molecules such as Vascular Cell Adhesion Molecule-1 (VCAM-1), and P-selectin. Chemical preconditioning by cobalt for 7 days (12.5 mg Co/kg b.w., oral) significantly attenuated cerebral vascular leakage and the expression of inflammatory mediators induced by hypoxia. Administration of NF{kappa}B inhibitor, curcumin (50 mg/kg b.w.; i.p.) appreciably inhibited hypoxia induced vascular leakage indicating the involvement of NF{kappa}B in causing vascular leakage. Interestingly, cobalt when administered at 12.5 mg Co/kg b.w. (i.p.), 1 h before hypoxia could not prevent the vascular leakage indicating that cobalt per se did not have an effect on NF{kappa}B. The lower levels of NF{kappa}B observed in the brains of cobalt administered animals might be due to higher levels of antioxidant and anti-inflammatory proteins (hemeoxygenase-1 and metallothionein). To conclude cobalt preconditioning inhibited hypobaric hypoxia induced cerebral vascular leakage by lowering NF{kappa}B DNA binding activity and its regulated pro-inflammatory mediators. This is contemplated to be mediated by cobalt induced reduction in ROS/NO and increase in HO-1 and MT.

  9. Lycium barbarum Polysaccharides Protect against Trimethyltin Chloride-Induced Apoptosis via Sonic Hedgehog and PI3K/Akt Signaling Pathways in Mouse Neuro-2a Cells

    PubMed Central

    Zhao, Wanyun; Pan, Xiaoqi; Li, Tao; Zhang, Changchun; Shi, Nian

    2016-01-01

    Trimethyltin chloride (TMT) is a classic neurotoxicant that can cause severe neurodegenerative diseases. Some signaling pathways involving cell death play pivotal roles in the central nervous system. In this study, the role of Sonic Hedgehog (Shh) and PI3K/Akt pathways in TMT-induced apoptosis and protective effect of Lycium barbarum polysaccharides (LBP) on mouse neuro-2a (N2a) cells were investigated. Results showed that TMT treatment significantly enhanced apoptosis, upregulated proapoptotic Bax, downregulated antiapoptotic Bcl-2 expression, and increased caspase-3 activity in a dose-dependent manner in N2a cells. TMT induced oxidative stress in cells, performing reactive oxygen species (ROS) and malondialdehyde (MDA) excessive generation, and superoxide dismutase (SOD) activity reduction. TMT significantly decreased phosphorylated glycogen synthase kinase-3β (GSK-3β) and inhibited Shh and PI3K/Akt pathways. However, the addition of LBP upregulated GSK-3β phosphorylation, activated Shh and PI3K/Akt pathways, and eventually reduced apoptosis and oxidative stress caused by TMT. The interaction between Shh and PI3K/Akt pathways was clarified by specific PI3K inhibitor LY294002 or Shh inhibitor GDC-0449. Moreover, LY294002 and GDC-0449 pretreatment both induced phosphorylated GSK-3β downregulation and significantly promoted apoptosis induced by TMT. These results suggest that LBP could reduce TMT-induced N2a cells apoptosis by regulating GSK-3β phosphorylation, Shh, and PI3K/Akt signaling pathways. PMID:27143997

  10. The AQP-3 water channel is a pivotal modulator of glycerol-induced chloride channel activation in nasopharyngeal carcinoma cells.

    PubMed

    Zhang, Haifeng; Deng, Zhiqin; Yang, Lili; Luo, Hai; Liu, Shanwen; Li, Yuan; Wei, Yan; Peng, Shuang; Zhu, Linyan; Wang, Liwei; Chen, Lixin

    2016-03-01

    Aquaporin (AQP) and chloride channels are ubiquitous in virtually all living cells, playing pivotal roles in cell proliferation, migration and apoptosis. We previously reported that AQP-3 aquaglyceroporin and ClC-3 chloride channels could form complexes to regulate cell volume in nasopharyngeal carcinoma cells. In this study, the roles of AQP-3 in their hetero-complexes were further investigated. Glycerol entered the cells via AQP-3 and induced two different Cl(-) currents through cell swelling-dependent or -independent pathways. The swelling-dependent Cl(-) current was significantly inhibited by pretreatment with CuCl2 and AQP-3-siRNA. After siRNA-induced AQP-3 knock-down, the 140 mM glycerol isoosmotic solution swelled cells by 22% (45% in AQP-3-intact cells) and induced a smaller Cl(-) current; this current was smaller than that activated by 8% cell volume swelling, which induced by the 140 mM glycerol hyperosmotic solution in AQP-3-intact cells. This suggests that the interaction between AQP-3 and ClC-3 plays an important role in cell volume regulation and that AQP-3 may be a modulator that opens volume-regulated chloride channels. The swelling-independent Cl(-) current, which was activated by extracellular glycerol, was reduced by CuCl2 and AQP-3-siRNA pretreatment. Dialyzing glycerol into cells via the pipette directly induced the swelling-independent Cl(-) current; however this current was blocked by AQP-3 down-regulation, suggesting AQP-3 is essential for the opening of chloride channels. In conclusion, AQP-3 is the pathway for water, glycerol and other small solutes to enter cells, and it may be an essential modulator for the gating of chloride channels. PMID:26794461

  11. Topical application of lithium chloride on the pulp induces dentin regeneration.

    PubMed

    Ishimoto, Kazuya; Hayano, Satoru; Yanagita, Takeshi; Kurosaka, Hiroshi; Kawanabe, Noriaki; Itoh, Shinsuke; Ono, Mitsuaki; Kuboki, Takuo; Kamioka, Hiroshi; Yamashiro, Takashi

    2015-01-01

    We herein describe a novel procedure for dentin regeneration that mimics the biological processes of tooth development in nature. The canonical Wnt signaling pathway is an important regulator of the Dentin sialophosphoprotein (Dspp) expression. Our approach mimics the biological processes underlying tooth development in nature and focuses on the activation of canonical Wnt signaling to trigger the natural process of dentinogenesis. The coronal portion of the dentin and the underlying pulp was removed from the first molars. We applied lithium chloride (LiCl), an activator of canonical Wnt signaling, on the amputated pulp surface to achieve transdifferentiation toward odontoblasts from the surrounding pulpal cells. MicroCT and microscopic analyses demonstrated that the topical application of LiCl induced dentin repair, including the formation of a complete dentin bridge. LiCl-induced dentin is a tubular dentin in which the pulp cells are not embedded within the matrix, as in primary dentin. In contrast, a dentin bridge was not induced in the control group treated with pulp capping with material carriers alone, although osteodentin without tubular formation was induced at a comparatively deeper position from the pulp exposure site. We also evaluated the influence of LiCl on differentiation toward odontoblasts in vitro. In the mDP odontoblast cell line, LiCl activated the mRNA expression of Dspp, Axin2 and Kallikrein 4 (Klk4) and downregulated the Osteopontin (Osp) expression. These results provide a scientific basis for the biomimetic regeneration of dentin using LiCl as a new capping material to activate dentine regeneration.

  12. Topical Application of Lithium Chloride on the Pulp Induces Dentin Regeneration

    PubMed Central

    Ishimoto, Kazuya; Hayano, Satoru; Yanagita, Takeshi; Kurosaka, Hiroshi; Kawanabe, Noriaki; Itoh, Shinsuke; Ono, Mitsuaki; Kuboki, Takuo; Kamioka, Hiroshi; Yamashiro, Takashi

    2015-01-01

    We herein describe a novel procedure for dentin regeneration that mimics the biological processes of tooth development in nature. The canonical Wnt signaling pathway is an important regulator of the Dentin sialophosphoprotein (Dspp) expression. Our approach mimics the biological processes underlying tooth development in nature and focuses on the activation of canonical Wnt signaling to trigger the natural process of dentinogenesis. The coronal portion of the dentin and the underlying pulp was removed from the first molars. We applied lithium chloride (LiCl), an activator of canonical Wnt signaling, on the amputated pulp surface to achieve transdifferentiation toward odontoblasts from the surrounding pulpal cells. MicroCT and microscopic analyses demonstrated that the topical application of LiCl induced dentin repair, including the formation of a complete dentin bridge. LiCl-induced dentin is a tubular dentin in which the pulp cells are not embedded within the matrix, as in primary dentin. In contrast, a dentin bridge was not induced in the control group treated with pulp capping with material carriers alone, although osteodentin without tubular formation was induced at a comparatively deeper position from the pulp exposure site. We also evaluated the influence of LiCl on differentiation toward odontoblasts in vitro. In the mDP odontoblast cell line, LiCl activated the mRNA expression of Dspp, Axin2 and Kallikrein 4 (Klk4) and downregulated the Osteopontin (Osp) expression. These results provide a scientific basis for the biomimetic regeneration of dentin using LiCl as a new capping material to activate dentine regeneration. PMID:25812134

  13. Case report of occupational asthma induced by polyvinyl chloride and nickel.

    PubMed

    Song, Ga-Won; Ban, Ga-Young; Nam, Young-Hee; Park, Hae-Sim; Ye, Young-Min

    2013-10-01

    Polyvinyl chloride (PVC) is a widely used chemical for production of plastics. However occupational asthma (OA) caused by PVC has been reported only rarely. We report a 34-yr-old male wallpaper factory worker with OA due to PVC and nickel (Ni) whose job was mixing PVC with plasticizers. He visited the emergency room due to an asthma attack with moderate airflow obstruction and markedly increased sputum eosinophil numbers. A methacholine challenge test was positive (PC20 2.5 mg/mL). Bronchoprovocation tests with both PVC and Ni showed early and late asthmatic responses, respectively. Moreover, the fractional concentration of exhaled nitric oxide (FeNO) was increased after challenge with PVC. To our knowledge, this is the first case of OA in Korea induced by exposure to both PVC and Ni. We suggest that eosinophilic inflammation may be involved in the pathogenesis of PVC-induced OA and that FeNO monitoring can be used for its diagnosis.

  14. Acrolein induces oxidative stress in brain mitochondria.

    PubMed

    Luo, Jian; Shi, Riyi

    2005-02-01

    Acrolein, a byproduct of lipid peroxidation, has been shown to inflict significant structural and functional damage to isolated guinea pig spinal cord. Reactive oxygen species (ROS) are thought to mediate such detrimental effects. The current study demonstrates that acrolein can directly stimulate mitochondrial oxidative stress. Specifically, exposure of purified brain mitochondria to acrolein resulted in a dose-dependent increase of ROS and decreases in glutathione content and aconitase activity. This effect was not accompanied by significant intramitochondrial calcium influx or mitochondrial permeability transition, but rather by impaired function of the mitochondrial electron transport system. As well, we detected a significant inhibition of mitochondrial adenine nucleotide translocase (ANT) in the presence of acrolein. This inhibition of ANT likely contributes to acrolein-induced ROS elevation since application of atractyloside, a specific ANT inhibitor, induced significant increase of ROS. We hypothesize that inhibition of ANT may mediate, in part, the acrolein-induced ROS increase in mitochondria.

  15. Changes in metabolites, antioxidant system, and gene expression in Microcystis aeruginosa under sodium chloride stress.

    PubMed

    Chen, Lei; Mao, Feijian; Kirumba, George Chira; Jiang, Cheng; Manefield, Mike; He, Yiliang

    2015-12-01

    Microcystis (M.) aeruginosa, one of the most common bloom-forming cyanobacteria, occurs worldwide. The Qingcaosha (QCS) Reservoir is undergoing eutrophication and faces the problem of saltwater intrusion. The aim of this study was to investigate the effects of sudden salinity changes on physiological parameters and related gene transcription in M. aeruginosa under controlled laboratory conditions. The results showed that sodium chloride (50, 200 and 500 mg L(-1) NaCl) inhibited the algal growth and decreased pigment concentrations (chlorophyll a, carotenoid and phycocyanin). Sodium chloride increased both the intracellular and extracellular microcystin contents and elevated the mcyD transcript level in M. aeruginosa. It also increased the malondialdehyde (MDA) content and caused cytomembrane damage. This damage caused the release of intracellular toxins into the culture medium. In addition, NaCl decreased the maximum electron transport rate, increased the levels of reactive oxygen species (ROS) and changed the cellular redox status. Consequently, NaCl inhibited the expression of cpcB, psbA and rbcL. Furthermore, NaCl increased the activities of superoxide dismutases (SOD), catalase (CAT), glutathione reductase (GR), and total glutathione peroxidase (GPx). The transcript levels of sod and reduced glutathione (gsh) were also increased after exposure to NaCl. Our results indicate that a sudden increase in salinity increases the production and excretion of microcystin, changes the cellular redox status, enhances the activities of antioxidant enzymes, inhibits photosynthesis, and affects transcript levels of related genes in M. aeruginosa. PMID:26232039

  16. Changes in metabolites, antioxidant system, and gene expression in Microcystis aeruginosa under sodium chloride stress.

    PubMed

    Chen, Lei; Mao, Feijian; Kirumba, George Chira; Jiang, Cheng; Manefield, Mike; He, Yiliang

    2015-12-01

    Microcystis (M.) aeruginosa, one of the most common bloom-forming cyanobacteria, occurs worldwide. The Qingcaosha (QCS) Reservoir is undergoing eutrophication and faces the problem of saltwater intrusion. The aim of this study was to investigate the effects of sudden salinity changes on physiological parameters and related gene transcription in M. aeruginosa under controlled laboratory conditions. The results showed that sodium chloride (50, 200 and 500 mg L(-1) NaCl) inhibited the algal growth and decreased pigment concentrations (chlorophyll a, carotenoid and phycocyanin). Sodium chloride increased both the intracellular and extracellular microcystin contents and elevated the mcyD transcript level in M. aeruginosa. It also increased the malondialdehyde (MDA) content and caused cytomembrane damage. This damage caused the release of intracellular toxins into the culture medium. In addition, NaCl decreased the maximum electron transport rate, increased the levels of reactive oxygen species (ROS) and changed the cellular redox status. Consequently, NaCl inhibited the expression of cpcB, psbA and rbcL. Furthermore, NaCl increased the activities of superoxide dismutases (SOD), catalase (CAT), glutathione reductase (GR), and total glutathione peroxidase (GPx). The transcript levels of sod and reduced glutathione (gsh) were also increased after exposure to NaCl. Our results indicate that a sudden increase in salinity increases the production and excretion of microcystin, changes the cellular redox status, enhances the activities of antioxidant enzymes, inhibits photosynthesis, and affects transcript levels of related genes in M. aeruginosa.

  17. Paternal Transmission of Stressed-Induced Pathologies

    PubMed Central

    Dietz, David M.; LaPlant, Quincey; Watts, Emily L.; Hodes, Georgia E.; Russo, Scott J.; Feng, Jian; Oosting, Ronald S.; Vialou, Vincent; Nestler, Eric J.

    2011-01-01

    Background There has been recent interest in the possibility that epigenetic mechanisms might contribute to the trans-generational transmission of stress-induced vulnerability. Here, we focused on possible paternal transmission using the social defeat stress paradigm. Methods Adult male mice exposed to chronic social defeat stress, or control non-defeated mice, were bred with normal female mice and their offspring were assessed behaviorally for depressive- and anxiety-like measures. Plasma levels of corticosterone and vascular endothelial growth factor (VEGF) were also assayed. To directly assess the role of epigenetic mechanisms, we used in vitro fertilization (IVF); behavioral assessments were conducted on offspring of mice from IVF-control and IVF-defeated fathers. Results We show that both male and female offspring from defeated fathers exhibit increased measures of several depression- and anxiety-like behaviors. The male offspring of defeated fathers also display increased baseline plasma levels of corticosterone and decreased levels of VEGF. However, most of these behavioral changes were not observed when offspring were generated through IVF. Conclusion These results suggest that, while behavioral adaptations that occur after chronic social defeat stress can be transmitted from the father to his male and female F1 progeny, only very subtle changes might be transmitted epigenetically under the conditions tested. PMID:21679926

  18. Studies on effect of stress preconditioning in restrain stress-induced behavioral alterations.

    PubMed

    Kaur, Rajneet; Jaggi, Amteshwar Singh; Singh, Nirmal

    2010-02-01

    Stress preconditioning has been documented to confer on gastroprotective effects on stress-induced gastric ulcerations. However, the effects of prior exposure of stress preconditioning episodes on stress-induced behavioral changes have not been explored yet. Therefore the present study was designed to investigate the ameliorative effects of stress preconditioning in immobilization stress-induced behavioral alterations in rats. The rats were subjected to restrain stress by placing in restrainer (5.5 cm in diameter and 18 cm in length) for 3.5 h. Stress preconditioning was induced by subjecting the rats to two cycles of restraint and restrain-free periods of 15 min each. Furthermore, a similar type of stress preconditioning was induced using different time cycles of 30 and 45 min. The extent and severity of the stress-induced behavioral alterations were assessed using different behavioral tests such as hole-board test, social interaction test, open field test, and actophotometer. Restrain stress resulted in decrease in locomotor activity, frequency of head dips and rearing in hole board, line crossing and rearing in open field, and decreased following and increased avoidance in social interaction test. Stress preconditioning with two cycles of 15, 30 or 45 min respectively, did not attenuate stress-induced behavioral changes to any extent. It may be concluded that stress preconditioning does not seem to confer any protective effect in modulating restrain stress-induced behavioral alterations.

  19. Effects of applied potential on the stress corrosion cracking behavior of 7003 aluminum alloy in acid and alkaline chloride solutions

    NASA Astrophysics Data System (ADS)

    Zhang, Xiao-yan; Song, Ren-guo; Sun, Bin; Lu, Hai; Wang, Chao

    2016-07-01

    Potentiodynamic polarization tests and slow strain rate test (SSRT) in combination with fracture morphology observations were conducted to investigate the stress corrosion cracking (SCC) behavior of 7003 aluminum alloy (AA7003) in acid and alkaline chloride solutions under various applied potentials ( E a). The results show that AA7003 is to a certain extent susceptible to SCC via anodic dissolution (AD) at open-circuit potential (OCP) and is highly susceptible to hydrogen embrittlement (HE) at high negative E a in the solutions with pH levels of 4 and 11. The susceptibility increases with negative shift in the potential when E a is less than -1000 mV vs. SCE. However, the susceptibility distinctly decreases because of the inhibition of AD when E a is equal to -1000 mV vs. SCE. In addition, the SCC susceptibility of AA7003 in the acid chloride solution is higher than that in the alkaline solution at each potential. Moreover, the effect of hydrogen on SCC increases with increasing hydrogen ion concentration.

  20. Effects of chronic exposure to benzalkonium chloride in Oncorhynchus mykiss: cholinergic neurotoxicity, oxidative stress, peroxidative damage and genotoxicity.

    PubMed

    Antunes, S C; Nunes, B; Rodrigues, S; Nunes, R; Fernandes, J; Correia, A T

    2016-07-01

    Benzalkonium chloride (BAC) is one of the most used conservatives in pharmaceutical preparations. However, its use is limited to a small set of external use formulations, due to its high toxicity. Benzalkonium chloride effects are related to the potential exertion of deleterious effects, mediated via oxidative stress and through interaction with membrane enzymes, leading to cellular damage. To address the ecotoxicity of this specific compound rainbow trouts were chronically exposed to BAC at environmental relevant concentrations (ranging from 0.100 to 1.050mg/L), and the biological response of cholinergic neurotoxicity, modulation of the antioxidant defense, phase II metabolism, lipid peroxidation and genotoxicity was studied. The obtained results showed a dual pattern of antioxidant response, with significant alterations in catalase activity (starting at 0.180mg/L), and lipid peroxidation, for intermediate (0.180 and 0.324mg/L) concentrations. No significant alterations occurred for glutathione-S-transferases activity. An unexpected increased of the acetylcholinesterase activity was also recorded for the individuals exposed to higher concentrations of BAC (starting at 0.180mg/L). Furthermore, exposure to BAC resulted in the establishment of genotoxic alterations, observable (for the specific case of the comet assay results) for all tested BAC concentrations. However, and considering that the oxidative response was not devisable, other mechanisms may be involved in the genotoxic effects reported here. PMID:27280532

  1. Differences in GABA-induced chloride ion influx in brain of inbred mouse strains

    SciTech Connect

    Yu, O.; Chiu, T.H.; Rosenberg, H.C.

    1986-03-01

    Audiogenic seizure-susceptible (AS) mice (DBA2J) are a widely used model of epilepsy. The precise pathophysiology of this mouse strain is not fully understood. One of the proposed mechanisms was a difference in GABA/BZ receptor affinity and population from that of audiogenic seizure resistant (ASR) mice. This study attempted to determine the difference in function of GABA/BZ receptor between DBA2J (AS) and C57BL6J (ASR) mice by directly measuring the GABA-induced chloride ion (/sup 36/Cl/sup -/) influx in twice washed crude brain homogenates. /sup 36/Cl/sup -/ influx was terminated by ice-cold buffer and collected by filtration. A concentration range of 2-1000 ..mu..M GABA and two age-matched groups (20-22 days and 40-42 days) were used. GABA-induced /sup 36/Cl/sup -/ influx was dose-dependent, and brain homogenates from DBA2J mice (20-22 days) were less sensitive to GABA-induced Cl/sup -/ ion influx than C57BL6J mice at both age groups. However, in older DBA2J mice (40-42 days), the sensitivity to GABA was intermediate between that of the younger AS mice and the control ASR mice. No significant difference in basal influx of Cl/sup -/ was observed between age groups and mouse strains, nor was there any significant difference between 20-22 days old and 40-42 days old C57BL6J mice. In conclusion, this study had demonstrated a malfunction may recover with age.

  2. Stress-induced mutagenesis and complex adaptation

    PubMed Central

    Ram, Yoav; Hadany, Lilach

    2014-01-01

    Because mutations are mostly deleterious, mutation rates should be reduced by natural selection. However, mutations also provide the raw material for adaptation. Therefore, evolutionary theory suggests that the mutation rate must balance between adaptability—the ability to adapt—and adaptedness—the ability to remain adapted. We model an asexual population crossing a fitness valley and analyse the rate of complex adaptation with and without stress-induced mutagenesis (SIM)—the increase of mutation rates in response to stress or maladaptation. We show that SIM increases the rate of complex adaptation without reducing the population mean fitness, thus breaking the evolutionary trade-off between adaptability and adaptedness. Our theoretical results support the hypothesis that SIM promotes adaptation and provide quantitative predictions of the rate of complex adaptation with different mutational strategies. PMID:25143032

  3. Symbiosis-induced adaptation to oxidative stress.

    PubMed

    Richier, Sophie; Furla, Paola; Plantivaux, Amandine; Merle, Pierre-Laurent; Allemand, Denis

    2005-01-01

    Cnidarians in symbiosis with photosynthetic protists must withstand daily hyperoxic/anoxic transitions within their host cells. Comparative studies between symbiotic (Anemonia viridis) and non-symbiotic (Actinia schmidti) sea anemones show striking differences in their response to oxidative stress. First, the basal expression of SOD is very different. Symbiotic animal cells have a higher isoform diversity (number and classes) and a higher activity than the non-symbiotic cells. Second, the symbiotic animal cells of A. viridis also maintain unaltered basal values for cellular damage when exposed to experimental hyperoxia (100% O(2)) or to experimental thermal stress (elevated temperature +7 degrees C above ambient). Under such conditions, A. schmidti modifies its SOD activity significantly. Electrophoretic patterns diversify, global activities diminish and cell damage biomarkers increase. These data suggest symbiotic cells adapt to stress while non-symbiotic cells remain acutely sensitive. In addition to being toxic, high O(2) partial pressure (P(O(2))) may also constitute a preconditioning step for symbiotic animal cells, leading to an adaptation to the hyperoxic condition and, thus, to oxidative stress. Furthermore, in aposymbiotic animal cells of A. viridis, repression of some animal SOD isoforms is observed. Meanwhile, in cultured symbionts, new activity bands are induced, suggesting that the host might protect its zooxanthellae in hospite. Similar results have been observed in other symbiotic organisms, such as the sea anemone Aiptasia pulchella and the scleractinian coral Stylophora pistillata. Molecular or physical interactions between the two symbiotic partners may explain such variations in SOD activity and might confer oxidative stress tolerance to the animal host. PMID:15634847

  4. Symbiosis-induced adaptation to oxidative stress.

    PubMed

    Richier, Sophie; Furla, Paola; Plantivaux, Amandine; Merle, Pierre-Laurent; Allemand, Denis

    2005-01-01

    Cnidarians in symbiosis with photosynthetic protists must withstand daily hyperoxic/anoxic transitions within their host cells. Comparative studies between symbiotic (Anemonia viridis) and non-symbiotic (Actinia schmidti) sea anemones show striking differences in their response to oxidative stress. First, the basal expression of SOD is very different. Symbiotic animal cells have a higher isoform diversity (number and classes) and a higher activity than the non-symbiotic cells. Second, the symbiotic animal cells of A. viridis also maintain unaltered basal values for cellular damage when exposed to experimental hyperoxia (100% O(2)) or to experimental thermal stress (elevated temperature +7 degrees C above ambient). Under such conditions, A. schmidti modifies its SOD activity significantly. Electrophoretic patterns diversify, global activities diminish and cell damage biomarkers increase. These data suggest symbiotic cells adapt to stress while non-symbiotic cells remain acutely sensitive. In addition to being toxic, high O(2) partial pressure (P(O(2))) may also constitute a preconditioning step for symbiotic animal cells, leading to an adaptation to the hyperoxic condition and, thus, to oxidative stress. Furthermore, in aposymbiotic animal cells of A. viridis, repression of some animal SOD isoforms is observed. Meanwhile, in cultured symbionts, new activity bands are induced, suggesting that the host might protect its zooxanthellae in hospite. Similar results have been observed in other symbiotic organisms, such as the sea anemone Aiptasia pulchella and the scleractinian coral Stylophora pistillata. Molecular or physical interactions between the two symbiotic partners may explain such variations in SOD activity and might confer oxidative stress tolerance to the animal host.

  5. Stress corrosion cracking of a titanium alloy in chloride-containing liquid environments

    NASA Technical Reports Server (NTRS)

    Smyrl, W. H.; Blackburn, M. J.

    1974-01-01

    Ti-8 Al-1 Mo-1 V was tested in solvents containing chloride, bromide or iodide ions. It was found that the region II plateau velocity could be correlated with the inverse of the viscosity for several solvents. It seems most likely that this reflects the influence of the viscosity on the diffusion coefficient of some species involved in a mass transfer process which limits the crack growth. Associated tests were performed in which the potential, pH and concentration of Cl- were varied, in some of the same solutions as used for the viscosity tests. It is concluded from these tests that the absence of cathodic protection against cracking in solutions of low pH arises from an ohmic effect which isolates the crack tip from external potential control.

  6. Modification of nylon-6 fibres by radiation-induced graft polymerisation of vinylbenzyl chloride

    NASA Astrophysics Data System (ADS)

    Ting, T. M.; Nasef, Mohamed Mahmoud; Hashim, Kamaruddin

    2015-04-01

    Modification of nylon-6 fibres by radiation-induced graft copolymerisation (RIGP) of vinylbenzyl chloride (VBC) using the preirradiation method was investigated. A number of grafting parameters such as type of solvent, total dose, monomer concentrations, reaction temperature and reaction time were studied to obtain desired degree of grafting (DG). The DG was found to be a function of reaction parameters and achieved a maximum value of 130 wt% at 20 vol% VBC concentration in methanol, 300 kGy dose, 30 °C temperature and 3 h reaction time. Fourier-transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) and X-ray diffraction (XRD) were employed to evaluate the chemical, morphological and structural changes that occurred in the grafted fibres, respectively. Thermogravimetric analysis (TGA) was also applied to determine the thermal stability, whereas differential scanning calorimeter (DSC) and universal mechanical tester were used to analyse respective thermal and mechanical properties of the grafted fibres. The results of these analyses provide strong evidence for successful grafting of VBC onto nylon-6, and the variation in the properties of the grafted fibres depends on DG.

  7. Modulatory Role of Simvastatin against Aluminium Chloride-Induced Behavioural and Biochemical Changes in Rats

    PubMed Central

    Nampoothiri, Madhavan; John, Jessy; Kumar, Nitesh; Mudgal, Jayesh; Nampurath, Gopalan Kutty; Chamallamudi, Mallikarjuna Rao

    2015-01-01

    Objectives. Aluminium, a neurotoxic agent in humans, has been implicated in the pathogenesis of neurodegenerative disorders. In this study, we examined the behavioral and biochemical effects of aluminium in rats with special emphasis on memory centres, namely, hippocampus and frontal cortex. Further, the effect of simvastatin treatment on aluminium intoxication was evaluated. Methods. Rats were exposed to aluminium chloride (AlCl3) for 60 days. Simvastatin (10 mg/kg/p.o.) and rivastigmine (1 mg/kg/p.o.) were administered daily prior to AlCl3. Behavioral parameters were assessed using Morris water maze test and actophotometer followed by biochemical investigations, namely, acetylcholinesterase (AChE) activity, TNF-α level, antioxidant enzymes (GSH, catalase), lipid peroxidation, and nitrite level in hippocampus and frontal cortex. Triglycerides, total cholesterol, LDL, and HDL levels in serum were also determined. Key Findings. Simvastatin treatment improved cognitive function and locomotor activity in rats. Simvastatin reversed hyperlipidemia and significantly rectified the deleterious effect of AlCl3 on AChE activity. Further, in hippocampus and frontal cortex, aluminium-induced elevation in nitrite and TNF-α and reduction in antioxidant enzymes were inhibited by simvastatin. Conclusion. To conclude, the present study suggests that simvastatin per se protects the neurons in hippocampus and frontal cortex from AlCl3, an environmental toxin. PMID:25802481

  8. Electron-induced chemistry of methyl chloride caged within amorphous solid water

    NASA Astrophysics Data System (ADS)

    Horowitz, Yonatan; Asscher, Micha

    2013-10-01

    The interaction of low energy electrons (1.0-25 eV) with methyl-chloride (CD3Cl) molecules, caged within Amorphous Solid Water (ASW) films, 10-120 monolayer (ML) thick, has been studied on top of a Ru(0001) substrate under Ultra High Vacuum (UHV) conditions. While exposing the ASW film to 3 eV electrons a static electric field up to 8 × 108 V/m is developed inside the ASW film due to the accumulation of trapped electrons that produce a plate capacitor voltage of exactly 3 V. At the same time while the electrons continuously strike the ASW surface, they are transmitted through the ASW film at currents of ca. 3 × 10-7 A. These electrons transiently attach to the caged CD3Cl molecules leading to C-Cl bond scission via Dissociative Electron Attachment (DEA) process. The electron induced dissociation cross sections and product formation rate constants at 3.0 eV incident electrons at ASW film thicknesses of 10 ML and 40 ML were derived from model simulations supported by Thermal Programmed Desorption (TPD) experimental data. For 3.0 eV electrons the CD3Cl dissociation cross section is 3.5 × 10-16 cm2, regardless of ASW film thickness. TPD measurements reveal that the primary product is deuterated methane (D3CH) and the minor one is deuterated ethane (C2D6).

  9. Electron-induced chemistry of methyl chloride caged within amorphous solid water.

    PubMed

    Horowitz, Yonatan; Asscher, Micha

    2013-10-21

    The interaction of low energy electrons (1.0-25 eV) with methyl-chloride (CD3Cl) molecules, caged within Amorphous Solid Water (ASW) films, 10-120 monolayer (ML) thick, has been studied on top of a Ru(0001) substrate under Ultra High Vacuum (UHV) conditions. While exposing the ASW film to 3 eV electrons a static electric field up to 8 × 10(8) V∕m is developed inside the ASW film due to the accumulation of trapped electrons that produce a plate capacitor voltage of exactly 3 V. At the same time while the electrons continuously strike the ASW surface, they are transmitted through the ASW film at currents of ca. 3 × 10(-7) A. These electrons transiently attach to the caged CD3Cl molecules leading to C-Cl bond scission via Dissociative Electron Attachment (DEA) process. The electron induced dissociation cross sections and product formation rate constants at 3.0 eV incident electrons at ASW film thicknesses of 10 ML and 40 ML were derived from model simulations supported by Thermal Programmed Desorption (TPD) experimental data. For 3.0 eV electrons the CD3Cl dissociation cross section is 3.5 × 10(-16) cm(2), regardless of ASW film thickness. TPD measurements reveal that the primary product is deuterated methane (D3CH) and the minor one is deuterated ethane (C2D6).

  10. Formation Of Vinyl Chloride And Vinylidene Fluoride By UV-Laser Induced Chain Reactions

    NASA Astrophysics Data System (ADS)

    Wolfrum, J.; Schneider, M.

    1984-05-01

    Thermal elimination of hydrogen chloride from 1,2-dichloroethane and 1,1,1-chlorodifluoroethane is a main industrial route to some important monomer compounds. Two reaction paths are possible - unimolecular four-center-elimination and a radical chain mechanism. The latter is started by the endothermic C-Cl bond rupture, followed by the chain consisting of an abstraction reaction and a monomolecular decomposition step. Inducing the chain by photo-initiation offers the advantage that the monomolecular process becomes the rate determining step leading to a lower activation energy for the total reaction. This allows lower process temperatures, therefore decreasing energy expense and avoiding the high temperature formation of byproducts. In our investigation we used as photolysis source several lines of an UV-Exciplex-Laser which provide short pulses of monochromatic UV-radiation with high energy. It was possible to study the effects of initial radical concentration on the quantum yield 0 as function of the temperature. Long reaction chains and a decrease of 0 inversely proportional to the square root of irradiation intensity were observed. The formation of the monomers was detected by a time-resolved UV-absorption technique. Experimental results were analysed in order to yield information about the temperature and pressure dependence of the rate determining reaction. By application of our data in computer simulations wP were able to extrapolate the reaction behaviour to various technical conditions.

  11. Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel.

    PubMed

    Bonnard, Thomas; Hagemeyer, Christoph E

    2015-06-29

    Severe thrombosis and its ischemic consequences such as myocardial infarction, pulmonary embolism and stroke are major worldwide health issues. The ferric chloride injury is now a well-established technique to rapidly and accurately induce the formation of thrombi in exposed veins or artery of small and large diameter. This model has played a key role in the study of the pathophysiology of thrombosis, in the discovery and validation of novel antithrombotic drugs and in the understanding of the mechanism of action of these new agents. Here, the implementation of this technique on a mesenteric vessel and carotid artery in mice is presented. The method describes how to label circulating leukocytes and platelets with a fluorescent dye and to observe, by intravital microscopy on the exposed mesentery, their accumulation at the injured vessel wall which leads to the formation of a thrombus. On the carotid artery, the occlusion caused by the clot formation is measured by monitoring the blood flow with a Doppler probe.

  12. Neuroprotective effect of hesperidin on aluminium chloride induced Alzheimer's disease in Wistar rats.

    PubMed

    Justin Thenmozhi, Arokiasamy; Raja, Tharsius Raja William; Janakiraman, Udaiyappan; Manivasagam, Thamilarasan

    2015-04-01

    The present study was aimed to evaluate the protective effect of hesperidin (Hes) on aluminium chloride (AlCl3) induced neurobehavioral and pathological changes in Alzheimeric rats. Intraperitonial injection of AlCl3 (100 mg/kg body weight) for 60 days significantly elevated the levels of aluminium (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP), β amyloid (Aβ 1-42), β and γ secretases as compared to control group in hippocampus and cortex of rat brain. Hes administration orally along with AlCl3 injection for 60 days, significantly revert the Al concentration, AChE activity and Aβ synthesis-related molecules in the studied brain regions. Our results showed that aluminum exposure was significantly reduced the spontaneous locomotor and exploratory activities in open field test and enhanced the learning and memory impairments in morris water maze test. The behavioral impairments caused by aluminum were significantly attenuated by Hes. The histopathological studies in the hippocampus and cortex of rat brain also supported that Hes (100 mg/kg) markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that hesperidin can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.

  13. Biophysical analysis of phaseolin denaturation induced by urea, guanidinium chloride, pH, and temperature.

    PubMed

    Dyer, J M; Nelson, J W; Murai, N

    1992-06-01

    The structural stability of phaseolin was determined by using absorbance, circular dichroism (CD), fluorescence emission, and fluorescence polarization anisotropy to monitor denaturation induced by urea, guanidinium chloride (GdmCl), pH changes, increasing temperature, or a combination thereof. Initial results indicated that phaseolin remained folded to a similar extent in the presence or absence of 6.0 M urea or GdmCl at room temperature. In 6.0 M GdmCl, phaseolin denatures at approximately 65 degrees C when probed with absorbance, CD, and fluorescence polarization anisotropy. The transition occurs at lower temperatures by decreasing pH. Kinetic measurements of denaturation using CD indicated that the denaturation is slow below 55 degrees C and is associated with an activation energy of 52 kcal/mol in 6.0 M GdmCl. In addition, kinetic measurement using fluorescence emission indicated that the single tryptophan residue was sensitive to at least two steps of the denaturation process. The fluorescence emission appeared to reflect some other structural perturbation than protein denaturation, as fluorescence inflection occurred approximately 5 degrees C prior to the changes observed in absorbance, CD, and fluorescence polarization anisotropy.

  14. Chelerythrine chloride induces apoptosis in renal cancer HEK-293 and SW-839 cell lines

    PubMed Central

    CHEN, XIAO-MENG; ZHANG, MENG; FAN, PENG-LI; QIN, YU-HUA; ZHAO, HONG-WEI

    2016-01-01

    Previous studies have demonstrated that the benzo[c]phenanthridine alkaloid chelerythrine chloride (CC) has inhibitory effects on various tumors. However, the anticancer activity of CC and its underlying mechanisms have not been elucidated in renal cancer cells. The present study examined the effects of CC on growth inhibition and apoptosis of renal cancer cells in vitro and in vivo. Flow cytometry and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays revealed that CC markedly suppressed the growth of HEK-293 and human renal cancer SW-839 cells in a time- and dose-dependent manner. The xenograft mouse model, which was performed in nude mice, exhibited a reduced tumor growth following CC treatment. In addition, the present study revealed that CC significantly decreased the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, which was accompanied by upregulation of p53, B-cell lymphoma 2 (Bcl-2)-associated X protein, cleaved caspase-3 and cleaved poly (adenosine diphosphate-ribose) polymerase (PARP), and downregulation of Bcl-2, caspase-3 and PARP. Furthermore, the use of PD98059, a specific mitogen-activated protein kinase kinase inhibitor, potentiated the proapoptotic effects of CC, which indicated that CC may induce apoptosis in renal cancer cells partly via inhibition of ERK activity. Overall, the results of the present study demonstrated that CC may be developed as a potential anticancer treatment for patients with renal cancer. PMID:27313717

  15. Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel.

    PubMed

    Bonnard, Thomas; Hagemeyer, Christoph E

    2015-01-01

    Severe thrombosis and its ischemic consequences such as myocardial infarction, pulmonary embolism and stroke are major worldwide health issues. The ferric chloride injury is now a well-established technique to rapidly and accurately induce the formation of thrombi in exposed veins or artery of small and large diameter. This model has played a key role in the study of the pathophysiology of thrombosis, in the discovery and validation of novel antithrombotic drugs and in the understanding of the mechanism of action of these new agents. Here, the implementation of this technique on a mesenteric vessel and carotid artery in mice is presented. The method describes how to label circulating leukocytes and platelets with a fluorescent dye and to observe, by intravital microscopy on the exposed mesentery, their accumulation at the injured vessel wall which leads to the formation of a thrombus. On the carotid artery, the occlusion caused by the clot formation is measured by monitoring the blood flow with a Doppler probe. PMID:26167713

  16. Stress state in turbopump bearing induced by shrink fitting

    NASA Technical Reports Server (NTRS)

    Sims, P.; Zee, R.

    1991-01-01

    The stress generated by shrink fitting in bearing-like geometries is studied. The feasibility of using strain gages to determine the strain induced by shrink fitting process is demonstrated. Results from a ring with a uniform cross section reveal the validity of simple stress mechanics calculations for determining the stress state induced in this geometry by shrink fitting.

  17. Chloride channels mediate sodium sulphide-induced relaxation in rat uteri

    PubMed Central

    Mijušković, Ana; Kokić, Aleksandra Nikolić; Dušić, Zorana Oreščanin; Slavić, Marija; Spasić, Mihajlo B; Blagojević, Duško

    2015-01-01

    Background and Purpose Hydrogen sulphide reduces uterine contractility and is of potential interest as a treatment for uterine disorders. The aim of this study was to explore the mechanism of sodium sulphide (Na2S)-induced relaxation of rat uterus, investigate the importance of redox effects and ion channel-mediated mechanisms, and any interactions between these two mechanisms. Experimental Approach Organ bath studies were employed to assess the pharmacological effects of Na2S in uterine strips by exposing them to Na2S with or without Cl− channel blockers (DIDS, NFA, IAA-94, T16Ainh-A01, TA), raised KCl (15 and 75 mM), K+ channel inhibitors (glibenclamide, TEA, 4-AP), L-type Ca2+ channel activator (S-Bay K 8644), propranolol and methylene blue. The activities of antioxidant enzymes were measured in homogenates of treated uteri. The expression of bestrophin channel 1 (BEST-1) was determined by Western blotting and RT-PCR. Key Results Na2S caused concentration-dependent reversible relaxation of spontaneously active and calcium-treated uteri, affecting both amplitude and frequency of contractions. Uteri exposed to 75 mM KCl were less sensitive to Na2S compared with uteri in 15 mM KCl. Na2S-induced relaxations were abolished by DIDS, but unaffected by other modulators or by the absence of extracellular HCO3−, suggesting the involvement of chloride ion channels. Na2S in combination with different modulators provoked specific changes in the anti-oxidant profiles of uteri. The expression of BEST-1, both mRNA and protein, was demonstrated in rat uteri. Conclusions and Implications The relaxant effects of Na2S in rat uteri are mediated mainly via a DIDS-sensitive Cl−-pathway. Components of the relaxation are redox- and Ca2+-dependent. PMID:25857480

  18. Melamine Induces Oxidative Stress in Mouse Ovary

    PubMed Central

    Dai, Xiao-Xin; Duan, Xing; Cui, Xiang-Shun; Kim, Nam-Hyung; Xiong, Bo; Sun, Shao-Chen

    2015-01-01

    Melamine is a nitrogen heterocyclic triazine compound which is widely used as an industrial chemical. Although melamine is not considered to be acutely toxic with a high LD50 in animals, food contaminated with melamine expose risks to the human health. Melamine has been reported to be responsible for the renal impairment in mammals, its toxicity on the reproductive system, however, has not been adequately assessed. In the present study, we examined the effect of melamine on the follicle development and ovary formation. The data showed that melamine increased reactive oxygen species (ROS) levels, and induced granulosa cell apoptosis as well as follicle atresia. To further analyze the mechanism by which melamine induces oxidative stress, the expression and activities of two key antioxidant enzymes superoxide dismutase (SOD) and glutathi-one peroxidase (GPX) were analyzed, and the concentration of malondialdehyde (MDA) were compared between control and melamine-treated ovaries. The result revealed that melamine changed the expression and activities of SOD and GPX in the melamine-treated mice. Therefore, we demonstrate that melamine causes damage to the ovaries via oxidative stress pathway. PMID:26545251

  19. Melamine Induces Oxidative Stress in Mouse Ovary.

    PubMed

    Dai, Xiao-Xin; Duan, Xing; Cui, Xiang-Shun; Kim, Nam-Hyung; Xiong, Bo; Sun, Shao-Chen

    2015-01-01

    Melamine is a nitrogen heterocyclic triazine compound which is widely used as an industrial chemical. Although melamine is not considered to be acutely toxic with a high LD50 in animals, food contaminated with melamine expose risks to the human health. Melamine has been reported to be responsible for the renal impairment in mammals, its toxicity on the reproductive system, however, has not been adequately assessed. In the present study, we examined the effect of melamine on the follicle development and ovary formation. The data showed that melamine increased reactive oxygen species (ROS) levels, and induced granulosa cell apoptosis as well as follicle atresia. To further analyze the mechanism by which melamine induces oxidative stress, the expression and activities of two key antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) were analyzed, and the concentration of malondialdehyde (MDA) were compared between control and melamine-treated ovaries. The result revealed that melamine changed the expression and activities of SOD and GPX in the melamine-treated mice. Therefore, we demonstrate that melamine causes damage to the ovaries via oxidative stress pathway.

  20. Capsaicin induces NKCC1 internalization and inhibits chloride secretion in colonic epithelial cells independently of TRPV1.

    PubMed

    Bouyer, Patrice G; Tang, Xu; Weber, Christopher R; Shen, Le; Turner, Jerrold R; Matthews, Jeffrey B

    2013-01-15

    Colonic chloride secretion is regulated via the neurohormonal and immune systems. Exogenous chemicals (e.g., butyrate, propionate) can affect chloride secretion. Capsaicin, the pungent ingredient of the chili peppers, exerts various effects on gastrointestinal function. Capsaicin is known to activate the transient receptor potential vanilloid type 1 (TRPV1), expressed in the mesenteric nervous system. Recent studies have also demonstrated its presence in epithelial cells but its role remains uncertain. Because capsaicin has been reported to inhibit colonic chloride secretion, we tested whether this effect of capsaicin could occur by direct action on epithelial cells. In mouse colon and model T84 human colonic epithelial cells, we found that capsaicin inhibited forskolin-dependent short-circuit current (FSK-I(sc)). Using PCR and Western blot, we demonstrated the presence of TRPV1 in colonic epithelial cells. In T84 cells, TRPV1 localized at the basolateral membrane and in vesicular compartments. In permeabilized monolayers, capsaicin activated apical chloride conductance, had no effect on basolateral potassium conductance, but induced NKCC1 internalization demonstrated by immunocytochemistry and basolateral surface biotinylation. AMG-9810, a potent inhibitor of TRPV1, did not prevent the inhibition of the FSK-I(sc) by capsaicin. Neither resiniferatoxin nor N-oleoyldopamine, two selective agonists of TRPV1, blocked the FSK-I(sc). Conversely capsaicin, resiniferatoxin, and N-oleoyldopamine raised intracellular calcium ([Ca(2+)](i)) in T84 cells and AMG-9810 blocked the rise in [Ca(2+)](i) induced by capsaicin and resiniferatoxin suggesting the presence of a functional TRPV1 channel. We conclude that capsaicin inhibits chloride secretion in part by causing NKCC1 internalization, but by a mechanism that appears to be independent of TRPV1. PMID:23139219

  1. Zingerone protects against stannous chloride-induced and hydrogen peroxide-induced oxidative DNA damage in vitro.

    PubMed

    Rajan, Iyappan; Narayanan, Nithya; Rabindran, Remitha; Jayasree, P R; Manish Kumar, P R

    2013-12-01

    In this paper, we report the dose-dependent antioxidant activity and DNA protective effects of zingerone. At 500 μg/mL, the DPPH radical scavenging activity of zingerone and ascorbic acid as a standard was found to be 86.7 and 94.2 % respectively. At the same concentration, zingerone also showed significant reducing power (absorbance 0.471) compared to that of ascorbic acid (absorbance 0.394). The in vitro toxicity of stannous chloride (SnCl2) was evaluated using genomic and plasmid DNA. SnCl2-induced degradation of genomic DNA was found to occur at a concentration of 0.8 mM onwards with complete degradation at 1.02 mM and above. In the case of plasmid DNA, conversion of supercoiled DNA into the open circular form indicative of DNA nicking activity was observed at a concentration of 0.2 mM onwards; complete conversion was observed at a concentration of 1.02 mM and above. Zingerone was found to confer protection against SnCl2-induced oxidative damage to genomic and plasmid DNA at concentrations of 500 and 750 μg/mL onwards, respectively. This protective effect was further confirmed in the presence of UV/H2O2-a known reactive oxygen species (ROS) generating system-wherein protection by zingerone against ROS-mediated DNA damage was observed at a concentration of 250 μg/mL onwards in a dose-dependent manner. This study clearly indicated the in vitro DNA protective property of zingerone against SnCl2-induced, ROS-mediated DNA damage.

  2. DHEA administration modulates stress-induced analgesia in rats.

    PubMed

    Cecconello, Ana Lúcia; Torres, Iraci L S; Oliveira, Carla; Zanini, Priscila; Niches, Gabriela; Ribeiro, Maria Flávia Marques

    2016-04-01

    An important aspect of adaptive stress response is the pain response suppression that occurs during or following stress exposure, which is often referred to as acute stress-induced analgesia. Dehydroepiandrosterone (DHEA) participates in the modulation of adaptive stress response, changing the HPA axis activity. The effect of DHEA on the HPA axis activity is dependent on the state and uses the same systems that participate in the regulation of acute stress-induced analgesia. The impact of DHEA on nociception has been studied; however, the effect of DHEA on stress-induced analgesia is not known. Thus, the aim of the present study was to evaluate the effect of DHEA on stress-induced analgesia and determine the best time for hormone administration in relation to exposure to stressor stimulus. The animals were stressed by restraint for 1h in a single exposure and received treatment with DHEA by a single injection before the stress or a single injection after the stress. Nociception was assessed with a tail-flick apparatus. Serum corticosterone levels were measured. DHEA administered before exposure to stress prolonged the acute stress-induced analgesia. This effect was not observed when the DHEA was administered after the stress. DHEA treatment in non-stressed rats did not alter the nociceptive threshold, suggesting that the DHEA effect on nociception is state-dependent. The injection of DHEA had the same effect as exposure to acute stress, with both increasing the levels of corticosterone. In conclusion, acute treatment with DHEA mimics the response to acute stress indexed by an increase in activity of the HPA axis. The treatment with DHEA before stress exposure may facilitate adaptive stress response, prolonging acute stress-induced analgesia, which may be a therapeutic strategy of interest to clinics.

  3. DHEA administration modulates stress-induced analgesia in rats.

    PubMed

    Cecconello, Ana Lúcia; Torres, Iraci L S; Oliveira, Carla; Zanini, Priscila; Niches, Gabriela; Ribeiro, Maria Flávia Marques

    2016-04-01

    An important aspect of adaptive stress response is the pain response suppression that occurs during or following stress exposure, which is often referred to as acute stress-induced analgesia. Dehydroepiandrosterone (DHEA) participates in the modulation of adaptive stress response, changing the HPA axis activity. The effect of DHEA on the HPA axis activity is dependent on the state and uses the same systems that participate in the regulation of acute stress-induced analgesia. The impact of DHEA on nociception has been studied; however, the effect of DHEA on stress-induced analgesia is not known. Thus, the aim of the present study was to evaluate the effect of DHEA on stress-induced analgesia and determine the best time for hormone administration in relation to exposure to stressor stimulus. The animals were stressed by restraint for 1h in a single exposure and received treatment with DHEA by a single injection before the stress or a single injection after the stress. Nociception was assessed with a tail-flick apparatus. Serum corticosterone levels were measured. DHEA administered before exposure to stress prolonged the acute stress-induced analgesia. This effect was not observed when the DHEA was administered after the stress. DHEA treatment in non-stressed rats did not alter the nociceptive threshold, suggesting that the DHEA effect on nociception is state-dependent. The injection of DHEA had the same effect as exposure to acute stress, with both increasing the levels of corticosterone. In conclusion, acute treatment with DHEA mimics the response to acute stress indexed by an increase in activity of the HPA axis. The treatment with DHEA before stress exposure may facilitate adaptive stress response, prolonging acute stress-induced analgesia, which may be a therapeutic strategy of interest to clinics. PMID:26852948

  4. [Central Circuit Mechanism for Psychological Stress-Induced Hyperthermia].

    PubMed

    Nakamura, Kazuhiro

    2015-10-01

    Many types of psychological stress induce hyperthermia. The stress-induced elevation of body temperature is caused by sympathetic responses including brown adipose tissue thermogenesis, tachycardia, and cutaneous vasoconstriction as well as by neuroendocrine responses including stress hormone release via the hypothalamo-pituitary-adrenal (HPA) axis. Recent studies have revealed that the hypothalamic and medullary neural circuitry for driving these stress responses. In this circuitry, the dorsomedial hypothalamus serves as a hub for the central stress signaling: first, it connects the sympathetic efferents with medullary sympathetic premotor neurons to drive the sympathetic responses; second, it connects the neuroendocrine efferents with the HPA axis to drive the stress hormone release. The findings from the animal experiments would be relevant to understand the etiology of the chronic stress-induced hyperthermia "psychogenic fever", a psychosomatic symptom in humans. In this review, I describe the current understanding of the central circuit mechanism for the development of psychological stress-induced hyperthermia, incorporating recent important discoveries.

  5. Hydrogen sulfide attenuates ferric chloride-induced arterial thrombosis in rats.

    PubMed

    Qin, Yi-Ren; You, Shou-Jiang; Zhang, Yan; Li, Qian; Wang, Xian-Hui; Wang, Fen; Hu, Li-Fang; Liu, Chun-Feng

    2016-06-01

    Hydrogen sulfide (H2S) is a novel gaseous transmitter, regulating a multitude of biological processes in the cardiovascular and other systems. However, it remains unclear whether it exerts any effect on arterial thrombosis. In this study, we examined the effect of H2S on ferric chloride (FeCl3)-induced thrombosis in the rat common carotid artery (CCA). The results revealed a decrease of the H2S-producing enzyme cystathionine γ-lyase (CSE) expression and H2S production that persisted until 48 h after FeCl3 application. Intriguingly, administration with NaHS at appropriate regimen reduced the thrombus formation and enhanced the blood flow, accompanied with the alleviation of CSE and CD31 downregulation, and endothelial cell apoptosis in the rat CCA following FeCl3 application. Moreover, the antithrombotic effect of H2S was also observed in Rose Bengal photochemical model in which the development of thrombosis is contributed by oxidative injury to the endothelium. The in vitro study demonstrated that the mRNA and protein expression of CSE, as well as H2S production, was decreased in hydrogen peroxide (H2O2)-treated endothelial cells. Exogenous supplement of NaHS and CSE overexpression consistently alleviated the increase of cleaved caspase-3 and endothelial cell damage caused by H2O2. Taken together, our findings suggest that endogenous H2S generation in the endothelium may be impaired during arterial thrombosis and that modulation of H2S, either exogenous supplement or boost of endogenous production, may become a potential venue for arterial thrombosis therapy.

  6. Ammonium Chloride Ingestion Attenuates Exercise-Induced mRNA Levels in Human Muscle.

    PubMed

    Edge, Johann; Mündel, Toby; Pilegaard, Henriette; Hawke, Emma; Leikis, Murray; Lopez-Villalobos, Nicolas; Oliveira, Rodrigo S F; Bishop, David J

    2015-01-01

    Minimizing the decrease in intracellular pH during high-intensity exercise training promotes greater improvements in mitochondrial respiration. This raises the intriguing hypothesis that pH may affect the exercise-induced transcription of genes that regulate mitochondrial biogenesis. Eight males performed 10x2-min cycle intervals at 80% VO2speak intensity on two occasions separated by ~2 weeks. Participants ingested either ammonium chloride (ACID) or calcium carbonate (PLA) the day before and on the day of the exercise trial in a randomized, counterbalanced order, using a crossover design. Biopsies were taken from the vastus lateralis muscle before and after exercise. The mRNA level of peroxisome proliferator-activated receptor co-activator 1α (PGC-1α), citrate synthase, cytochome c and FOXO1 was elevated at rest following ACID (P<0.05). During the PLA condition, the mRNA content of mitochondrial- and glucose-regulating proteins was elevated immediately following exercise (P<0.05). In the early phase (0-2 h) of post-exercise recovery during ACID, PGC-1α, citrate synthase, cytochome C, FOXO1, GLUT4, and HKII mRNA levels were not different from resting levels (P>0.05); the difference in PGC-1α mRNA content 2 h post-exercise between ACID and PLA was not significant (P = 0.08). Thus, metabolic acidosis abolished the early post-exercise increase of PGC-1α mRNA and the mRNA of downstream mitochondrial and glucose-regulating proteins. These findings indicate that metabolic acidosis may affect mitochondrial biogenesis, with divergent responses in resting and post-exercise skeletal muscle. PMID:26656911

  7. Ammonium Chloride Ingestion Attenuates Exercise-Induced mRNA Levels in Human Muscle

    PubMed Central

    Mündel, Toby; Pilegaard, Henriette; Hawke, Emma; Leikis, Murray; Lopez-Villalobos, Nicolas; Oliveira, Rodrigo S. F.; Bishop, David J.

    2015-01-01

    Minimizing the decrease in intracellular pH during high-intensity exercise training promotes greater improvements in mitochondrial respiration. This raises the intriguing hypothesis that pH may affect the exercise-induced transcription of genes that regulate mitochondrial biogenesis. Eight males performed 10x2-min cycle intervals at 80% V˙O2peak intensity on two occasions separated by ~2 weeks. Participants ingested either ammonium chloride (ACID) or calcium carbonate (PLA) the day before and on the day of the exercise trial in a randomized, counterbalanced order, using a crossover design. Biopsies were taken from the vastus lateralis muscle before and after exercise. The mRNA level of peroxisome proliferator-activated receptor co-activator 1α (PGC-1α), citrate synthase, cytochome c and FOXO1 was elevated at rest following ACID (P<0.05). During the PLA condition, the mRNA content of mitochondrial- and glucose-regulating proteins was elevated immediately following exercise (P<0.05). In the early phase (0–2 h) of post-exercise recovery during ACID, PGC-1α, citrate synthase, cytochome C, FOXO1, GLUT4, and HKII mRNA levels were not different from resting levels (P>0.05); the difference in PGC-1α mRNA content 2 h post-exercise between ACID and PLA was not significant (P = 0.08). Thus, metabolic acidosis abolished the early post-exercise increase of PGC-1α mRNA and the mRNA of downstream mitochondrial and glucose-regulating proteins. These findings indicate that metabolic acidosis may affect mitochondrial biogenesis, with divergent responses in resting and post-exercise skeletal muscle. PMID:26656911

  8. Potassium nitrate application alleviates sodium chloride stress in winter wheat cultivars differing in salt tolerance.

    PubMed

    Zheng, Yanhai; Jia, Aijun; Ning, Tangyuan; Xu, Jialin; Li, Zengjia; Jiang, Gaoming

    2008-09-29

    A sand culture experiment was conducted to answer the question whether or not exogenous KNO(3) can alleviate adverse effects of salt stress in winter wheat by monitoring plant growth, K(+)/Na(+) accumulation and the activity of some antioxidant enzymes. Seeds of two wheat cultivars (CVs), DK961 (salt-tolerant) and JN17 (salt-sensitive), were planted in sandboxes and controls germinated and raised with Hoagland nutrient solution (6 mM KNO(3), no NaCl). Experimental seeds were exposed to seven modified Hoagland solutions containing increased levels of KNO(3) (11, 16, 21 mM) or 100 mM NaCl in combination with the four KNO(3) concentrations (6, 11, 16 and 21 mM). Plants were harvested 30 d after imbibition, with controls approximately 22 cm in height. Both CVs showed significant reduction in plant height, root length and dry weight of shoots and roots under KNO(3) or NaCl stress. However, the combination of increased KNO(3) and NaCl alleviated symptoms of the individual salt stresses by improving growth of shoots and roots, reducing electrolyte leakage, malondialdehyde and soluble sugar contents and enhancing the activities of antioxidant enzymes. The salt-tolerant cultivar accumulated more K(+) in both shoots and roots compared with the higher Na(+) accumulation typical for the salt-sensitive cultivar. Soluble sugar content and activities of antioxidant enzymes were found to be more stable in the salt-tolerant cultivar. Our findings suggest that the optimal K(+)/Na(+) ratio of the nutrient solution should be 16:100 for both the salt-tolerant and the salt-sensitive cultivar under the experimental conditions used, and that the alleviation of NaCl stress symptoms through simultaneously applied elevated KNO(3) was more effective in the salt-tolerant than in the salt-sensitive cultivar.

  9. Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice.

    PubMed

    Tabrizian, Kaveh; Yazdani, Abdolmajid; Baheri, Behnam; Payandemehr, Borna; Sanati, Mehdi; Hashemzaei, Mahmoud; Miri, Abdolhossein; Zandkarimi, Majid; Belaran, Maryam; Fanoudi, Sahar; Sharifzadeh, Mohammad

    2016-01-01

    It is very important to investigate the neurotoxic effects of metals on learning and memory processes. In this study, we tried to investigate the effects and time course properties of oral administration of zinc chloride (25, 50, and 75 mg/kg, for 2 weeks), lead acetate (250, 750, 1,500, and 2,500 ppm for 4, 6 and 8 weeks), and their possible mechanisms on a model of memory function. For this matter, we examined the intra-peritoneal injections of nicotine (0.25, 0.5, 1, and 1.5 mg/kg) and bucladesine (50, 100, 300, and 600 nM/mouse) for 4 days alone and in combination with mentioned metals in the step-through passive avoidance task. Control animals received saline, drinking water, saline, and DMSO (dimethyl sulfoxide)/deionized water (1:9), respectively. At the end of each part of studies, animals were trained for 1 day in step-through task. The avoidance memory retention alterations were evaluated 24 and 48 h later in singular and combinational studies. Zinc chloride (75 mg/kg) oral gavage for 2 weeks decreased latency times compared to control animals. Also, lead acetate (750 ppm oral administrations for 8 weeks) caused significant lead blood levels and induced avoidance memory retention impairments. Four-days intra-peritoneal injection of nicotine (1 mg/kg) increased latency time compared to control animals. Finally, findings of this research showed that treatment with intra-peritoneal injections of nicotine (1 mg/kg) and/or bucladesine (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments. Taken together, these results showed the probable role of cholinergic system and protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.

  10. Stress induced phase transitions in silicon

    NASA Astrophysics Data System (ADS)

    Budnitzki, M.; Kuna, M.

    2016-10-01

    Silicon has a tremendous importance as an electronic, structural and optical material. Modeling the interaction of a silicon surface with a pointed asperity at room temperature is a major step towards the understanding of various phenomena related to brittle as well as ductile regime machining of this semiconductor. If subjected to pressure or contact loading, silicon undergoes a series of stress-driven phase transitions accompanied by large volume changes. In order to understand the material's response for complex non-hydrostatic loading situations, dedicated constitutive models are required. While a significant body of literature exists for the dislocation dominated high-temperature deformation regime, the constitutive laws used for the technologically relevant rapid low-temperature loading have severe limitations, as they do not account for the relevant phase transitions. We developed a novel finite deformation constitutive model set within the framework of thermodynamics with internal variables that captures the stress induced semiconductor-to-metal (cd-Si → β-Si), metal-to-amorphous (β-Si → a-Si) as well as amorphous-to-amorphous (a-Si → hda-Si, hda-Si → a-Si) transitions. The model parameters were identified in part directly from diamond anvil cell data and in part from instrumented indentation by the solution of an inverse problem. The constitutive model was verified by successfully predicting the transformation stress under uniaxial compression and load-displacement curves for different indenters for single loading-unloading cycles as well as repeated indentation. To the authors' knowledge this is the first constitutive model that is able to adequately describe cyclic indentation in silicon.

  11. An Arabidopsis ATPase gene involved in nematode-induced syncytium development and abiotic stress responses

    PubMed Central

    Ali, Muhammad Amjad; Plattner, Stephan; Radakovic, Zoran; Wieczorek, Krzysztof; Elashry, Abdelnaser; Grundler, Florian MW; Ammelburg, Moritz; Siddique, Shahid; Bohlmann, Holger

    2013-01-01

    The beet cyst nematode Heterodera schachtii induces syncytia in the roots of Arabidopsis thaliana, which are its only nutrient source. One gene, At1g64110, that is strongly up-regulated in syncytia as shown by RT-PCR, quantitative RT-PCR, in situ RT-PCR and promoter::GUS lines, encodes an AAA+-type ATPase. Expression of two related genes in syncytia, At4g28000 and At5g52882, was not detected or not different from control root segments. Using amiRNA lines and T-DNA mutants, we show that At1g64110 is important for syncytium and nematode development. At1g64110 was also inducible by wounding, jasmonic acid, salicylic acid, heat and cold, as well as drought, sodium chloride, abscisic acid and mannitol, indicating involvement of this gene in abiotic stress responses. We confirmed this using two T-DNA mutants that were more sensitive to abscisic acid and sodium chloride during seed germination and root growth. These mutants also developed significantly smaller roots in response to abscisic acid and sodium chloride. An in silico analysis showed that ATPase At1g64110 (and also At4g28000 and At5g52882) belong to the ‘meiotic clade’ of AAA proteins that includes proteins such as Vps4, katanin, spastin and MSP1. PMID:23480402

  12. Stress-induced flowering: the third category of flowering response.

    PubMed

    Takeno, Kiyotoshi

    2016-09-01

    The switch from vegetative growth to reproductive growth, i.e. flowering, is the critical event in a plant's life. Flowering is regulated either autonomously or by environmental factors; photoperiodic flowering, which is regulated by the duration of the day and night periods, and vernalization, which is regulated by low temperature, have been well studied. Additionally, it has become clear that stress also regulates flowering. Diverse stress factors can induce or accelerate flowering, or inhibit or delay it, in a wide range of plant species. This article focuses on the positive regulation of flowering via stress, i.e. the induction or acceleration of flowering in response to stress that is known as stress-induced flowering - a new category of flowering response. This review aims to clarify the concept of stress-induced flowering and to summarize the full range of characteristics of stress-induced flowering from a predominately physiological perspective. PMID:27382113

  13. Memory recuperative potential of rifampicin in aluminum chloride-induced dementia: role of pregnane X receptors.

    PubMed

    Kaur, P; Sodhi, R K

    2015-03-12

    The present study has been designed to investigate the potential of rifampicin [Pregnane X receptors (PXR) agonist] in experimental dementia. Aluminum chloride (AlCl3) [100mg/kg, p.o. for 42days] was administered to Wistar rats (n=6) to induce dementia. Morris water maze (MWM) test was used to assess learning and memory and rota rod test was used to assess locomotor activity of the animals. A battery of biochemical tests and histopathological evaluation using hematoxylin and eosin (H&E) and Congo Red stains were performed at the end of the study. AlCl3-treated rats demonstrated impaired cognition and locomotor activity on MWM apparatus and rota rod test, respectively. These animals exhibited a significant rise in acetylcholinesterase (AChE) activity (138±3.6), thiobarbituric acid reactive species (TBARS) level (15±1.6), nitrite (56±2.4) level and myeloperoxidase (MPO) activity (4.1±0.9) along with decline in reduced glutathione (GSH) level (22±1.3) in comparison to the control group (p<0.05). Further the H&E and Congo Red-stained cerebral cortex sections of AlCl3-treated rats indicated severe neutrophilic infiltration and amyloid deposition. Rifampicin-treated AlCl3-rats exhibited significant attenuation in memory deficits, biochemical parameters like AChE activity (33±1.4), TBARS level (4.1±1.0), nitrite level (64±2.6), MPO activity (3.6±1.0) and GSH level (53±2.4) along with improved histopathological alterations and locomotor activity when compared with AlCl3-treated rats (p<0.05). Combined administration of ketoconazole (a PXR antagonist) and rifampicin to AlCl3-treated animals reversed the rifampicin-induced protective effects. Therefore the results obtained from the study indicate a defensive role of rifampicin in memory dysfunction which may probably be due to its anti-cholinesterase, anti-oxidative, anti-inflammatory and amyloid lowering effects. Moreover the study speculates the potential of PXR in the pathophysiology of dementia which is subject

  14. UV-induced Lactobacillus gasseri mutants resisting sodium chloride and sodium nitrite for meat fermentation.

    PubMed

    Arihara, K; Itoh, M

    2000-06-01

    Lactobacillus gasseri, one of the predominant lactobacilli in human intestinal tracts, is utilized for probiotics and dairy starter cultures. However, since L. gasseri is relatively sensitive to sodium chloride and sodium nitrite (essential compounds for meat products), it is difficult to utilize this species for conventional fermented meat products. In this study, efforts were directed to generate mutants of L. gasseri resisting sodium chloride and sodium nitrite. UV irradiation of the strain of L. gasseri JCM1131(T) generated several mutants resisting these compounds. A mutant strain 1131-M8 demonstrated satisfactory growth in meat containing 3.3% sodium chloride and 200 ppm sodium nitrite. Although proteins extracted from the cell surface of 1131-M8 were slightly different from those of the original strain, other biochemical characteristics of both strains were indistinguishable. These results suggest that the L. gasseri mutant obtained in this study could be utilized as a starter culture to develop probiotic meat products.

  15. Abiotic stresses induce different localizations of anthocyanins in Arabidopsis

    PubMed Central

    Kovinich, Nik; Kayanja, Gilbert; Chanoca, Alexandra; Otegui, Marisa S; Grotewold, Erich

    2015-01-01

    Anthocyanins are induced in plants in response to abiotic stresses such as drought, high salinity, excess light, and cold, where they often correlate with enhanced stress tolerance. Numerous roles have been proposed for anthocyanins induced during abiotic stresses including functioning as ROS scavengers, photoprotectants, and stress signals. We have recently found different profiles of anthocyanins in Arabidopsis (Arabidopsis thaliana) plants exposed to different abiotic stresses, suggesting that not all anthocyanins have the same function. Here, we discuss these findings in the context of other studies and show that anthocyanins induced in Arabidopsis in response to various abiotic stresses have different localizations at the organ and tissue levels. These studies provide a basis to clarify the role of particular anthocyanin species during abiotic stress. PMID:26179363

  16. TIA1 oxidation inhibits stress granule assembly and sensitizes cells to stress-induced apoptosis

    PubMed Central

    Arimoto-Matsuzaki, Kyoko; Saito, Haruo; Takekawa, Mutsuhiro

    2016-01-01

    Cytoplasmic stress granules (SGs) are multimolecular aggregates of stalled translation pre-initiation complexes that prevent the accumulation of misfolded proteins, and that are formed in response to certain types of stress including ER stress. SG formation contributes to cell survival not only by suppressing translation but also by sequestering some apoptosis regulatory factors. Because cells can be exposed to various stresses simultaneously in vivo, the regulation of SG assembly under multiple stress conditions is important but unknown. Here we report that reactive oxygen species (ROS) such as H2O2 oxidize the SG-nucleating protein TIA1, thereby inhibiting SG assembly. Thus, when cells are confronted with a SG-inducing stress such as ER stress caused by protein misfolding, together with ROS-induced oxidative stress, they cannot form SGs, resulting in the promotion of apoptosis. We demonstrate that the suppression of SG formation by oxidative stress may underlie the neuronal cell death seen in neurodegenerative diseases. PMID:26738979

  17. Stress, stress-induced cortisol responses, and eyewitness identification performance.

    PubMed

    Sauerland, Melanie; Raymaekers, Linsey H C; Otgaar, Henry; Memon, Amina; Waltjen, Thijs T; Nivo, Maud; Slegers, Chiel; Broers, Nick J; Smeets, Tom

    2016-07-01

    In the eyewitness identification literature, stress and arousal at the time of encoding are considered to adversely influence identification performance. This assumption is in contrast with findings from the neurobiology field of learning and memory, showing that stress and stress hormones are critically involved in forming enduring memories. This discrepancy may be related to methodological differences between the two fields of research, such as the tendency for immediate testing or the use of very short (1-2 hours) retention intervals in eyewitness research, while neurobiology studies insert at least 24 hours. Other differences refer to the extent to which stress-responsive systems (i.e., the hypothalamic-pituitary-adrenal axis) are stimulated effectively under laboratory conditions. The aim of the current study was to conduct an experiment that accounts for the contemporary state of knowledge in both fields. In all, 123 participants witnessed a live staged theft while being exposed to a laboratory stressor that reliably elicits autonomic and glucocorticoid stress responses or while performing a control task. Salivary cortisol levels were measured to control for the effectiveness of the stress induction. One week later, participants attempted to identify the thief from target-present and target-absent line-ups. According to regression and receiver operating characteristic analyses, stress did not have robust detrimental effects on identification performance. Copyright © 2016 John Wiley & Sons, Ltd. © 2016 The Authors Behavioral Sciences & the Law Published by John Wiley & Sons Ltd. PMID:27417874

  18. Glucagon orchestrates stress-induced hyperglycaemia.

    PubMed

    Harp, J B; Yancopoulos, G D; Gromada, J

    2016-07-01

    Hyperglycaemia is commonly observed on admission and during hospitalization for medical illness, traumatic injury, burn and surgical intervention. This transient hyperglycaemia is referred to as stress-induced hyperglycaemia (SIH) and frequently occurs in individuals without a history of diabetes. SIH has many of the same underlying hormonal disturbances as diabetes mellitus, specifically absolute or relative insulin deficiency and glucagon excess. SIH has the added features of elevated blood levels of catecholamines and cortisol, which are not typically present in people with diabetes who are not acutely ill. The seriousness of SIH is highlighted by its greater morbidity and mortality rates compared with those of hospitalized patients with normal glucose levels, and this increased risk is particularly high in those without pre-existing diabetes. Insulin is the treatment standard for SIH, but new therapies that reduce glucose variability and hypoglycaemia are desired. In the present review, we focus on the key role of glucagon in SIH and discuss the potential use of glucagon receptor blockers and glucagon-like peptide-1 receptor agonists in SIH to achieve target glucose control. PMID:27027662

  19. Differentiating stress to wheat fields induced by Diuraphis noxia from other stress causing factors

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The objective of this study was to develop a method to differentiate two categories of stress to wheat fields, stress induced by the Russian wheat aphid, Diuraphis noxia (Mordvilko), and stress caused by other factors. The study used a set of 11 spatial pattern metrics derived from multispectral im...

  20. Prenatal stress induces vulnerability to stress together with the disruption of central serotonin neurons in mice.

    PubMed

    Miyagawa, Kazuya; Tsuji, Minoru; Ishii, Daisuke; Takeda, Kotaro; Takeda, Hiroshi

    2015-01-15

    A growing body of evidence suggests that prenatal stress increases the vulnerability to neuropsychiatric disorders. On the other hand, the ability to adapt to stress is an important defensive function of a living body, and disturbance of this stress adaptability may be related, at least in part, to the pathophysiology of stress-related psychiatric disorders. The aim of the present study was to clarify the relationship between exposure to prenatal stress and the ability to adapt to stress in mice. Naive and prenatally stressed mice were exposed to repeated restraint stress for 60 min/day for 7 days. After the final exposure to restraint stress, the emotionality of mice was evaluated in terms of exploratory activity, i.e., total distance moved as well as the number and duration of rearing and head-dipping behaviors, using an automatic hole-board apparatus. A single exposure to restraint stress for 60 min induced a decrease in head-dipping behavior in the hole-board test. This acute emotional stress response disappeared in naive mice that had been exposed to repeated restraint stress for 60 min/day for 7 days, which confirmed the development of stress adaptation. In contrast, prenatally stressed mice did not develop this stress adaptation, and still showed a decrease in head-dipping behavior after the repeated exposure to restraint stress. Biochemical studies showed that the rate-limiting enzyme in 5-HT synthesis, tryptophan hydroxylase, was increased in raphe obtained from stress-adapted mice. In contrast, a decrease in tryptophan hydroxylase was observed in stress-maladaptive mice. In addition, the transcription factor Lmx1b, which is essential for differentiation and the maintenance of normal functions in central 5-HT neurons, was decreased in the embryonic hindbrain and adult raphe of prenatally stressed mice. These findings suggest that exposure to excessive prenatal stress may induce a vulnerability to stress and disrupt the development of 5-HT neurons.

  1. Stress- and Allostasis-Induced Brain Plasticity

    PubMed Central

    McEwen, Bruce S.; Gianaros, Peter J.

    2014-01-01

    The brain is the key organ of stress processes. It determines what individuals will experience as stressful, it orchestrates how individuals will cope with stressful experiences, and it changes both functionally and structurally as a result of stressful experiences. Within the brain, a distributed, dynamic, and plastic neural circuitry coordinates, monitors, and calibrates behavioral and physiological stress response systems to meet the demands imposed by particular stressors. These allodynamic processes can be adaptive in the short term (allostasis) and maladaptive in the long term (allostatic load). Critically, these processes involve bidirectional signaling between the brain and body. Consequently, allostasis and allostatic load can jointly affect vulnerability to brain-dependent and stress-related mental and physical health conditions. This review focuses on the role of brain plasticity in adaptation to, and pathophysiology resulting from, stressful experiences. It also considers interventions to prevent and treat chronic and prevalent health conditions via allodynamic brain mechanisms. PMID:20707675

  2. Induced stresses due to fluid extraction from axisymmetric reservoirs

    USGS Publications Warehouse

    Segall, P.

    1992-01-01

    Earthquakes can be induced by fluid extraction, as well as by fluid injection. Segall (1989) proposed that poroelastic stresses are responsible for inducing earthquakes associated with fluid extraction. Here, I present methods for computing poroelastic stress changes due to fluid extraction for general axisymmetric reservoir geometries. The results of Geertsma (1973) for a thin disk reservoir with uniform pressure drop are recovered as a special case. Predicted surface subsidence agrees very well with measured leveling changes over the deep Lacq gas field in southwestern France. The induced stresses are finite if the reservoir pressure changes are continuous. Computed stress changes are on the order of several bars, suggesting that the preexisting stress states in regions of extraction induced seismicity are very close to frictional instability prior to production. ?? 1992 Birkha??user Verlag.

  3. OGG1 is essential in oxidative stress induced DNA demethylation.

    PubMed

    Zhou, Xiaolong; Zhuang, Ziheng; Wang, Wentao; He, Lingfeng; Wu, Huan; Cao, Yan; Pan, Feiyan; Zhao, Jing; Hu, Zhigang; Sekhar, Chandra; Guo, Zhigang

    2016-09-01

    DNA demethylation is an essential cellular activity to regulate gene expression; however, the mechanism that triggers DNA demethylation remains unknown. Furthermore, DNA demethylation was recently demonstrated to be induced by oxidative stress without a clear molecular mechanism. In this manuscript, we demonstrated that 8-oxoguanine DNA glycosylase-1 (OGG1) is the essential protein involved in oxidative stress-induced DNA demethylation. Oxidative stress induced the formation of 8-oxoguanine (8-oxoG). We found that OGG1, the 8-oxoG binding protein, promotes DNA demethylation by interacting and recruiting TET1 to the 8-oxoG lesion. Downregulation of OGG1 makes cells resistant to oxidative stress-induced DNA demethylation, while over-expression of OGG1 renders cells susceptible to DNA demethylation by oxidative stress. These data not only illustrate the importance of base excision repair (BER) in DNA demethylation but also reveal how the DNA demethylation signal is transferred to downstream DNA demethylation enzymes.

  4. Biological effects of laser-induced stress waves

    SciTech Connect

    Doukas, A.; Lee, S.; McAuliffe, D.

    1995-12-31

    Laser-induced stress waves can be generated by one of the following mechanisms: Optical breakdown, ablation or rapid heating of an absorbing medium. These three modes of laser interaction with matter allow the investigation of cellular and tissue responses to stress waves with different characteristics and under different conditions. The most widely studied phenomena are those of the collateral damage seen in photodisruption in the eye and in 193 run ablation of cornea and skin. On the other hand, the therapeutic application of laser-induced stress waves has been limited to the disruption of noncellular material such as renal stones, atheromatous plaque and vitreous strands. The effects of stress waves to cells and tissues can be quite disparate. Stress waves can fracture tissue, damage cells, and increase the permeability of the plasma membrane. The viability of cell cultures exposed to stress waves increases with the peak stress and the number of pulses applied. The rise time of the stress wave also influences the degree of cell injury. In fact, cell viability, as measured by thymidine incorporation, correlates better with the stress gradient than peak stress. Recent studies have also established that stress waves induce a transient increase of the permeability of the plasma membrane in vitro. In addition, if the stress gradient is below the damage threshhold, the cells remain viable. Thus, stress waves can be useful as a means of drug delivery, increasing the intracellular drug concentration and allowing the use of drugs which are impermeable to the cell membrane. The present studies show that it is important to create controllable stress waves. The wavelength tunability and the micropulse structure of the free electron laser is ideal for generating stress waves with independently adjustable parameters, such as rise time, duration and peak stress.

  5. Paxillus involutus strains MAJ and NAU mediate K(+)/Na(+) homeostasis in ectomycorrhizal Populus x canescens under sodium chloride stress.

    PubMed

    Li, Jing; Bao, Siqin; Zhang, Yuhong; Ma, Xujun; Mishra-Knyrim, Manika; Sun, Jian; Sa, Gang; Shen, Xin; Polle, Andrea; Chen, Shaoliang

    2012-08-01

    Salt-induced fluxes of H(+), Na(+), K(+), and Ca(2+) were investigated in ectomycorrhizal (EM) associations formed by Paxillus involutus (strains MAJ and NAU) with the salt-sensitive poplar hybrid Populus × canescens. A scanning ion-selective electrode technique was used to measure flux profiles in non-EM roots and axenically grown EM cultures of the two P. involutus isolates to identify whether the major alterations detected in EM roots were promoted by the fungal partner. EM plants exhibited a more pronounced ability to maintain K(+)/Na(+) homeostasis under salt stress. The influx of Na(+) was reduced after short-term (50 mm NaCl, 24 h) and long-term (50 mm NaCl, 7 d) exposure to salt stress in mycorrhizal roots, especially in NAU associations. Flux data for P. involutus and susceptibility to Na(+)-transport inhibitors indicated that fungal colonization contributed to active Na(+) extrusion and H(+) uptake in the salinized roots of P. × canescens. Moreover, EM plants retained the ability to reduce the salt-induced K(+) efflux, especially under long-term salinity. Our study suggests that P. involutus assists in maintaining K(+) homeostasis by delivering this nutrient to host plants and slowing the loss of K(+) under salt stress. EM P. × canescens plants exhibited an enhanced Ca(2+) uptake ability, whereas short-term and long-term treatments caused a marked Ca(2+) efflux from mycorrhizal roots, especially from NAU-colonized roots. We suggest that the release of additional Ca(2+) mediated K(+)/Na(+) homeostasis in EM plants under salt stress.

  6. Gadolinium chloride reduces cytochrome P450: relevance to chemical-induced hepatotoxicity.

    PubMed

    Badger, D A; Kuester, R K; Sauer, J M; Sipes, I G

    1997-08-15

    The Kupffer cell inhibitor, gadolinium chloride (GdCl3), protects the liver from a number of toxicants that require biotransformation to elicit toxicity (i.e. 1,2-dichlorobenzene and CCl4), as well as compounds that do not (i.e. cadmium chloride and beryllium sulfate). The mechanism of this protection is thought to result from reduced secretion of inflammatory and cytotoxic products from Kupffer cells (KC). However, since other lanthanides have been shown to decrease cytochrome P450 (P450) activity, the following studies were designed to determine if GdCl3 pretreatment alters hepatic P450 levels or activity. The toxicological relevance of GdCl3-mediated alterations in P450 activity was also estimated by determining the effect of GdCl3 pretreatment on the susceptibility of primary cultured hepatocytes to CCl4 and cadmium chloride (CdCl2). Male and female Sprague-Dawley rats were given GdCl3 (i.v., 10 mg/kg). Twenty-four hours later, livers were either processed for preparation of microsomes or for primary cultures of hepatocytes. Gadolinium chloride treatment reduced total hepatic microsomal P450 as well as aniline hydroxylase activity by approximately 30% in males and 20% in females. In hepatocytes isolated from rats pretreated with GdCl3, the toxicity caused by CCl4, but not CdCl2 was reduced. Interestingly, when GdCl3 was administered in vitro to microsomes, there was no effect on either the microsomal P450 difference spectra or p-hydroxylation of aniline. However, when GdCl3 was incubated with isolated hepatocytes, the cytotoxicity of CCl4 (but not CdCl2) was partially attenuated. These results suggest that, in addition to its inhibitory effects on KC, GdCl3 produces other effects which may alter the susceptibility of hepatocytes to toxicity caused by certain chemicals.

  7. Chloride ions induce order-disorder transition at water-oxide interfaces.

    PubMed

    Deshmukh, Sanket; Kamath, Ganesh; Ramanathan, Shriram; Sankaranarayanan, Subramanian K R S

    2013-12-01

    Water can form quasi-two-dimensional ordered layers near a solid interface. The solvation dynamics and ionic transport phenomena through this ordered water structure is of direct relevance to a variety of problems in interface science. Molecular dynamics simulations are used to study the impact of local fluctuation of the chloride ion density in the vicinity of an oxide surface on the structure and dynamics of water layers. We demonstrate that local increase in chloride ions beyond a threshold concentration near the water-MgO (100) interface introduces an order-disorder transition of this two-dimensional layered network into bulklike water, leading to increased diffusional characteristics and reduced hydrogen bonding lifetimes. We find that the extent of this order-disorder transition can be tuned by modifying the defect chemistry and nature of the underlying substrate. The kinetic fluidity resulting from order-disorder transition at high chloride ion concentration has significance for a broad range of phenomena, ranging from freezing point depression of brine to onset of aqueous corrosion. PMID:24483398

  8. Chloride ions induce order-disorder transition at water-oxide interfaces

    NASA Astrophysics Data System (ADS)

    Deshmukh, Sanket; Kamath, Ganesh; Ramanathan, Shriram; Sankaranarayanan, Subramanian K. R. S.

    2013-12-01

    Water can form quasi-two-dimensional ordered layers near a solid interface. The solvation dynamics and ionic transport phenomena through this ordered water structure is of direct relevance to a variety of problems in interface science. Molecular dynamics simulations are used to study the impact of local fluctuation of the chloride ion density in the vicinity of an oxide surface on the structure and dynamics of water layers. We demonstrate that local increase in chloride ions beyond a threshold concentration near the water-MgO (100) interface introduces an order-disorder transition of this two-dimensional layered network into bulklike water, leading to increased diffusional characteristics and reduced hydrogen bonding lifetimes. We find that the extent of this order-disorder transition can be tuned by modifying the defect chemistry and nature of the underlying substrate. The kinetic fluidity resulting from order-disorder transition at high chloride ion concentration has significance for a broad range of phenomena, ranging from freezing point depression of brine to onset of aqueous corrosion.

  9. Stress antagonizes morphine-induced analgesia in rats

    NASA Technical Reports Server (NTRS)

    Vernikos, J.; Shannon, L.; Heybach, J. P.

    1981-01-01

    Exposure to restraint stress resulted in antagonism of the analgesic effect of administered morphine in adult male rats. This antagonism of morphine-induced analgesia by restraint stress was not affected by adrenalectomy one day prior to testing, suggesting that stress-induced secretion of corticosteroids is not critical to this antagonism. In addition, parenteral administration of exogenous adrenocorticotropin (ACTH) mimicked the effect of stress in antagonizing morphine's analgesic efficacy. The hypothesis that ACTH is an endogenous opiate antagonist involved in modulating pain sensitivity is supported.

  10. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro.

    PubMed

    Hu, H; Möller, G; Abedi-Valugerdi, M

    1997-10-01

    Autoimmune diseases induced by mercuric chloride are genetically determined, at least one gene being major histocompatibility complex (MHC)-linked. Previously, we showed that in vitro mercury stimulation induced a high proliferative response in lymphocytes from susceptible mice (high-responders) and that the proliferative response could be restored in lymphocytes from low-responders by pretreating the cells with mercury. We also found that the continuous presence of mercury induced IL-2 and IFN-gamma production, while pretreatment with mercury induced IL-4 production. In this study, we showed that anti-MHC class II monoclonal antibodies blocked both the mercury-induced proliferative responses in lymphocytes from high-responders and the restored proliferative responses in low-responders. In addition, anti-MHC class II antibodies also inhibited the mercury-induced IL-2, IFN-gamma and IL-4 cytokine production in vitro. The results demonstrate that MHC class II antigens directly participate in mercury-induced cytokine production and cell activation, and are required at the onset of the initiation.

  11. Aluminum Induces Oxidative Stress Genes in Arabidopsis thaliana1

    PubMed Central

    Richards, Keith D.; Schott, Eric J.; Sharma, Yogesh K.; Davis, Keith R.; Gardner, Richard C.

    1998-01-01

    Changes in gene expression induced by toxic levels of Al were characterized to investigate the nature of Al stress. A cDNA library was constructed from Arabidopsis thaliana seedlings treated with Al for 2 h. We identified five cDNA clones that showed a transient induction of their mRNA levels, four cDNA clones that showed a longer induction period, and two down-regulated genes. Expression of the four long-term-induced genes remained at elevated levels for at least 48 h. The genes encoded peroxidase, glutathione-S-transferase, blue copper-binding protein, and a protein homologous to the reticuline:oxygen oxidoreductase enzyme. Three of these genes are known to be induced by oxidative stresses and the fourth is induced by pathogen treatment. Another oxidative stress gene, superoxide dismutase, and a gene for Bowman-Birk protease inhibitor were also induced by Al in A. thaliana. These results suggested that Al treatment of Arabidopsis induces oxidative stress. In confirmation of this hypothesis, three of four genes induced by Al stress in A. thaliana were also shown to be induced by ozone. Our results demonstrate that oxidative stress is an important component of the plant's reaction to toxic levels of Al. PMID:9449849

  12. Psychological stress, cocaine and natural reward each induce endoplasmic reticulum stress genes in rat brain.

    PubMed

    Pavlovsky, A A; Boehning, D; Li, D; Zhang, Y; Fan, X; Green, T A

    2013-08-29

    Our prior research has shown that the transcription of endoplasmic reticulum (ER) stress transcription factors activating transcription factor 3 (ATF3) and ATF4 are induced by amphetamine and restraint stress in rat striatum. However, presently the full extent of ER stress responses to psychological stress or cocaine, and which of the three ER stress pathways is activated is unknown. The current study examines transcriptional responses of key ER stress target genes subsequent to psychological stress or cocaine. Rats were subjected to acute or repeated restraint stress or cocaine treatment and mRNA was isolated from dorsal striatum, medial prefrontal cortex and nucleus accumbens brain tissue. ER stress gene mRNA expression was measured using quantitative polymerase chain reaction (PCR) and RNA sequencing. Restraint stress and cocaine-induced transcription of the classic ER stress-induced genes (BIP, CHOP, ATF3 and GADD34) and of two other ER stress components x-box binding protein 1 (XBP1) and ATF6. In addition, rats living in an enriched environment (large group cage with novel toys changed daily) exhibited rapid induction of GADD34 and ATF3 after 30 min of exploring novel toys, suggesting these genes are also involved in normal non-pathological signaling. However, environmental enrichment, a paradigm that produces protective addiction and depression phenotypes in rats, attenuated the rapid induction of ATF3 and GADD34 after restraint stress. These experiments provide a sensitive measure of ER stress and, more importantly, these results offer good evidence of the activation of ER stress mechanisms from psychological stress, cocaine and natural reward. Thus, ER stress genes may be targets for novel therapeutic targets for depression and addiction. PMID:23644055

  13. Psychological Stress, Cocaine and Natural Reward Each Induce Endoplasmic Reticulum Stress Genes in Rat Brain

    PubMed Central

    Pavlovsky, Ashly A.; Boehning, Darren; Li, Dingge; Zhang, Yafang; Fan, Xiuzhen; Green, Thomas A.

    2013-01-01

    Our prior research has shown that the transcription of endoplasmic reticulum (ER) stress transcription factors Activating Transcription Factor 3 (ATF3) and ATF4 are induced by amphetamine and restraint stress in rat striatum. However, presently it is unknown the full extent of ER stress responses to psychological stress or cocaine, and which of the three ER stress pathways is activated. The current study examines transcriptional responses of key ER stress target genes subsequent to psychological stress or cocaine. Rats were subjected to acute or repeated restraint stress or cocaine treatment and mRNA was isolated from dorsal striatum, medial prefrontal cortex and nucleus accumbens brain tissue. ER stress gene mRNA expression was measured using quantitative PCR and RNA sequencing. Restraint stress and cocaine induced transcription of the classic ER stress-induced genes (BIP, CHOP, ATF3 and GADD34) and of two other ER stress components XBP1 and ATF6. In addition, rats living in an enriched environment (large group cage with novel toys changed daily) exhibited rapid induction of GADD34 and ATF3 after 30 min of exploring novel toys, suggesting these genes are also involved in normal non-pathological signaling. However, environmental enrichment, a paradigm that produces protective addiction and depression phenotypes in rats, attenuated the rapid induction of ATF3 and GADD34 after restraint stress. These experiments provide a sensitive measure of ER stress and, more importantly, these results offer good evidence of the activation of ER stress mechanisms from psychological stress, cocaine and natural reward. Thus, ER stress genes may be targets for novel therapeutic targets for depression and addiction. PMID:23644055

  14. Effects of crocin and zinc chloride on blood levels of zinc and metabolic and oxidative parameters in streptozotocin-induced diabetic rats

    PubMed Central

    Asri-Rezaei, Siamak; Tamaddonfard, Esmaeal; Ghasemsoltani-Momtaz, Behnaz; Erfanparast, Amir; Gholamalipour, Sima

    2015-01-01

    Objectives: Crocin is one of constituents of saffron and has antioxidant property. Zinc chloride is one of the common compounds of zinc with antioxidant activity. The present study was aimed to investigate separate and combined treatment effects of crocin and zinc chloride on blood levels of zinc and metabolic and oxidative parameters in diabetic rats. Materials and Methods: Diabetes was induced by intraperitoneal (i.p.) injection of 50 mg/kg of streptozotocin (STZ) and was confirmed by blood glucose levels higher than 250 mg/dL. After confirmation of diabetes, injections (i.p.) of crocin and zinc chloride were performed for six weeks. At the end of the experiment, blood levels of zinc, glucose, insulin, malodialdehyde (MDA), and total antioxidant capacity (TAC) were measured. ‎ Results: Crocin (25 and 50 mg/kg) and zinc chloride (5 mg/kg) significantly recovered the decreased levels of zinc, insulin, and TAC and improved the increased levels of glucose and MDA in STZ-induced diabetic rats. In a combination treatment performed with an ineffective dose of crocin (12.5 mg/kg) and a low dose of zinc chloride (1.25 mg/kg), improving effects were observed on the above-mentioned biochemical parameters.‎ Conclusion: The results indicated that separate and combined treatments with crocin and zinc chloride produced improving effects on the blood levels of zinc, glucose, insulin, MDA and TAC in STZ-induced diabetic rats. PMID:26468459

  15. Effects of supplemental potassium and sodium chloride salts on ruminal turnover rates, acid-base and mineral status of lactating dairy cows during heat stress.

    PubMed

    Schneider, P L; Beede, D K; Wilcox, C J

    1988-01-01

    Effects of added dietary sodium and potassium chloride salts on ruminal turnover rates, acid-base balance and mineral status of lactating dairy cows experiencing a nycterohemeral cycle of heat stress were examined. Black globe-humidity index in the chambers averaged 94 during the daytime and 68 during the nighttime. Four ruminally cannulated multiparous Holstein cows in mid-lactation were confined in climatic chambers for a single-reversal experiment consisting of two 17-d periods. To the basal diet (50% corn silage: 50% concentrate, which contained .97% potassium, .19% sodium and .20% chloride), 1.25% sodium chloride plus 1.85% potassium chloride were added, making the high mineral treatment (1.93% potassium, 68% sodium and 1.85% chloride). Liquid dilution rates from the rumen were measured by chromium-ethylenediaminetetraacetate disappearance. Turnover rates of solids were determined by appearance of ytterbium in feces. Ruminal contents, arterial blood and urine were collected hourly for 26 h. Grab samples of feces were sampled over 6 d. Dry matter intakes and milk yields were not affected by the diets (averaging 17.8 and 21.1 kg/d, respectively). Cows fed the high mineral diet drank 17% more water (P less than .01). Tests for homogeneity of regression were utilized to compare chromium disappearance and ytterbium appearance data, which were best described by second-order polynomial functions. Increased ruminal chromium disappearance (P less than .01) and decreased total volatile fatty acid concentrations (P less than .01) suggested faster liquid dilution rates with high mineral diet, but turnover rates of solids were not affected. Urinary potassium secretion compensated for the high potassium content of the high mineral diet without an alkalogenic effect on acid-base status. Lower urine pH and higher urine ammonium concentrations during cool hours suggested that the high chloride content of the high mineral diet had an acidogenic effect. The results are

  16. Stress-induced changes in wheat grain composition and quality.

    PubMed

    Ashraf, M

    2014-01-01

    Abiotic stresses such as drought, salinity, waterlogging, and high temperature cause a myriad of changes in the metabolism of plants, and there is a lot of overlap in these changes in plants in response to different stresses such as drought and salinity. These stress-induced metabolic changes cause impaired crop growth thereby resulting in poor yield. The metabolic changes taking place in several plant species due to a particular abiotic stress have been revealed from the whole plant to the molecular level by researchers, but most studies have focused on organs such as leaf, stem, and root. Information on such stress-induced changes in seed or grains is infrequent in the literature. From the information that is available, it is now evident that abiotic stress can induce considerable changes in the composition and quality of cereal grains including those of wheat, the premier staple food crop in the world. Thus, the present review discusses how far different types of stresses, mainly salinity, drought, high temperature, and waterlogging, can alter the wheat grain composition and quality. By fully uncovering the stress-induced changes in the nutritional values of wheat grains it would be possible to establish whether balanced supplies of essential nutrients are available to the human population from the wheat crop grown on stress-affected areas.

  17. Caffeine attenuated ER stress-induced leptin resistance in neurons.

    PubMed

    Hosoi, Toru; Toyoda, Keisuke; Nakatsu, Kanako; Ozawa, Koichiro

    2014-05-21

    Exposing the endoplasmic reticulum (ER) to stress causes the accumulation of unfolded proteins, and subsequently results in ER stress. ER stress may be involved in various disorders such as obesity, diabetes, and neurodegenerative diseases. Leptin is an important circulating hormone, that inhibits food intake and accelerates energy consumption, which suppresses body weight gain. Recent studies demonstrated that leptin resistance is one of the main factors involved in the development of obesity. We and other groups recently reported the role of ER stress in the development of leptin resistance. Therefore, identifying drugs that target ER stress may be a promising fundamental strategy for the treatment of obesity. In the present study, we investigated whether caffeine could affect ER stress and the subsequent development of leptin resistance. We showed that caffeine exhibited chaperone activity, which attenuated protein aggregation. Caffeine also inhibited the ER stress-induced activation of IRE1 and PERK, which suggested the attenuation of ER stress. Moreover, caffeine markedly improved ER stress-induced impairments in the leptin-induced phosphorylation of STAT3. Therefore, these results suggest caffeine may have pharmacological properties that ameliorate leptin resistance by reducing ER stress. PMID:24699176

  18. Social factors modulate restraint stress induced hyperthermia in mice.

    PubMed

    Watanabe, Shigeru

    2015-10-22

    Stress-induced hyperthermia (SIH) was examined in three different social conditions in mice by thermographic measurement of the body surface temperature. Placing animals in cylindrical holders induced restraint stress. I examined the effect of the social factors in SIH using the thermograph (body surface temperature). Mice restrained in the holders alone showed SIH. Mice restrained in the holders at the same time as other similarly restrained cage mates (social equality condition) showed less hyperthermia. Interestingly, restrained mice with free moving cage mates (social inequality condition) showed the highest hyperthermia. These results are consistent with a previous experiment measuring the memory-enhancing effects of stress and the stress-induced elevation of corticosterone, and suggest that social inequality enhances stress.

  19. Social factors modulate restraint stress induced hyperthermia in mice.

    PubMed

    Watanabe, Shigeru

    2015-10-22

    Stress-induced hyperthermia (SIH) was examined in three different social conditions in mice by thermographic measurement of the body surface temperature. Placing animals in cylindrical holders induced restraint stress. I examined the effect of the social factors in SIH using the thermograph (body surface temperature). Mice restrained in the holders alone showed SIH. Mice restrained in the holders at the same time as other similarly restrained cage mates (social equality condition) showed less hyperthermia. Interestingly, restrained mice with free moving cage mates (social inequality condition) showed the highest hyperthermia. These results are consistent with a previous experiment measuring the memory-enhancing effects of stress and the stress-induced elevation of corticosterone, and suggest that social inequality enhances stress. PMID:26232073

  20. Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress.

    PubMed

    Carda, Ana P P; Marchi, Katia C; Rizzi, Elen; Mecawi, André S; Antunes-Rodrigues, José; Padovan, Claudia M; Tirapelli, Carlos R

    2015-01-01

    We hypothesized that acute stress would induce endothelial dysfunction. Male Wistar rats were restrained for 2 h within wire mesh. Functional and biochemical analyses were conducted 24 h after the 2-h period of restraint. Stressed rats showed decreased exploration on the open arms of an elevated-plus maze (EPM) and increased plasma corticosterone concentration. Acute restraint stress did not alter systolic blood pressure, whereas it increased the in vitro contractile response to phenylephrine and serotonin in endothelium-intact rat aortas. NG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase, NOS, inhibitor) did not alter the contraction induced by phenylephrine in aortic rings from stressed rats. Tiron, indomethacin and SQ29548 reversed the increase in the contractile response to phenylephrine induced by restraint stress. Increased systemic and vascular oxidative stress was evident in stressed rats. Restraint stress decreased plasma and vascular nitrate/nitrite (NOx) concentration and increased aortic expression of inducible (i) NOS, but not endothelial (e) NOS. Reduced expression of cyclooxygenase (COX)-1, but not COX-2, was observed in aortas from stressed rats. Restraint stress increased thromboxane (TX)B(2) (stable TXA(2) metabolite) concentration but did not affect prostaglandin (PG)F2α concentration in the aorta. Restraint reduced superoxide dismutase (SOD) activity, whereas concentrations of hydrogen peroxide (H(2)O(2)) and reduced glutathione (GSH) were not affected. The major new finding of our study is that restraint stress increases vascular contraction by an endothelium-dependent mechanism that involves increased oxidative stress and the generation of COX-derived vasoconstrictor prostanoids. Such stress-induced endothelial dysfunction could predispose to the development of cardiovascular diseases.

  1. Endothelin-1-induced endoplasmic reticulum stress in disease.

    PubMed

    Jain, Arjun

    2013-08-01

    The accumulation of unfolded proteins in the endoplasmic reticulum (ER) represents a cellular stress induced by multiple stimuli and pathologic conditions. Recent evidence implicates endothelin-1 (ET-1) in the induction of placental ER stress in pregnancy disorders. ER stress has previously also been implicated in various other disease states, including neurodegenerative disorders, diabetes, and cardiovascular diseases, as has ET-1 in the pathophysiology of these conditions. However, to date, there has been no investigation of the link between ET-1 and the induction of ER stress in these disease states. Based on recent evidence and mechanistic insight into the role of ET-1 in the induction of placental ER stress, the following review attempts to outline the broader implications of ET-1-induced ER stress, as well as strategies for therapeutic intervention based around ET-1. PMID:23740603

  2. Stress-Induced Tau Phosphorylation: Functional Neuroplasticity or Neuronal Vulnerability?

    PubMed Central

    Rissman, Robert A.

    2010-01-01

    Abnormally phosphorylated tau protein is a key component of the pathology seen in neurodegenerative tauopathies, such as Alzheimer's disease (AD). Despite its association with disease, tau phosphorylation (tau-P) also plays an important role in neuroplasticity, such as dendritic/synaptic remodeling seen in the hippocampus in response to environmental challenges, such as stress. To define the boundaries between neuroplasticity and neuropathology, studies have attempted to characterize the paradigms, stimuli, and signaling intermediates involved in stress-induced tau-P. Supporting an involvement of stress in AD are data demonstrating alterations in stress pathways and peptides in the AD brain and epidemiological data implicating stress exposure as a risk factor for AD. In this review, the question of whether stress-induced tau-P can be used as a model for examining the relationship between functional neuroplasticity and neuronal vulnerability will be discussed. PMID:19584431

  3. Exercise-induced stress response as an adaptive tolerance strategy.

    PubMed Central

    Sonneborn, J S; Barbee, S A

    1998-01-01

    Interaction between the quality of the environment and the health of the exposed population determines the survival response of living organisms. The phenomenon of induced tolerance by exposure to threshold levels of stressors to stimulate natural defense mechanisms has potential therapeutic value. The paucity of information on predictability of individual response and information on the operative fundamental mechanisms limit applicability of the adaptive tolerance strategy. A potential biomarker of the stress response includes members of the stress-inducible ubiquitin gene family. Transcript sizes detected with Northern blot analysis identify different classes of ubiquitin gene family members and the intensity of the radioactive signal allows abundance determinations. Using moderate exercise as the stressor, significant increase (p < 0.028) in abundance of inducible polyubiquitin genes was found in human blood. Both the potential of exercise as a model system of a natural stress inducer and polyubiquitin as a biomarker of stress were established in these studies. Images Figure 1 Figure 2 PMID:9539026

  4. Possible Biomarkers of Chronic Stress Induced Exhaustion - A Longitudinal Study

    PubMed Central

    Wallensten, Johanna; Åsberg, Marie; Nygren, Åke; Szulkin, Robert; Wallén, Håkan; Mobarrez, Fariborz; Nager, Anna

    2016-01-01

    Background Vascular endothelial growth factor (VEGF), epidermal growth factor (EGF) and monocyte chemotactic protein-1 (MCP-1) have previously been suggested to be potential biomarkers for chronic stress induced exhaustion. The knowledge about VEGF has increased during the last decades and supports the contention that VEGF plays an important role in stress and depression. There is scarce knowledge on the possible relationship of EGF and MCP-1 in chronic stress and depression. This study further examines the role of VEGF, EGF and MCP-1 in women with chronic stress induced exhaustion and healthy women during a follow-up period of two years. Methods and Findings Blood samples were collected from 105 women with chronic stress induced exhaustion on at least 50% sick leave for at least three months, at inclusion (T0), after 12 months (T12) and after 24 months (T24). Blood samples were collected at inclusion (T0) in 116 physically and psychiatrically healthy women. The plasma levels of VEGF, EGF and MCP-1 were analyzed using Biochip Array Technology. Women with chronic stress induced exhaustion had significantly higher plasma levels of VEGF and EGF compared to healthy women at baseline, T12 and at T24. There was no significant difference in plasma levels of MCP-1. Plasma levels of VEGF and EGF decreased significantly in women with chronic stress induced exhaustion during the two years follow-up. Conclusions The replicated findings of elevated levels of VEGF and EGF in women with chronic stress induced exhaustion and decreasing plasma levels of VEGF and EGF during the two years follow-up add important knowledge to the pathophysiology of chronic stress induced exhaustion. PMID:27145079

  5. Biochemical and biophysical response to calcium chloride stress in Aspergillus niger and its role in malachite green degradation.

    PubMed

    Gomaa, Ola M; Selim, Nabila S; Linz, John E

    2013-04-01

    Filamentous fungi show great promise in remediation of environmental contaminants such as industrial dyes. In the current study, Aspergillus niger (Genbank ID: JF437542) decolorized 82 % of the test dye malachite green (MG; 50 mg/l) during cultivation for 24 h. The organism decolorized only 6 % of the MG at higher concentration (250 mg MG/l) during the same time period and growth was inhibited at this higher MG concentration. Exposing A. niger to different types of stress resulted in variable impacts on ability to decolorize MG. CaCl2 had the largest positive impact on decolorization. A. niger cultures treated with CaCl2 (1 M) decolorized 46 % of the MG (250 mg/l) in 1 h compared to 6 % in untreated control cultures. CaCl2 also increased catalase production in A. niger which strongly supported a direct relationship between stress response and decolorizing ability. Spectrophotometric measurement confirmed MG decolorization while Fourier transform infrared spectroscopy suggested that biodegradation of MG occurred. Cultures treated with CaCl2 accumulated fewer toxic MG by-products than untreated cultures. CaCl2-induced stress increased the permeability and conductivity of the fungal cell membrane. An observed increase in medium [H(+)] also suggested a change in Ca(2+)/H(+) exchange capacity in the fungal cell. Calcium ions had a pronounced effect on membrane properties and this may have had an important impact on signal transduction. We conclude that A. niger decolorizes MG and that CaCl2 enhances this process; the CaCl2 effect appears to be associated with stress response.

  6. Proline betaine accumulation and metabolism in alfalfa plants under sodium chloride stress. Exploring its compartmentalization in nodules.

    PubMed

    Trinchant, Jean-Charles; Boscari, Alexandre; Spennato, Guillaume; Van de Sype, Ghislaine; Le Rudulier, Daniel

    2004-07-01

    The osmoprotectant Pro betaine is the main betaine identified in alfalfa (Medicago sativa). We have investigated the long-term responses of nodulated alfalfa plants to salt stress, with a particular interest for Pro betaine accumulation, compartmentalization, and metabolism. Exposure of 3-week-old nodulated alfalfa plants to 0.2 m NaCl for 4 weeks was followed by a 10-, 4-, and 8-fold increase in Pro betaine in shoots, roots, and nodules, respectively. Isotope-labeling studies in alfalfa shoots indicate that [14C]Pro betaine was synthesized from l-[14C]Pro. [14C]Pro betaine was efficiently catabolized through sequential demethylations via N-methylPro and Pro. Salt stress had a minor effect on Pro betaine biosynthesis, whereas it strongly reduced Pro betaine turnover. Analysis of Pro betaine and Pro compartmentalization within nodules revealed that 4 weeks of salinization of the host plants induced a strong increase in cytosol and bacteroids. The estimated Pro betaine and Pro concentrations in salt-stressed bacteroids reached 7.4 and 11.8 mm, respectively, compared to only 0.8 mm in control bacteroids. Na+ content in nodule compartments was also enhanced under salinization, leading to a concentration of 14.7 mm in bacteroids. [14C]Pro betaine and [14C]Pro were taken up by purified symbiosomes and free bacteroids. There was no indication of saturable carrier(s), and the rate of uptake was moderately enhanced by salinization. Ultrastructural analysis showed a large peribacteroid space in salt-stressed nodules, suggesting an increased turgor pressure inside the symbiosomes, which might partially be due to an elevated concentration in Pro, Pro betaine, and Na+ in this compartment.

  7. Rebound rib: stress-induced first rib fracture.

    PubMed

    Sacchetti, A D; Beswick, D R; Morse, S D

    1983-03-01

    Reported are two cases of stress-induced fracture of the first rib in young, healthy basketball players. Presumably the fractures resulted from violent contraction of the scalene musculature. This is the usual method of production of stress-induced first rib fracture, but basketball-related cases have not been reported previously. This entity probably is underdiagnosed, and is amenable to conservative outpatient management in most cases.

  8. Altered Gravity Induces Oxidative Stress in Drosophila Melanogaster

    NASA Technical Reports Server (NTRS)

    Bhattacharya, Sharmila; Hosamani, Ravikumar

    2015-01-01

    Altered gravity environments can induce increased oxidative stress in biological systems. Microarray data from our previous spaceflight experiment (FIT experiment on STS-121) indicated significant changes in the expression of oxidative stress genes in adult fruit flies after spaceflight. Currently, our lab is focused on elucidating the role of hypergravity-induced oxidative stress and its impact on the nervous system in Drosophila melanogaster. Biochemical, molecular, and genetic approaches were combined to study this effect on the ground. Adult flies (2-3 days old) exposed to acute hypergravity (3g, for 1 hour and 2 hours) showed significantly elevated levels of Reactive Oxygen Species (ROS) in fly brains compared to control samples. This data was supported by significant changes in mRNA expression of specific oxidative stress and antioxidant defense related genes. As anticipated, a stress-resistant mutant line, Indy302, was less vulnerable to hypergravity-induced oxidative stress compared to wild-type flies. Survival curves were generated to study the combined effect of hypergravity and pro-oxidant treatment. Interestingly, many of the oxidative stress changes that were measured in flies showed sex specific differences. Collectively, our data demonstrate that altered gravity significantly induces oxidative stress in Drosophila, and that one of the organs where this effect is evident is the brain.

  9. FMRFamide signaling promotes stress-induced sleep in Drosophila.

    PubMed

    Lenz, Olivia; Xiong, Jianmei; Nelson, Matthew D; Raizen, David M; Williams, Julie A

    2015-07-01

    Enhanced sleep in response to cellular stress is a conserved adaptive behavior across multiple species, but the mechanism of this process is poorly understood. Drosophila melanogaster increases sleep following exposure to septic or aseptic injury, and Caenorhabditis elegans displays sleep-like quiescence following exposure to high temperatures that stress cells. We show here that, similar to C. elegans, Drosophila responds to heat stress with an increase in sleep. In contrast to Drosophila infection-induced sleep, heat-induced sleep is not sensitive to the time-of-day of the heat pulse. Moreover, the sleep response to heat stress does not require Relish, the NFκB transcription factor that is necessary for infection-induced sleep, indicating that sleep is induced by multiple mechanisms from different stress modalities. We identify a sleep-regulating role for a signaling pathway involving FMRFamide neuropeptides and their receptor FR. Animals mutant for either FMRFamide or for the FMRFamide receptor (FR) have a reduced recovery sleep in response to heat stress. FR mutants, in addition, show reduced sleep responses following infection with Serratia marcescens, and succumb to infection at a faster rate than wild-type controls. Together, these findings support the hypothesis that FMRFamide and its receptor promote an adaptive increase in sleep following stress. Because an FMRFamide-like neuropeptide plays a similar role in C. elegans, we propose that FRMFamide neuropeptide signaling is an ancient regulator of recovery sleep which occurs in response to cellular stress.

  10. FMRFamide signaling promotes stress-induced sleep in Drosophila

    PubMed Central

    Lenz, Olivia; Xiong, Jianmei; Nelson, Matthew D.; Raizen, David M.; Williams, Julie A.

    2015-01-01

    Enhanced sleep in response to cellular stress is a conserved adaptive behavior across multiple species, but the mechanism of this process is poorly understood. Drosophila melanogaster increases sleep following exposure to septic or aseptic injury, and Caenorhabditis elegans displays sleep-like quiescence following exposure to high temperatures that stress cells. We show here that, similar to C. elegans, Drosophila responds to heat stress with an increase in sleep. In contrast to Drosophila infection-induced sleep, heat-induced sleep is not sensitive to the time-of-day of the heat pulse. Moreover, the sleep response to heat stress does not require Relish, the NFκB transcription factor that is necessary for infection-induced sleep, indicating that sleep is induced by multiple mechanisms from different stress modalities. We identify a sleep-regulating role for a signaling pathway involving FMRFamide neuropeptides and their receptor FR. Animals mutant for either FMRFamide or for the FMRFamide receptor (FR) have a reduced recovery sleep in response to heat stress. FR mutants, in addition, show reduced sleep responses following infection with Serratia marcescens, and succumb to infection at a faster rate than wild-type controls. Together, these findings support the hypothesis that FMRFamide and its receptor promote an adaptive increase in sleep following stress. Because an FMRFamide-like neuropeptide plays a similar role in C. elegans, we propose that FRMFamide neuropeptide signaling is an ancient regulator of recovery sleep which occurs in response to cellular stress. PMID:25668617

  11. Emotional Intelligence, Personality, and Task-Induced Stress

    ERIC Educational Resources Information Center

    Matthews, Gerald; Emo, Amanda K.; Funke, Gregory; Zeidner, Moshe; Roberts, Richard D.; Costa, Paul T.; Schulze, Ralf

    2006-01-01

    Emotional intelligence (EI) may predict stress responses and coping strategies in a variety of applied settings. This study compares EI and the personality factors of the Five Factor Model (FFM) as predictors of task-induced stress responses. Participants (N = 200) were randomly assigned to 1 of 4 task conditions, 3 of which were designed to be…

  12. Histone deacetylase inhibition abolishes stress-induced spatial memory impairment.

    PubMed

    Vargas-López, Viviana; Lamprea, Marisol R; Múnera, Alejandro

    2016-10-01

    Acute stress induced before spatial training impairs memory consolidation. Although non-epigenetic underpinning of such effect has been described, the epigenetic mechanisms involved have not yet been studied. Since spatial training and intense stress have opposite effects on histone acetylation balance, it is conceivable that disruption of such balance may underlie acute stress-induced spatial memory consolidation impairment and that inhibiting histone deacetylases prevents such effect. Trichostatin-A (TSA, a histone deacetylase inhibitor) was used to test its effectiveness in preventing stress' deleterious effect on memory. Male Wistar rats were trained in a spatial task in the Barnes maze; 1-h movement restraint was applied to half of them before training. Immediately after training, stressed and non-stressed animals were randomly assigned to receive either TSA (1mg/kg) or vehicle intraperitoneal injection. Twenty-four hours after training, long-term spatial memory was tested; plasma and brain tissue were collected immediately after the memory test to evaluate corticosterone levels and histone H3 acetylation in several brain areas. Stressed animals receiving vehicle displayed memory impairment, increased plasma corticosterone levels and markedly reduced histone H3 acetylation in prelimbic cortex and hippocampus. Such effects did not occur in stressed animals treated with TSA. The aforementioned results support the hypothesis that acute stress induced-memory impairment is related to histone deacetylation.

  13. Histone deacetylase inhibition abolishes stress-induced spatial memory impairment.

    PubMed

    Vargas-López, Viviana; Lamprea, Marisol R; Múnera, Alejandro

    2016-10-01

    Acute stress induced before spatial training impairs memory consolidation. Although non-epigenetic underpinning of such effect has been described, the epigenetic mechanisms involved have not yet been studied. Since spatial training and intense stress have opposite effects on histone acetylation balance, it is conceivable that disruption of such balance may underlie acute stress-induced spatial memory consolidation impairment and that inhibiting histone deacetylases prevents such effect. Trichostatin-A (TSA, a histone deacetylase inhibitor) was used to test its effectiveness in preventing stress' deleterious effect on memory. Male Wistar rats were trained in a spatial task in the Barnes maze; 1-h movement restraint was applied to half of them before training. Immediately after training, stressed and non-stressed animals were randomly assigned to receive either TSA (1mg/kg) or vehicle intraperitoneal injection. Twenty-four hours after training, long-term spatial memory was tested; plasma and brain tissue were collected immediately after the memory test to evaluate corticosterone levels and histone H3 acetylation in several brain areas. Stressed animals receiving vehicle displayed memory impairment, increased plasma corticosterone levels and markedly reduced histone H3 acetylation in prelimbic cortex and hippocampus. Such effects did not occur in stressed animals treated with TSA. The aforementioned results support the hypothesis that acute stress induced-memory impairment is related to histone deacetylation. PMID:27544851

  14. Ameliorating effect of black tea extract on cadmium chloride-induced alteration of serum lipid profile and liver histopathology in rats.

    PubMed

    Mantur, Venkappa S; Somannavarib, Manjunath S; Yendigeri, Saeed; Das, Kusal K; Goudar, Shivaprasad S

    2014-01-01

    Cadmium is one among the most environmental pollutants that affects many organs like kidney, liver and testis. The present study was aimed to assess the simultaneous effects of black tea extracts (BTE) on cadmium chloride induced alterations in lipid profile and liver histology. Adult rats were divided into four groups (n=6/group), group I (normal saline), group II (CdCl2, 1.0 mg/kg, b.wt; i.p), group III (black tea extract, 2.5 gm tea leaf/dl of water that is 2.5% of aqueous BTE) and group IV (cadmium chloride + BTE). Cadmium chloride intoxicated rats showed significant increase in serum total cholesterol, triglycerides, and low density lipoprotein-cholesterol and there is a significant decrease in the serum high density lipoprotein-cholesterol. In the liver, cadmium chloride showed changes in normal architecture, swollen hepatocytes, kupffer cells hyperplasia, dilation and congestion of central vein. Oral administration of black tea extracts with cadmium chloride significantly improves lipid profile and liver architecture as compared to the cadmium chloride group. The results indicate that BTE is beneficial in preventing cadmium-induced lipid alterations and hepatocellular damage.

  15. Potential role of punicalagin against oxidative stress induced testicular damage

    PubMed Central

    Rao, Faiza; Tian, Hui; Li, Wenqing; Hung, Helong; Sun, Fei

    2016-01-01

    Punicalagin is isolated from pomegranate and widely used for the treatment of different diseases in Chinese traditional medicine. This study aimed to evaluate the effect of Punicalagin (purity ≥98%) on oxidative stress induced testicular damage and its effect on fertility. We detected the antioxidant potential of punicalagin in lipopolysaccharide (LPS) induced oxidative stress damage in testes, also tried to uncover the boosting fertility effect of Punicalagin (PU) against oxidative stress-induced infertility. Results demonstrated that 9 mg kg−1 for 7 days treatment significantly decreases LPS induced oxidative damage in testes and nitric oxide production. The administration of oxidative stress resulted in a significant reduction in testes antioxidants GSH, T-SOD, and CAT raised LPO, but treatment with punicalagin for 7 days increased antioxidant defense GSH, T-SOD, and CAT by the end of the experiment and reduced LPO level as well. PU also significantly activates Nrf2, which is involved in regulation of antioxidant defense systems. Hence, the present research categorically elucidates the protective effect of punicalagin against LPS induced oxidative stress induced perturbation in the process of spermatogenesis and significantly increased sperm health and number. Moreover, fertility success significantly decreased in LPS-injected mice compared to controls. Mice injected with LPS had fertility indices of 12.5%, while others treated with a combination of PU + LPS exhibited 75% indices. By promoting fertility and eliminating oxidative stress and inflammation, PU may be a useful nutrient for the treatment of infertility. PMID:26763544

  16. Stress-induced asymmetric frontal brain activity and aggression risk.

    PubMed

    Verona, Edelyn; Sadeh, Naomi; Curtin, John J

    2009-02-01

    Impersonal stressors, not only interpersonal provocation, can instigate aggression through an associative network linking negative emotions to behavioral activation (L. Berkowitz, 1990). Research has not examined the brain mechanisms that are engaged by different types of stress and serve to promote hostility and aggression. The present study examined whether stress exposure elicits more left than right frontal brain activity implicated in behavioral approach motivation and whether this lateralized brain activity predicts stress-induced aggression and hostile/aggressive tendencies. Results showed that (a) participants in the impersonal (assigned to stress by a computer) and interpersonal (assigned to stress by a provoking confederate) stress conditions both showed more left than right frontal electroencephalogram activity after condition assignment and stress exposure and (b) the 2 stress groups exhibited subsequent increases in aggression relative to the no-stress group. Importantly, left frontal asymmetry in response to stress exposure predicted increases in subsequent aggressive behavior, a finding that did not emerge in the no-stress condition. Thus, both the interpersonal and impersonal stressors impacted state changes in brain activity related to behavioral approach, suggesting that stress reactivity involving approach activation represents risk for behavioral dysregulation.

  17. Rosa rugosa Aqueous Extract Alleviates Endurance Exercise-Induced Stress.

    PubMed

    Seo, Eunjin; You, Yanghee; Yoon, Ho-Geun; Kim, Boemjeong; Kim, Kyungmi; Lee, Yoo-Hyun; Lee, Jeongmin; Chung, Jin Woong; Shim, Sangin; Jun, Woojin

    2015-06-01

    This study was performed to investigate the effect of water extract from Rosa rugosa (RRW) on endurance exercise-induced stress in mice. The mice were orally administered with distilled water or RRW, respectively. The endurance capacity was evaluated by exhaustive swimming using an adjustable-current water pool. Mice administered RRW swam longer before becoming exhausted. Also, RRW administration resulted in less lipid peroxidation, lower muscular antioxidant enzyme activities, and lower cortisol level. The results suggest that RRW can prevent exercise-induced stress by decreasing oxidative stress levels.

  18. Cytopathology induced by mercuric chloride and methylmercury in cultured renal cells of the Atlantic spotted dolphin (Stenella plagiodon).

    PubMed

    Wang, A; Pfeiffer, C J

    2001-01-01

    High mercury concentrations have been reported in various tissues of cetaceans, but the toxicological effects of mercury on cetaceans remain unclear. In vivo study is difficult due to the endangered status of these marine mammals and co-exposure to both mercury and selenium (antagonist of mercury) in the oceanic environment. The present data are the first ultrastructural information on dolphin renal cells exposed to mercury in vitro. Multiple organelle changes were observed in Atlantic spotted dolphin (Stenella plagiodon) renal cells treated with mercuric chloride (HgCl2) or methylmercury chloride (MeHgCl2). Mitochondria and rough endoplasmic reticula were swollen after treatment with HgCl2 or MeHgCl. Mitochondrial dense bodies and small cytoplasmic spherical granules of high electron density were also observed after exposure to MeHgCl. Cytoplasmic vacuoles and myelin-like figures were induced by both HgCl2 and MeHgCl. Nuclear changes included karyolysis, nuclear buds, and a novel observation in mercury-treated cells, vacuolization of (micro-)nucleoli after treatment with HgCl2. These morphological changes (multiple organelle damage and nuclear budding) indicated mercury-treated dolphin renal cells underwent oncosis and necrosis, and supported earlier pathophysiologic findings of diverse toxic actions on genetic, respiratory and other cellular functions. PMID:11686411

  19. Stress-induced sensitization to amphetamine and morphine psychomotor effects depend on stress-induced corticosterone secretion.

    PubMed

    Deroche, V; Piazza, P V; Casolini, P; Maccari, S; Le Moal, M; Simon, H

    1992-12-11

    Repeated exposure to stressful situations has been shown to increase individual reactivity to addictive drugs. However, the biological factors involved in such stress-induced changes are largely unknown. In this study, we investigated the role of corticosterone in the effects of restraint stress on the response to psychostimulants and opioids. The effects of repeated stress on amphetamine- and morphine-induced locomotor activity were compared in: (i) animals with an intact hypothalamo-pituitary-adrenal (HPA) axis; (ii) animals in which stress-induced corticosterone secretion was blocked by adrenalectomy, but who received exogenous corticosterone from a subcutaneous implant. The implanted pellets (50 mg) slowly release corticosterone producing a stable plasma level within the normal physiological range over a period of 20 days. Restraint stress increased the locomotor response to both amphetamine (1.5 mg/kg i.p.) and morphine (2 mg/kg s.c.) in animals with an intact HPA axis, but not in animals in which stress-induced corticosterone secretion was suppressed. These results suggest that corticosterone secretion may be one of the mechanisms by which repeated stress amplifies behavioral responses to amphetamine and morphine. Since an enhanced locomotor reactivity to addictive drugs has been found to be frequently associated with an enhanced vulnerability to drug self-administration, these findings point to a role for glucocorticoids in the susceptibility to drug abuse. PMID:1486498

  20. Folate levels modulate oncogene-induced replication stress and tumorigenicity

    PubMed Central

    Lamm, Noa; Maoz, Karin; Bester, Assaf C; Im, Michael M; Shewach, Donna S; Karni, Rotem; Kerem, Batsheva

    2015-01-01

    Chromosomal instability in early cancer stages is caused by replication stress. One mechanism by which oncogene expression induces replication stress is to drive cell proliferation with insufficient nucleotide levels. Cancer development is driven by alterations in both genetic and environmental factors. Here, we investigated whether replication stress can be modulated by both genetic and non-genetic factors and whether the extent of replication stress affects the probability of neoplastic transformation. To do so, we studied the effect of folate, a micronutrient that is essential for nucleotide biosynthesis, on oncogene-induced tumorigenicity. We show that folate deficiency by itself leads to replication stress in a concentration-dependent manner. Folate deficiency significantly enhances oncogene-induced replication stress, leading to increased DNA damage and tumorigenicity in vitro. Importantly, oncogene-expressing cells, when grown under folate deficiency, exhibit a significantly increased frequency of tumor development in mice. These findings suggest that replication stress is a quantitative trait affected by both genetic and non-genetic factors and that the extent of replication stress plays an important role in cancer development. PMID:26197802

  1. Role of endoplasmic reticulum stress in drug-induced toxicity.

    PubMed

    Foufelle, Fabienne; Fromenty, Bernard

    2016-02-01

    Drug-induced toxicity is a key issue for public health because some side effects can be severe and life-threatening. These adverse effects can also be a major concern for the pharmaceutical companies since significant toxicity can lead to the interruption of clinical trials, or the withdrawal of the incriminated drugs from the market. Recent studies suggested that endoplasmic reticulum (ER) stress could be an important event involved in drug liability, in addition to other key mechanisms such as mitochondrial dysfunction and oxidative stress. Indeed, drug-induced ER stress could lead to several deleterious effects within cells and tissues including accumulation of lipids, cell death, cytolysis, and inflammation. After recalling important information regarding drug-induced adverse reactions and ER stress in diverse pathophysiological situations, this review summarizes the main data pertaining to drug-induced ER stress and its potential involvement in different adverse effects. Drugs presented in this review are for instance acetaminophen (APAP), arsenic trioxide and other anticancer drugs, diclofenac, and different antiretroviral compounds. We also included data on tunicamycin (an antibiotic not used in human medicine because of its toxicity) and thapsigargin (a toxic compound of the Mediterranean plant Thapsia garganica) since both molecules are commonly used as prototypical toxins to induce ER stress in cellular and animal models. PMID:26977301

  2. HCV-Induced Oxidative Stress: Battlefield-Winning Strategy.

    PubMed

    Rebbani, Khadija; Tsukiyama-Kohara, Kyoko

    2016-01-01

    About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. PMID:27293514

  3. Melatonin ameliorates chronic mild stress induced behavioral dysfunctions in mice.

    PubMed

    Haridas, Seenu; Kumar, Mayank; Manda, Kailash

    2013-07-01

    Melatonin, a neurohormone, is known to regulate several physiological functions, especially the circadian homeostasis, mood and behavior. Chronic exposure to stress is involved in the etiology of human affective disorders, and depressed patients have been reported to show changes in the circadian rhythms and nocturnal melatonin concentration. The present study was conducted to evaluate a possible beneficial action of chronic night-time melatonin treatment against chronic mild stress (CMS) induced behavioral impairments. As expected in the present study, the stress exposed mice showed reduced weight gain, hedonic deficit, cognitive deficits and decreased mobility in behavioral despair test. Interestingly, CMS exposed mice showed less anxiety. Chronic night-time melatonin administration significantly ameliorated the stress-induced behavioral disturbances, especially the cognitive dysfunction and depressive phenotypes. In conclusion, the present findings suggest the mitigating role of melatonin against CMS-induced behavioral changes, including the cognitive dysfunctions and reaffirm its potential role as an antidepressant.

  4. HCV-Induced Oxidative Stress: Battlefield-Winning Strategy

    PubMed Central

    Rebbani, Khadija; Tsukiyama-Kohara, Kyoko

    2016-01-01

    About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. PMID:27293514

  5. Oxidative stress-induced autophagy: Role in pulmonary toxicity

    SciTech Connect

    Malaviya, Rama; Laskin, Jeffrey D.; Laskin, Debra L.

    2014-03-01

    Autophagy is an evolutionarily conserved catabolic process important in regulating the turnover of essential proteins and in elimination of damaged organelles and protein aggregates. Autophagy is observed in the lung in response to oxidative stress generated as a consequence of exposure to environmental toxicants. Whether autophagy plays role in promoting cell survival or cytotoxicity is unclear. In this article recent findings on oxidative stress-induced autophagy in the lung are reviewed; potential mechanisms initiating autophagy are also discussed. A better understanding of autophagy and its role in pulmonary toxicity may lead to the development of new strategies to treat lung injury associated with oxidative stress. - Highlights: • Exposure to pulmonary toxicants is associated with oxidative stress. • Oxidative stress is known to induce autophagy. • Autophagy is upregulated in the lung following exposure to pulmonary toxicants. • Autophagy may be protective or pathogenic.

  6. Juvenile stress impairs body temperature regulation and augments anticipatory stress-induced hyperthermia responses in rats.

    PubMed

    Yee, Nicole; Plassmann, Kerstin; Fuchs, Eberhard

    2011-09-01

    Clinical studies have implicated adolescence as an important and vulnerable period during which traumatic experiences can predispose individuals to anxiety and mood disorders. As such, a stress model in juvenile rats (age 27-29 d) was previously developed to investigate the long-term effects of stress exposure during adolescence on behavior and physiology. This paradigm involves exposing rats to different stressors on consecutive days over a 3-day period. Here, we studied the effects of juvenile stress on long-term core body temperature regulation and acute stress-induced hyperthermia (SIH) responses using telemetry. We found no differences between control and juvenile stress rats in anxiety-related behavior on the elevated plus maze, which we attribute to stress associated with surgical implantation of telemetry devices. This highlights the severe impact of surgical stress on the results of subsequent behavioral measurements. Nonetheless, juvenile stress disrupted the circadian rhythmicity of body temperature and decreased circadian amplitude. It also induced chronic hypothermia during the dark phase of the day, when rats are most active. When subjected to acute social defeat stress as adults, juvenile stress had no impact on the SIH response relative to controls. However, 24 h later, juvenile stress rats displayed an elevated SIH response in anticipation of social defeat when re-exposed to the social defeat environment. Taken together, our findings indicate that juvenile stress can induce long-term alterations in body temperature regulation and heighten the increase in temperature associated with anticipation of social defeat. The outcomes of behavioral measurements in these experiments, however, are severely affected by surgical stress. PMID:21557956

  7. Phloroglucinol Attenuates Free Radical-induced Oxidative Stress

    PubMed Central

    So, Mi Jung; Cho, Eun Ju

    2014-01-01

    The protective role of phloroglucinol against oxidative stress and stress-induced premature senescence (SIPS) was investigated in vitro and in cell culture. Phloroglucinol had strong and concentration-dependent radical scavenging effects against nitric oxide (NO), superoxide anions (O2−), and hydroxyl radicals. In this study, free radical generators were used to induce oxidative stress in LLC-PK1 renal epithelial cells. Treatment with phloroglucinol attenuated the oxidative stress induced by peroxyl radicals, NO, O2−, and peroxynitrite. Phloroglucinol also increased cell viability and decreased lipid peroxidation in a concentration-dependent manner. WI-38 human diploid fibroblast cells were used to investigate the protective effect of phloroglucinol against hydrogen peroxide (H2O2)-induced SIPS. Phloroglucinol treatment attenuated H2O2-induced SIPS by increasing cell viability and inhibited lipid peroxidation, suggesting that treatment with phloroglucinol should delay the aging process. The present study supports the promising role of phloroglucinol as an antioxidative agent against free radical-induced oxidative stress and SIPS. PMID:25320709

  8. Crocin "saffron" protects against beryllium chloride toxicity in rats through diminution of oxidative stress and enhancing gene expression of antioxidant enzymes.

    PubMed

    El-Beshbishy, Hesham A; Hassan, Memy H; Aly, Hamdy A A; Doghish, Ahmed S; Alghaithy, Abdulaziz A A

    2012-09-01

    Beryllium chloride (BeCl(2)) is a highly toxic substance that accumulates in different tissues after absorption. The purpose of this study was to investigate protective role of crocin against BeCl(2)-intoxication in rats. Male Wistar rats were used in this study and categorised into four groups (n=8). Group I served as normal control rats. Group II treated orally with BeCl(2) 86 mg/kg b.w. for five consecutive days. This dose was equivalent to experimental LD(50). Group III treated intraperitoneally with crocin 200 mg/kg b.w. for seven consecutive days. Group IV received crocin for seven consecutive days before BeCl(2) administration. Blood samples and liver and brain homogenates were obtained for haematological, biochemical and RT-PCR examinations. The haematocrit value, RBCs count and haemoglobin concentration were significantly decreased in BeCl(2)-treated rats. A significant increase was observed in rat liver and brain malondialdehyde level and protein carbonyls content in BeCl(2) exposed group compared to the control group, and these values were significantly declined upon administration of crocin. Lactate dehydrogenase levels in rat liver and brain significantly increased compared to the control group and was associated with significant decrease in catalase and superoxide dismutase activities. Reduced glutathione hepatic contents of BeCl(2)-treated rats were significantly decreased. There was significant decline in mRNA expression of catalase and superoxide dismutase genes in BeCl(2)-intoxicated rats compared to the normal rats. Crocin treatment prior to BeCl(2) intake resulted in significant increase in mRNA expressions of catalase and superoxide dismutase genes near to normalcy. The haematological and biochemical parameters were restored near to normal levels. Our results suggested that, BeCl(2) induced oxidation of cellular lipids and proteins and that administration of crocin reduced BeCl(2)-induced oxidative stress combined with initiation of m

  9. Water deficit stress induced gene expression

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Water deficit stress is one of the most challenging agricultural issues limiting sustainable cotton production. Many efforts have been incorporated using genetic and genomic approaches to identify valuable molecular resources. In this study, we aimed to identify a global set of transcript fragments ...

  10. [Stress-induced alteration of the anticonflict effect of anxiolytics].

    PubMed

    Molodavkin, G M; Voronina, T A; Ramkhin, E Ia; Aldarmaa, Zh

    2002-01-01

    The influence of stress of various etiology (prolonged isolation, anavoidable electrostimulation, paradoxical sleep deprivation, transport stress) on the activity of anxiolytics (tranquilizers) in the conflict situation was studied in inbreed white male rats. It was established that the anticonflict effect of highly effective anxiolytics decreases under the action of stress, the activity of gidazepam remains unchanged, while the drugs of moderate efficacy loose their activity. The degree of changes and the rate of restoration of the initial activity depends on the efficacy of anxiolytics, the strength and duration of stress, and on the duration of drug administration after stress. The possible mechanism of this phenomenon can be the stress-induced activation of the endogenous system of anxiogenic ligands.

  11. High sea-floor stress induced by extreme hurricane waves

    NASA Astrophysics Data System (ADS)

    Wijesekera, Hemantha W.; Wang, David W.; Teague, William J.; Jarosz, Ewa

    2010-06-01

    Strong surface waves and currents generated by major hurricanes can produce extreme forces at the seabed that scour the seafloor and cause massive underwater mudslides. Our understanding of these forces is poor due to lack of concurrent measurements of waves and currents under these storms. Using unique observations collected during the passage of a category-4 hurricane, Ivan, bottom stress due to currents and waves over the outer continental shelf in the Gulf of Mexico was examined. During the passage of Ivan, the bottom stress was highly correlated with the wind with a maximum of about 40% of the wind stress. The bottom stress was dominated by the wave-induced stresses, and exceeded critical levels at depths as large as 90 m. Surprisingly, the bottom damaging stress persisted after the passage of Ivan for about a week, and was modulated by near-inertial waves.

  12. Temporal pore pressure induced stress changes during injection and depletion

    NASA Astrophysics Data System (ADS)

    Müller, Birgit; Heidbach, Oliver; Schilling, Frank; Fuchs, Karl; Röckel, Thomas

    2016-04-01

    Induced seismicity is observed during injection of fluids in oil, gas or geothermal wells as a rather immediate response close to the injection wells due to the often high-rate pressurization. It was recognized even earlier in connection with more moderate rate injection of fluid waste on a longer time frame but higher induced event magnitudes. Today, injection-related induced seismicity significantly increased the number of events with M>3 in the Mid U.S. However, induced seismicity is also observed during production of fluids and gas, even years after the onset of production. E.g. in the Groningen gas field production was required to be reduced due to the increase in felt and damaging seismicity after more than 50 years of exploitation of that field. Thus, injection and production induced seismicity can cause severe impact in terms of hazard but also on economic measures. In order to understand the different onset times of induced seismicity we built a generic model to quantify the role of poro-elasticity processes with special emphasis on the factors time, regional crustal stress conditions and fault parameters for three case studies (injection into a low permeable crystalline rock, hydrothermal circulation and production of fluids). With this approach we consider the spatial and temporal variation of reservoir stress paths, the "early" injection-related induced events during stimulation and the "late" production induced ones. Furthermore, in dependence of the undisturbed in situ stress field conditions the stress tensor can change significantly due to injection and long-term production with changes of the tectonic stress regime in which previously not critically stressed faults could turn to be optimally oriented for fault reactivation.

  13. Beclin-1-independent autophagy mediates programmed cancer cell death through interplays with endoplasmic reticulum and/or mitochondria in colbat chloride-induced hypoxia.

    PubMed

    Sun, Lei; Liu, Ning; Liu, Shan-Shan; Xia, Wu-Yan; Liu, Meng-Yao; Li, Lin-Feng; Gao, Jian-Xin

    2015-01-01

    Autophagy has dual functions in cell survival and death. However, the effects of autophagy on cancer cell survival or death remain controversial. In this study, we show that Autophagy can mediate programmed cell death (PCD) of cancer cells in responding to cobalt chloride (CoCl2)-induced hypoxia in a Beclin-1-independent but autophagy protein 5 (ATG5)-dependent manner. Although ATG5 is not directly induced by CoCl2, its constitutive expression is essential for CoCl2-induced PCD. The ATG5-mediated autophagic PCD requires interplays with endoplasmic reticulum (ER) and/or mitochondria. In this process, ATG5 plays a central role in regulating ER stress protein CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) and mitochondrial protein second mitochondria derived activator of caspases (Smac). Two pathways for autophagic PCD in cancer cells responding to hypoxia have been identified: ATG5/CHOP/Smac pathway and ATG5/Smac pathway, which are probably dependent on the context of cell lines. The former is more potent than the latter for the induction of PCD at the early stage of hypoxia, although the ultimate efficiency of both pathways is comparable. In addition, both pathways may require ATG5-mediated conversion of LC3-I into LC3-II. Therefore, we have defined two autophagy-mediated pathways for the PCD of cancer cells in hypoxia, which are dependent on ATG5, interplayed with ER and mitochondria and tightly regulated by hypoxic status. The findings provide a new evidence that autophagy may inhibit tumor cell proliferation through trigger of PCD, facilitating the development of novel anti-cancer drugs. PMID:26609472

  14. Gravity-induced stresses in stratified rock masses

    USGS Publications Warehouse

    Amadei, B.; Swolfs, H.S.; Savage, W.Z.

    1988-01-01

    This paper presents closed-form solutions for the stress field induced by gravity in anisotropic and stratified rock masses. These rocks are assumed to be laterally restrained. The rock mass consists of finite mechanical units, each unit being modeled as a homogeneous, transversely isotropic or isotropic linearly elastic material. The following results are found. The nature of the gravity induced stress field in a stratified rock mass depends on the elastic properties of each rock unit and how these properties vary with depth. It is thermodynamically admissible for the induced horizontal stress component in a given stratified rock mass to exceed the vertical stress component in certain units and to be smaller in other units; this is not possible for the classical unstratified isotropic solution. Examples are presented to explore the nature of the gravity induced stress field in stratified rock masses. It is found that a decrease in rock mass anisotropy and a stiffening of rock masses with depth can generate stress distributions comparable to empirical hyperbolic distributions previously proposed in the literature. ?? 1988 Springer-Verlag.

  15. (+)-Catechin protects dermal fibroblasts against oxidative stress-induced apoptosis

    PubMed Central

    2014-01-01

    Background Oxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. Catechins, which are antioxidants contained in green tea, exert various actions such as anti-inflammatory, anti-bacterial, and anti-cancer actions. In this study, we investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts. Methods Fibroblasts (NIH3T3) under oxidative stress induced by hydrogen peroxide (0.1 mM) were treated with either vehicle or (+)-catechin (0–100 μM). The effect of (+)-catechin on cell viability, apoptosis, phosphorylation of c-Jun terminal kinases (JNK) and p38, and activation of caspase-3 in fibroblasts under oxidative stress were evaluated. Results Hydrogen peroxide induced apoptotic cell death in fibroblasts, accompanied by induction of phosphorylation of JNK and p38 and activation of caspase-3. Pretreatment of the fibroblasts with (+)-catechin inhibited hydrogen peroxide-induced apoptosis and reduced phosphorylation of JNK and p38 and activation of caspase-3. Conclusion (+)-Catechin protects against oxidative stress-induced cell death in fibroblasts, possibly by inhibiting phosphorylation of p38 and JNK. These results suggest that (+)-catechin has potential as a therapeutic agent for the prevention of skin aging. PMID:24712558

  16. ER Stress-induced Aberrant Neuronal Maturation and Neurodevelopmental Disorders.

    PubMed

    Kawada, Koichi; Iekumo, Takaaki; Kaneko, Masayuki; Nomura, Yasuyuki; Okuma, Yasunobu

    2016-01-01

    Neurodevelopmental disorders, which include autism spectrum disorder, are congenital impairments in the growth and development of the central nervous system. They are mainly accentuated during infancy and childhood. Autism spectrum disorder may be caused by environmental factors, genomic imprinting of chromosome 15q11-q13 regions, and gene defects such as those in genes encoding neurexin and neuroligin, which are involved in synaptogenesis and synaptic signaling. However, regardless of the many reports on neurodevelopmental disorders, the pathogenic mechanism and treatment of neurodevelopmental disorders remain unclear. Conversely, it has been reported that endoplasmic reticulum (ER) stress is involved in neurodegenerative diseases. ER stress is increased by environmental factors such as alcohol consumption and smoking. Here we show the recent results on ER stress-induced neurodevelopmental disorders. ER stress led to a decrease in the mRNA levels of the proneural factors Hes1/5 and Pax6, which maintain an undifferentiated state of the neural cells. This stress also led to a decrease in nestin expression and an increase in beta-III tubulin expression. In addition, dendrite length was shortened by ER stress in microtubule-associated protein-2 (MAP-2) positive cells. However, the ubiquitin ligase HRD1 expression was increased by ER stress. By suppressing HRD1 expression, the ER stress-induced decrease in nestin and MAP-2 expression and increase in beta-III tubulin returned to control levels. Therefore, we suggest that ER stress induces abnormalities in neuronal differentiation and maturation via HRD1 expression. These results suggest that targeting ER stress may facilitate quicker approaches toward the prevention and treatment of neurodevelopmental disorders. PMID:27252060

  17. Mono-2-ethylhexyl phthalate induces oxidative stress responses in human placental cells in vitro

    SciTech Connect

    Tetz, Lauren M.; Cheng, Adrienne A.; Korte, Cassandra S.; Giese, Roger W.; Wang, Poguang; Harris, Craig; Meeker, John D.; Loch-Caruso, Rita

    2013-04-01

    Di-2-ethylhexyl phthalate (DEHP) is an environmental contaminant commonly used as a plasticizer in polyvinyl chloride products. Exposure to DEHP has been linked to adverse pregnancy outcomes in humans including preterm birth, low birth-weight, and pregnancy loss. Although oxidative stress is linked to the pathology of adverse pregnancy outcomes, effects of DEHP metabolites, including the active metabolite, mono-2-ethylhexyl phthalate (MEHP), on oxidative stress responses in placental cells have not been previously evaluated. The objective of the current study is to identify MEHP-stimulated oxidative stress responses in human placental cells. We treated a human placental cell line, HTR-8/SVneo, with MEHP and then measured reactive oxygen species (ROS) generation using the dichlorofluorescein assay, oxidized thymine with mass-spectrometry, redox-sensitive gene expression with qRT-PCR, and apoptosis using a luminescence assay for caspase 3/7 activity. Treatment of HTR-8 cells with 180 μM MEHP increased ROS generation, oxidative DNA damage, and caspase 3/7 activity, and resulted in differential expression of redox-sensitive genes. Notably, 90 and 180 μM MEHP significantly induced mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS2), an enzyme important for synthesis of prostaglandins implicated in initiation of labor. The results from the present study are the first to demonstrate that MEHP stimulates oxidative stress responses in placental cells. Furthermore, the MEHP concentrations used were within an order of magnitude of the highest concentrations measured previously in human umbilical cord or maternal serum. The findings from the current study warrant future mechanistic studies of oxidative stress, apoptosis, and prostaglandins as molecular mediators of DEHP/MEHP-associated adverse pregnancy outcomes. - Highlights: ► MEHP increased reactive oxygen species, oxidative DNA damage, and caspase activity. ► MEHP induced expression of PTGS2, a gene

  18. An improved chloride-conducting channelrhodopsin for light-induced inhibition of neuronal activity in vivo

    PubMed Central

    Wietek, Jonas; Beltramo, Riccardo; Scanziani, Massimo; Hegemann, Peter; Oertner, Thomas G.; Simon Wiegert, J.

    2015-01-01

    Channelrhodopsins are light-gated cation channels that have been widely used for optogenetic stimulation of electrically excitable cells. Replacement of a glutamic acid in the central gate with a positively charged amino acid residue reverses the ion selectivity and produces chloride-conducting ChRs (ChloCs). Expressed in neurons, published ChloCs produced a strong shunting effect but also a small, yet significant depolarization from the resting potential. Depending on the state of the neuron, the net result of illumination might therefore be inhibitory or excitatory with respect to action potential generation. Here we report two additional amino acid substitutions that significantly shift the reversal potential of improved ChloC (iChloC) to the reversal potential of endogenous GABAA receptors. As a result, light-evoked membrane depolarization was strongly reduced and spike initiation after current injection or synaptic stimulation was reliably inhibited in iChloC-transfected neurons in vitro. In the primary visual cortex of anesthetized mice, activation of iChloC suppressed spiking activity evoked by visual stimulation. Due to its high operational light sensitivity, iChloC makes it possible to inhibit neurons in a large volume of brain tissue from a small, point-like light source. PMID:26443033

  19. Cadmium chloride strongly enhances cyclophosphamide-induced chromosome aberrations in mouse bone marrow cells

    SciTech Connect

    Pandurangarao, V.L.; Blazina, S.; Bherje, R.

    1997-10-01

    Earlier we reported that a single 5 mg cadmium chloride (CdCl{sub 2})/kg ip dose enhanced chromosome aberrations (ca) with 50 mg/kg cyclophosphamide (CP) in mouse bone marrow cells. In this report groups of 4 mice were injected ip with saline, 0.31, 0.62, 1.25, 2.5 or 5.0 mg/kg CdCl{sub 2}, followed by saline injections at 24 h. Other mice similarly uninjected at 0 h were injected with 50 mg/kg CP at 24 h. All the mice were injected ip with 4 mg colchicine/kg at 44 h. At 48 h the bone marrow cells were processed for chromosome spreads. After dissection, visual examination revealed obvious internal hemorrhaging of the testes at 1.25 CdCl{sub 2} mg/kg and higher doses. This effect was not further increased by CP treatment. The lowest ca enhancing dose of CdCl{sub 2} on CP was 0.625 mg/kg. Our hypothesis is that Cd replaces zinc presents in numerous DNA repair enzymes and proteins resulting in diminished repair. Subsequently, the excess of unrepaired DNA damage is seen as chromatid breaks, deletions, fragments and exchanges.

  20. Mechanical Stress Induces Biotic and Abiotic Stress Responses via a Novel cis-Element

    PubMed Central

    Walley, Justin W; Coughlan, Sean; Hudson, Matthew E; Covington, Michael F; Kaspi, Roy; Banu, Gopalan; Harmer, Stacey L; Dehesh, Katayoon

    2007-01-01

    Plants are continuously exposed to a myriad of abiotic and biotic stresses. However, the molecular mechanisms by which these stress signals are perceived and transduced are poorly understood. To begin to identify primary stress signal transduction components, we have focused on genes that respond rapidly (within 5 min) to stress signals. Because it has been hypothesized that detection of physical stress is a mechanism common to mounting a response against a broad range of environmental stresses, we have utilized mechanical wounding as the stress stimulus and performed whole genome microarray analysis of Arabidopsis thaliana leaf tissue. This led to the identification of a number of rapid wound responsive (RWR) genes. Comparison of RWR genes with published abiotic and biotic stress microarray datasets demonstrates a large overlap across a wide range of environmental stresses. Interestingly, RWR genes also exhibit a striking level and pattern of circadian regulation, with induced and repressed genes displaying antiphasic rhythms. Using bioinformatic analysis, we identified a novel motif overrepresented in the promoters of RWR genes, herein designated as the Rapid Stress Response Element (RSRE). We demonstrate in transgenic plants that multimerized RSREs are sufficient to confer a rapid response to both biotic and abiotic stresses in vivo, thereby establishing the functional involvement of this motif in primary transcriptional stress responses. Collectively, our data provide evidence for a novel cis-element that is distributed across the promoters of an array of diverse stress-responsive genes, poised to respond immediately and coordinately to stress signals. This structure suggests that plants may have a transcriptional network resembling the general stress signaling pathway in yeast and that the RSRE element may provide the key to this coordinate regulation. PMID:17953483

  1. Osmotic stress induces the phosphorylation of WNK4 Ser575 via the p38MAPK-MK pathway

    PubMed Central

    Maruyama, Junichi; Kobayashi, Yumie; Umeda, Tsuyoshi; Vandewalle, Alain; Takeda, Kohsuke; Ichijo, Hidenori; Naguro, Isao

    2016-01-01

    The With No lysine [K] (WNK)-Ste20-related proline/alanine-rich kinase (SPAK)/oxidative stress-responsive kinase 1 (OSR1) pathway has been reported to be a crucial signaling pathway for triggering pseudohypoaldosteronism type II (PHAII), an autosomal dominant hereditary disease that is characterized by hypertension. However, the molecular mechanism(s) by which the WNK-SPAK/OSR1 pathway is regulated remain unclear. In this report, we identified WNK4 as an interacting partner of a recently identified MAP3K, apoptosis signal-regulating kinase 3 (ASK3). We found that WNK4 is phosphorylated in an ASK3 kinase activity-dependent manner. By exploring the ASK3-dependent phosphorylation sites, we identified Ser575 as a novel phosphorylation site in WNK4 by LC-MS/MS analysis. ASK3-dependent WNK4 Ser575 phosphorylation was mediated by the p38MAPK-MAPK-activated protein kinase (MK) pathway. Osmotic stress, as well as hypotonic low-chloride stimulation, increased WNK4 Ser575 phosphorylation via the p38MAPK-MK pathway. ASK3 was required for the p38MAPK activation induced by hypotonic stimulation but was not required for that induced by hypertonic stimulation or hypotonic low-chloride stimulation. Our results suggest that the p38MAPK-MK pathway might regulate WNK4 in an osmotic stress-dependent manner but its upstream regulators might be divergent depending on the types of osmotic stimuli. PMID:26732173

  2. Intermittent Noise Induces Physiological Stress in a Coastal Marine Fish.

    PubMed

    Nichols, Tye A; Anderson, Todd W; Širović, Ana

    2015-01-01

    Anthropogenic noise in the ocean has increased substantially in recent decades, and motorized vessels produce what is likely the most common form of underwater noise pollution. Noise has the potential to induce physiological stress in marine fishes, which may have negative ecological consequences. In this study, physiological effects of increased noise (playback of boat noise recorded in the field) on a coastal marine fish (the giant kelpfish, Heterostichus rostratus) were investigated by measuring the stress responses (cortisol concentration) of fish to increased noise of various temporal dynamics and noise levels. Giant kelpfish exhibited acute stress responses when exposed to intermittent noise, but not to continuous noise or control conditions (playback of recorded natural ambient sound). These results suggest that variability in the acoustic environment may be more important than the period of noise exposure for inducing stress in a marine fish, and provide information regarding noise levels at which physiological responses occur. PMID:26402068

  3. Pneumococcal hydrogen peroxide-induced stress signaling regulates inflammatory genes.

    PubMed

    Loose, Maria; Hudel, Martina; Zimmer, Klaus-Peter; Garcia, Ernesto; Hammerschmidt, Sven; Lucas, Rudolf; Chakraborty, Trinad; Pillich, Helena

    2015-01-15

    Microbial infections can induce aberrant responses in cellular stress pathways, leading to translational attenuation, metabolic restriction, and activation of oxidative stress, with detrimental effects on cell survival. Here we show that infection of human airway epithelial cells with Streptococcus pneumoniae leads to induction of endoplasmic reticulum (ER) and oxidative stress, activation of mitogen-associated protein kinase (MAPK) signaling pathways, and regulation of their respective target genes. We identify pneumococcal H2O2 as the causative agent for these responses, as both catalase-treated and pyruvate oxidase-deficient bacteria lacked these activities. Pneumococcal H2O2 induced nuclear NF-κB translocation and transcription of proinflammatory cytokines. Inhibition of translational arrest and ER stress by salubrinal or of MAPK signaling pathways attenuate cytokine transcription. These results provide strong evidence for the notion that inhibition of translation is an important host pathway in monitoring harmful pathogen-associated activities, thereby enabling differentiation between pathogenic and nonpathogenic bacteria. PMID:25183769

  4. Intermittent Noise Induces Physiological Stress in a Coastal Marine Fish

    PubMed Central

    Nichols, Tye A.; Anderson, Todd W.; Širović, Ana

    2015-01-01

    Anthropogenic noise in the ocean has increased substantially in recent decades, and motorized vessels produce what is likely the most common form of underwater noise pollution. Noise has the potential to induce physiological stress in marine fishes, which may have negative ecological consequences. In this study, physiological effects of increased noise (playback of boat noise recorded in the field) on a coastal marine fish (the giant kelpfish, Heterostichus rostratus) were investigated by measuring the stress responses (cortisol concentration) of fish to increased noise of various temporal dynamics and noise levels. Giant kelpfish exhibited acute stress responses when exposed to intermittent noise, but not to continuous noise or control conditions (playback of recorded natural ambient sound). These results suggest that variability in the acoustic environment may be more important than the period of noise exposure for inducing stress in a marine fish, and provide information regarding noise levels at which physiological responses occur. PMID:26402068

  5. Cobalt chloride-mediated protein kinase Cα (PKCα) phosphorylation induces hypoxia-inducible factor 1α (HIF1α) in the nucleus of gastric cancer cell.

    PubMed

    Rath, Suvasmita; Anand, Aditya; Ghosh, Nilabh; Das, Lopamudra; Kokate, Shrikant B; Dixit, Pragyesh; Majhi, Swetapadma; Rout, Niranjan; Singh, Shivaram P; Bhattacharyya, Asima

    2016-02-26

    Hypoxia promotes cancer progression, and metastasis. The major protein expressed in hypoxic solid cancer is hypoxia-inducible factor 1 (HIF1). We show that enhanced phosphorylation of a conventional protein kinase C isoform, PKCα, at threonine 638 (T(638)) by hypoxia-mimetic cobalt chloride induces HIF1α in nuclei of gastric epithelial cells (GECs). Moreover, phospho-T(638)-PKCα (P-PKCα) interacts with p300-HIF1α complex in the nuclei of hypoxic GECs and PKCα phosphorylation at T(638) enhances transcriptional activity of HIF1α. High P-PKCα expression in neoplastic gastric cancer biopsy samples as compared to nonneoplastic samples suggests that P-PKCα might act as an indicator of gastric cancer progression.

  6. Intracellular accumulation of indium ions released from nanoparticles induces oxidative stress, proinflammatory response and DNA damage.

    PubMed

    Tabei, Yosuke; Sonoda, Akinari; Nakajima, Yoshihiro; Biju, Vasudevanpillai; Makita, Yoji; Yoshida, Yasukazu; Horie, Masanori

    2016-02-01

    Due to the widespread use of indium tin oxide (ITO), it is important to investigate its effect on human health. In this study, we evaluated the cellular effects of ITO nanoparticles (NPs), indium chloride (InCl3) and tin chloride (SnCl3) using human lung epithelial A549 cells. Transmission electron microscopy and inductively coupled plasma mass spectrometry were employed to study cellular ITO NP uptake. Interestingly, greater uptake of ITO NPs was observed, as compared with soluble salts. ITO NP species released could be divided into two types: 'indium release ITO' or 'tin release ITO'. We incubated A549 cells with indium release ITO, tin release ITO, InCl3 or SnCl2 and investigated oxidative stress, proinflammatory response, cytotoxicity and DNA damage. We found that intracellular reactive oxygen species were increased in cells incubated with indium release ITO, but not tin release ITO, InCl3 or SnCl2. Messenger RNA and protein levels of the inflammatory marker, interleukin-8, also increased following exposure to indium release ITO. Furthermore, the alkaline comet assay revealed that intracellular accumulation of indium ions induced DNA damage. Our results demonstrate that the accumulation of ionic indium, but not ionic tin, from ITO NPs in the intracellular matrix has extensive cellular effects.

  7. Study of inducer load and stress, volume 2

    NASA Technical Reports Server (NTRS)

    1972-01-01

    A program of analysis, design, fabrication and testing has been conducted to develop computer programs for predicting rocket engine turbopump inducer hydrodynamic loading, stress magnitude and distribution, and vibration characteristics. Methods of predicting blade loading, stress, and vibration characteristics were selected from a literature search and used as a basis for the computer programs. An inducer, representative of typical rocket engine inducers, was designed, fabricated, and tested with special instrumentation selected to provide measurements of blade surface pressures and stresses. Data from the tests were compared with predicted values and the computer programs were revised as required to improve correlation. For Volume 1 see N71-20403. For Volume 2 see N71-20404.

  8. The GST T1 and CYP2E1 genotypes are possible factors causing vinyl chloride induced abnormal liver function.

    PubMed

    Huang, C Y; Huang, K L; Cheng, T J; Wang, J D; Hsieh, L L

    1997-01-01

    Vinyl chloride monomer (VCM) is hepatotoxic as well as carcinogenic in humans. There are reports that exposure to VCM seems to induce abnormal liver function, liver fibrosis, cirrhosis, portal hypertension, and angiosarcoma of the liver. In vivo, VCM is metabolized by cytochrome P450 2E1 (CYP2E1) to form the electrophilic metabolites, chloroethylene oxide (CEO) and chloroacetaldehyde (CAA), which may either cause cell damage or be further metabolized and detoxified by glutathione S-transferases (GSTs). This study investigated whether or not the genotypes CYP2E1, glutathione S-transferase theta (GST T1) and mu (GST M1) correlated with abnormal liver function found in vinyl chloride exposed workers. For this study, 251 workers from five polyvinyl chloride plants were enrolled. The workers were classified into two exposure groups (high and low) and the degree of exposure was determined based on their job titles and airborne VCM concentration. The activity of serum alanine aminotransferase (ALT) was used as the parameter of liver function. The genotypes CYP2E1, GST T1 and GST M1 were determined by polymerase chain reaction and restriction fragment length polymorphism on peripheral white blood cell DNA. Other potential risk factors were also ascertained and the confounding effect was adjusted accordingly. Stratified analyses were used to explore the correlation between the alteration of liver function and the genotypes CYP2E1, GST T1 and GST M1 among the workers exposed to different levels of VCM. The following results were obtained (1) at low VCM exposure, the odds ratio (OR) of positive GST T1 on abnormal ALT was 3.8 (95% CI 1.2-14.5) but the CYP2E1 genotype was not associated with abnormal ALT. (2) At high VCM exposure, a c2c2 CYP2E1 genotype was associated with increased OR on abnormal ALT (OR 5.4, 95% CI 0.7-35.1) and positive GST T1 was significantly associated with decreased OR on abnormal ALT (OR 0.3, 95% CI 0.1-0.9). (3) Multiple linear and logistic regression

  9. Corneal Alternations Induced by Topical Application of Benzalkonium Chloride in Rabbit

    PubMed Central

    Chen, Wensheng; Li, Zhiyuan; Hu, Jiaoyue; Zhang, Zhenhao; Chen, Lelei; Chen, Yongxiong; Liu, Zuguo

    2011-01-01

    Benzalkonium chloride (BAC) is the most common preservative in ophthalmic preparations. Here, we investigated the corneal alternations in rabbits following exposure to BAC. Twenty-four adult male New Zealand albino rabbits were randomly divided into three groups. BAC at 0.01%, 0.05%, or 0.1% was applied twice daily to one eye each of rabbits for 4 days. The contralateral untreated eyes were used as control. Aqueous tear production and fluorescein staining scores of BAC-treated eyes were compared with those of controls. The structure of the central cornea was examined by in vivo confocal microscopy. Expression of mucin-5 subtype AC (MUC5AC) in conjunctiva was detected by immunostainig on cryosections. Corneal barrier function was assessed in terms of permeability to carboxy fluorescein (CF). The distribution and expression of ZO-1, a known marker of tight junction, and reorganization of the perijunctional actomyosin ring (PAMR) were examined by immunofluorescence analysis. Although there were no significant differences between control and BAC-treated eyes in Schirmer scores, corneal fluorescein scores and the number of conjunctival MUC5AC staining cells, in vivo confocal microscopy revealed significant epithelial and stromal defects in all BAC-treated corneas. Moreover, BAC at 0.1% resulted in significant increases in central corneal thickness and endothelial CF permeability, compared with those in control eyes, and endothelial cell damage with dislocation of ZO-1 and disruption of PAMR. Topical application of BAC can quickly impair the whole cornea without occurrence of dry eye. A high concentration of BAC breaks down the barrier integrity of corneal endothelium, concomitant with the disruption of PAMR and remodeling of apical junctional complex in vivo. PMID:22022526

  10. Upregulated autophagy protects cardiomyocytes from oxidative stress-induced toxicity.

    PubMed

    Dutta, Debapriya; Xu, Jinze; Kim, Jae-Sung; Dunn, William A; Leeuwenburgh, Christiaan

    2013-03-01

    Autophagy is a cellular self-digestion process that mediates protein quality control and serves to protect against neurodegenerative disorders, infections, inflammatory diseases and cancer. Current evidence suggests that autophagy can selectively remove damaged organelles such as the mitochondria. Mitochondria-induced oxidative stress has been shown to play a major role in a wide range of pathologies in several organs, including the heart. Few studies have investigated whether enhanced autophagy can offer protection against mitochondrially-generated oxidative stress. We induced mitochondrial stress in cardiomyocytes using antimycin A (AMA), which increased mitochondrial superoxide generation, decreased mitochondrial membrane potential and depressed cellular respiration. In addition, AMA augmented nuclear DNA oxidation and cell death in cardiomyocytes. Interestingly, although oxidative stress has been proposed to induce autophagy, treatment with AMA did not result in stimulation of autophagy or mitophagy in cardiomyocytes. Our results showed that the MTOR inhibitor rapamycin induced autophagy, promoted mitochondrial clearance and protected cardiomyocytes from the cytotoxic effects of AMA, as assessed by apoptotic marker activation and viability assays in both mouse atrial HL-1 cardiomyocytes and human ventricular AC16 cells. Importantly, rapamycin improved mitochondrial function, as determined by cellular respiration, mitochondrial membrane potential and morphology analysis. Furthermore, autophagy induction by rapamycin suppressed the accumulation of ubiquitinylated proteins induced by AMA. Inhibition of rapamycin-induced autophagy by pharmacological or genetic interventions attenuated the cytoprotective effects of rapamycin against AMA. We propose that rapamycin offers cytoprotection against oxidative stress by a combined approach of removing dysfunctional mitochondria as well as by degrading damaged, ubiquitinated proteins. We conclude that autophagy induction by

  11. Upregulated autophagy protects cardiomyocytes from oxidative stress-induced toxicity

    PubMed Central

    Dutta, Debapriya; Xu, Jinze; Kim, Jae-Sung; Dunn, Jr., William A.; Leeuwenburgh, Christiaan

    2013-01-01

    Autophagy is a cellular self-digestion process that mediates protein quality control and serves to protect against neurodegenerative disorders, infections, inflammatory diseases and cancer. Current evidence suggests that autophagy can selectively remove damaged organelles such as the mitochondria. Mitochondria-induced oxidative stress has been shown to play a major role in a wide range of pathologies in several organs, including the heart. Few studies have investigated whether enhanced autophagy can offer protection against mitochondrially-generated oxidative stress. We induced mitochondrial stress in cardiomyocytes using antimycin A (AMA), which increased mitochondrial superoxide generation, decreased mitochondrial membrane potential and depressed cellular respiration. In addition, AMA augmented nuclear DNA oxidation and cell death in cardiomyocytes. Interestingly, although oxidative stress has been proposed to induce autophagy, treatment with AMA did not result in stimulation of autophagy or mitophagy in cardiomyocytes. Our results showed that the MTOR inhibitor rapamycin induced autophagy, promoted mitochondrial clearance and protected cardiomyocytes from the cytotoxic effects of AMA, as assessed by apoptotic marker activation and viability assays in both mouse atrial HL-1 cardiomyocytes and human ventricular AC16 cells. Importantly, rapamycin improved mitochondrial function, as determined by cellular respiration, mitochondrial membrane potential and morphology analysis. Furthermore, autophagy induction by rapamycin suppressed the accumulation of ubiquitinylated proteins induced by AMA. Inhibition of rapamycin-induced autophagy by pharmacological or genetic interventions attenuated the cytoprotective effects of rapamycin against AMA. We propose that rapamycin offers cytoprotection against oxidative stress by a combined approach of removing dysfunctional mitochondria as well as by degrading damaged, ubiquitinated proteins. We conclude that autophagy induction by

  12. Silver nanoparticles induce endoplasmatic reticulum stress response in zebrafish

    SciTech Connect

    Christen, Verena; Capelle, Martinus; Fent, Karl

    2013-10-15

    Silver nanoparticles (AgNPs) find increasing applications, and therefore humans and the environment are increasingly exposed to them. However, potential toxicological implications are not sufficiently known. Here we investigate effects of AgNPs (average size 120 nm) on zebrafish in vitro and in vivo, and compare them to human hepatoma cells (Huh7). AgNPs are incorporated in zebrafish liver cells (ZFL) and Huh7, and in zebrafish embryos. In ZFL cells AgNPs lead to induction of reactive oxygen species (ROS), endoplasmatic reticulum (ER) stress response, and TNF-α. Transcriptional alterations also occur in pro-apoptotic genes p53 and Bax. The transcriptional profile differed in ZFL and Huh7 cells. In ZFL cells, the ER stress marker BiP is induced, concomitant with the ER stress marker ATF-6 and spliced XBP-1 after 6 h and 24 h exposure to 0.5 g/L and 0.05 g/L AgNPs, respectively. This indicates the induction of different pathways of the ER stress response. Moreover, AgNPs induce TNF-α. In zebrafish embryos exposed to 0.01, 0.1, 1 and 5 mg/L AgNPs hatching was affected and morphological defects occurred at high concentrations. ER stress related gene transcripts BiP and Synv are significantly up-regulated after 24 h at 0.1 and 5 mg/L AgNPs. Furthermore, transcriptional alterations occurred in the pro-apoptotic genes Noxa and p21. The ER stress response was strong in ZFL cells and occurred in zebrafish embryos as well. Our data demonstrate for the first time that AgNPs lead to induction of ER stress in zebrafish. The induction of ER stress can have several consequences including the activation of apoptotic and inflammatory pathways. - Highlights: • Effects of silver nanoparticles (120 nm AgNPs) are investigated in zebrafish. • AgNPs induce all ER stress reponses in vitro in zebrafish liver cells. • AgNPs induce weak ER stress in zebrafish embryos. • AgNPs induce oxidative stress and transcripts of pro-apoptosis genes.

  13. Gravity-induced stresses near a vertical cliff

    USGS Publications Warehouse

    Savage, W.Z.

    1993-01-01

    The exact solution for gravity-induced stresses beneath a vertical cliff presented here has application to the design of cut slopes in rock, compares favorably with published photoelastic and finite-element results for this problem, and satisfies the condition that shear and normal stresses vanish on the ground surface, except at the bottom corner where stress concentrations exist. The solution predicts that horizontal stresses are tensile away from the bottom of the cliff-effects caused by movement below the cliff in response to the gravity loading of the cliff. Also, it is shown that along the top of the cliff normal stresses reduce to those predicted for laterally constrained flat-lying topography. ?? 1993.

  14. Aneuploidy-induced cellular stresses limit autophagic degradation

    PubMed Central

    Santaguida, Stefano; Vasile, Eliza; White, Eileen; Amon, Angelika

    2015-01-01

    An unbalanced karyotype, a condition known as aneuploidy, has a profound impact on cellular physiology and is a hallmark of cancer. Aneuploid cells experience a number of stresses that are caused by aneuploidy-induced proteomic changes. How the aneuploidy-associated stresses affect cells and whether cells respond to them are only beginning to be understood. Here we show that autophagosomal cargo such as protein aggregates accumulate within lysosomes in aneuploid cells. This causes a lysosomal stress response. Aneuploid cells activate the transcription factor TFEB, a master regulator of autophagic and lysosomal gene expression, thereby increasing the expression of genes needed for autophagy-mediated protein degradation. Accumulation of autophagic cargo within the lysosome and activation of TFEB-responsive genes are also observed in cells in which proteasome function is inhibited, suggesting that proteotoxic stress causes TFEB activation. Our results reveal a TFEB-mediated lysosomal stress response as a universal feature of the aneuploid state. PMID:26404941

  15. Tau protein is essential for stress-induced brain pathology.

    PubMed

    Lopes, Sofia; Vaz-Silva, João; Pinto, Vitor; Dalla, Christina; Kokras, Nikolaos; Bedenk, Benedikt; Mack, Natalie; Czisch, Michael; Almeida, Osborne F X; Sousa, Nuno; Sotiropoulos, Ioannis

    2016-06-28

    Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer's-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory deficits. Here, we demonstrate that stress-driven hippocampal deficits in wild-type mice are accompanied by synaptic missorting of Tau and enhanced Fyn/GluN2B-driven synaptic signaling. In contrast, mice lacking Tau [Tau knockout (Tau-KO) mice] do not exhibit stress-induced pathological behaviors and atrophy of hippocampal dendrites or deficits of hippocampal connectivity. These findings implicate Tau as an essential mediator of the adverse effects of stress on brain structure and function. PMID:27274066

  16. OGG1 is essential in oxidative stress induced DNA demethylation.

    PubMed

    Zhou, Xiaolong; Zhuang, Ziheng; Wang, Wentao; He, Lingfeng; Wu, Huan; Cao, Yan; Pan, Feiyan; Zhao, Jing; Hu, Zhigang; Sekhar, Chandra; Guo, Zhigang

    2016-09-01

    DNA demethylation is an essential cellular activity to regulate gene expression; however, the mechanism that triggers DNA demethylation remains unknown. Furthermore, DNA demethylation was recently demonstrated to be induced by oxidative stress without a clear molecular mechanism. In this manuscript, we demonstrated that 8-oxoguanine DNA glycosylase-1 (OGG1) is the essential protein involved in oxidative stress-induced DNA demethylation. Oxidative stress induced the formation of 8-oxoguanine (8-oxoG). We found that OGG1, the 8-oxoG binding protein, promotes DNA demethylation by interacting and recruiting TET1 to the 8-oxoG lesion. Downregulation of OGG1 makes cells resistant to oxidative stress-induced DNA demethylation, while over-expression of OGG1 renders cells susceptible to DNA demethylation by oxidative stress. These data not only illustrate the importance of base excision repair (BER) in DNA demethylation but also reveal how the DNA demethylation signal is transferred to downstream DNA demethylation enzymes. PMID:27251462

  17. The effect of induced visual stress on three dimensional perception.

    PubMed

    Abd-Manan, F

    2000-07-01

    Previous studies have shown that stress on the vergence and accommodation systems, either artificially induced or naturally occurring, results in small misalignment of the visual axes, reduces binocular visual acuity and produces symptoms of ocular discomfort. This study examines the effect of artificially induced visual stress using ophthalmic prisms on three dimensional perception on 30 optometry students ages ranging from 19 to 29 years old. 6D base-in prisms, equally divided between the eyes (3D base-in each) was used to induce stress on the visual system producing misalignment of visual axes known as fixation disparity. The fixation disparity is quantified using near vision Mallett Unit and an enlarged scaled diagram. Stereoscopic perception was measured with the TNO test, with and without the presence of stress and the results was compared. Wilcoxon's matched pair ranked tests show statistically significant difference in the stereo thresholds of both conditions, p = 0.01 for advancing stereopsis and p = 0.01 for receding stereopsis, respectively. The study concludes that visual stress induced by prisms, produce misalignment of the visual axes and thus reduces three dimensional performance. PMID:22977386

  18. Stress-induced transverse isotropy in rocks

    SciTech Connect

    Schwartz, L.M.; Murphy, W.F. III; Berryman, J.G.

    1994-03-28

    The application of uniaxial pressure can induce elastic anisotropy in otherwise isotropic rock. We consider models based on two very different rock classes, granites and weakly consolidated granular systems. We show that these models share common underlying assumptions, that they lead to similar qualitative behavior, and that both provide a microscopic basis for elliptical anisotropy. In the granular case, we make experimentally verifiable predictions regarding the horizontally propagating modes based on the measured behavior of the vertical modes.

  19. Cannabinoid 2 (CB2) receptor agonism reduces lithium chloride-induced vomiting in Suncus murinus and nausea-induced conditioned gaping in rats.

    PubMed

    Rock, Erin M; Boulet, Nathalie; Limebeer, Cheryl L; Mechoulam, Raphael; Parker, Linda A

    2016-09-01

    We aimed to investigate the potential anti-emetic and anti-nausea properties of targeting the cannabinoid 2 (CB2) receptor. We investigated the effect of the selective CB2 agonist, HU-308, on lithium chloride- (LiCl) induced vomiting in Suncus murinus (S. murinus) and conditioned gaping (nausea-induced behaviour) in rats. Additionally, we determined whether these effects could be prevented by pretreatment with AM630 (a selective CB2 receptor antagonist/inverse agonist). In S. murinus, HU-308 (2.5, 5mg/kg, i.p.) reduced, but did not completely block, LiCl-induced vomiting; an effect that was prevented with AM630. In rats, HU-308 (5mg/kg, i.p.) suppressed, but did not completely block, LiCl-induced conditioned gaping to a flavour; an effect that was prevented by AM630. These findings are the first to demonstrate the ability of a selective CB2 receptor agonist to reduce nausea in animal models, indicating that targeting the CB2 receptor may be an effective strategy, devoid of psychoactive effects, for managing toxin-induced nausea and vomiting. PMID:27263826

  20. Mechanisms of Nanoparticle-Induced Oxidative Stress and Toxicity

    PubMed Central

    Wang, Liying

    2013-01-01

    The rapidly emerging field of nanotechnology has offered innovative discoveries in the medical, industrial, and consumer sectors. The unique physicochemical and electrical properties of engineered nanoparticles (NP) make them highly desirable in a variety of applications. However, these novel properties of NP are fraught with concerns for environmental and occupational exposure. Changes in structural and physicochemical properties of NP can lead to changes in biological activities including ROS generation, one of the most frequently reported NP-associated toxicities. Oxidative stress induced by engineered NP is due to acellular factors such as particle surface, size, composition, and presence of metals, while cellular responses such as mitochondrial respiration, NP-cell interaction, and immune cell activation are responsible for ROS-mediated damage. NP-induced oxidative stress responses are torch bearers for further pathophysiological effects including genotoxicity, inflammation, and fibrosis as demonstrated by activation of associated cell signaling pathways. Since oxidative stress is a key determinant of NP-induced injury, it is necessary to characterize the ROS response resulting from NP. Through physicochemical characterization and understanding of the multiple signaling cascades activated by NP-induced ROS, a systemic toxicity screen with oxidative stress as a predictive model for NP-induced injury can be developed. PMID:24027766

  1. Suppression of c-Kit signaling induces adult neurogenesis in the mouse intestine after myenteric plexus ablation with benzalkonium chloride.

    PubMed

    Tamada, Hiromi; Kiyama, Hiroshi

    2016-01-01

    Adult neurogenesis rarely occurs in the enteric nervous system (ENS). In this study, we demonstrated that, after intestinal myenteric plexus (MP) ablation with benzalkonium chloride (BAC), adult neurogenesis in the ENS was significantly induced in c-kit loss-of-function mutant mice (W/W(v)). Almost all neurons and fibers in the MP disappeared after BAC treatment. However, 1 week after ablation, substantial penetration of nerve fibers from the non-damaged area was observed in the MP, longitudinal muscle and subserosal layers in both wildtype and W/W(v) mice. Two weeks after BAC treatment, in addition to the penetrating fibers, a substantial number of ectopic neurons appeared in the subserosal and longitudinal muscle layers of W/W(v) mice, whereas only a few ectopic neurons appeared in wildtype mice. Such ectopic neurons expressed either excitatory or inhibitory intrinsic motor neuron markers and formed ganglion-like structures, including glial cells, synaptic vesicles and basal lamina. Furthermore, oral administration of imatinib, an inhibitor of c-Kit and an anticancer agent for gastrointestinal stromal tumors, markedly induced appearance of ectopic neurons after BAC treatment, even in wildtype mice. These results suggest that adult neurogenesis in the ENS is negatively regulated by c-Kit signaling in vivo. PMID:27572504

  2. Suppression of c-Kit signaling induces adult neurogenesis in the mouse intestine after myenteric plexus ablation with benzalkonium chloride

    PubMed Central

    Tamada, Hiromi; Kiyama, Hiroshi

    2016-01-01

    Adult neurogenesis rarely occurs in the enteric nervous system (ENS). In this study, we demonstrated that, after intestinal myenteric plexus (MP) ablation with benzalkonium chloride (BAC), adult neurogenesis in the ENS was significantly induced in c-kit loss-of-function mutant mice (W/Wv). Almost all neurons and fibers in the MP disappeared after BAC treatment. However, 1 week after ablation, substantial penetration of nerve fibers from the non-damaged area was observed in the MP, longitudinal muscle and subserosal layers in both wildtype and W/Wv mice. Two weeks after BAC treatment, in addition to the penetrating fibers, a substantial number of ectopic neurons appeared in the subserosal and longitudinal muscle layers of W/Wv mice, whereas only a few ectopic neurons appeared in wildtype mice. Such ectopic neurons expressed either excitatory or inhibitory intrinsic motor neuron markers and formed ganglion-like structures, including glial cells, synaptic vesicles and basal lamina. Furthermore, oral administration of imatinib, an inhibitor of c-Kit and an anticancer agent for gastrointestinal stromal tumors, markedly induced appearance of ectopic neurons after BAC treatment, even in wildtype mice. These results suggest that adult neurogenesis in the ENS is negatively regulated by c-Kit signaling in vivo. PMID:27572504

  3. Mice heterozygous for cathepsin D deficiency exhibit mania-related behavior and stress-induced depression.

    PubMed

    Zhou, Rui; Lu, Yi; Han, Yong; Li, Xia; Lou, Huifang; Zhu, Liya; Zhen, Xuechu; Duan, Shumin

    2015-12-01

    Mutations in cathepsin D (CTSD), an aspartic protease in the endosomal-lysosomal system, underlie congenital neuronal ceroid-lipofuscinosis (cNCL, also known as CLN10), a devastating neurodegenerative disease. CLN10 patients die within the first few days of life, and in the few patients who live into adulthood psychopathological symptoms have not been reported. Extensive neuropathology and altered neurotransmission have been reported in CTSD-deficient mice; however signs of neuropsychiatric behavior in these mice are not well characterized due to the severe movement disorder and premature death of the animal. In the present study, we show that heterozygous CTSD-deficient (CTSD HET) mice display an overall behavioral profile that is similar to human mania, including hyperlocomotion, d-amphetamine-induced hyperactivity, sleep-disturbance, and reduced anxiety-like behavior. However, under stressful conditions CTSD HET mice manifest depressive-like behavior, including anhedonia, behavioral despair, and enhanced learned helplessness. Chronic administration of lithium chloride or valproic acid, two clinically effective mood stabilizers, reverses the majority of these behavioral abnormalities. In addition, CTSD HET mice display stress-induced hypersecretion of corticosterone. These findings suggest an important role for CTSD in the regulation of mood stabilization.

  4. Stress-Induced Phenomena in Metallization 8th International Workshop on Stress-Induced Phenomena in Metallization

    NASA Astrophysics Data System (ADS)

    Zschech, Ehrenfried; Maex, Karen; Ho, Paul S.; Kawasaki, Hisao; Nakamura, Tomoji

    All papers were peer reviewed. This proceedings presents current research on issues related to stress-induced phenomena in on-chip metal interconnects and solder joints. Stresses arising in on-chip metal interconnects and surrounding dielectric materials due to thermal mismatch, electromigration, microstructure changes or process integration can lead to degradation and failure of microelectronic products. The implementation of low dielectric constant materials into the inlaid copper backend-of-line process has brought new challenges for process integration and reliability.

  5. Pharmacological modulation of stress-induced behavioral changes in the light/dark exploration test in male C57BL/6J mice.

    PubMed

    Ihne, Jessica L; Fitzgerald, Paul J; Hefner, Kathryn R; Holmes, Andrew

    2012-01-01

    Psychological stress is a major risk factor for mood and anxiety disorders. However, the phenotypic manifestation of stress effects varies across individuals, likely due, in part, to genetic variation. Modeling the behavioral and neural consequences of stress across genetically diverse inbred mouse strains is a valuable approach to studying gene × stress interactions. Recent work has shown that C57BL/6J mice exposed to ten daily sessions of restraint stress exhibited increased exploration of the aversive light compartment in the light/dark exploration (LDE) test. Here we sought to clarify the nature of this stress-induced phenotype by testing the ability of treatment with various clinically efficacious drugs of different therapeutic classes to rescue it. Ten days of restraint increased light compartment exploration, reduced body weight and sensitized the corticosterone response to swim stress. Subchronic administration (during stress and LDE testing) of fluoxetine, and to a lesser extent, lithium chloride, rescued stress-induced LDE behavior. Chronic fluoxetine treatment prior to (plus during stress and testing) failed to block the LDE stress effect. Acute administration of antipsychotic haloperidol, anti-ADHD medication methylphenidate or anxiolytic drug chlordiazepoxide, prior to LDE testing, was also unable to normalize the LDE stress effect. Collectively, these data demonstrate a treatment-selective prophylactic rescue of a restraint stress-induced behavioral abnormality in the C57BL/6J inbred strain. Further work with this novel model could help elucidate genetic and neural mechanisms mediating stress-induced changes in mouse 'emotion-relevant' behaviors and, ultimately, further understanding of the pathophysiology of stress-related neuropsychiatric disorders. This article is part of a Special Issue entitled 'Anxiety and Depression'.

  6. Protective effect of low dose gadolinium chloride against isoproterenol-induced myocardial injury in rat.

    PubMed

    Zheng, Yuan-Yuan; Zhang, Hai-Hong; Yan, Xin-Xin; Chen, Min; Qi, Tian-Yu; Zhang, Lan-E; Luo, Da-Li

    2015-09-01

    Acute myocardial injury remains a leading cause of morbidity and mortality worldwide, and large amount of released arachidonic acid (AA) is found to be related to cardiomyocyte apoptosis and necrosis. Previous study suggested that GdCl3 completely abolished AA-induced Ca(2+) response. Thus, this study aims to investigate possible cardioprotection effect of GdCl3 on isoproterenol (ISO)-induced myocardial injury and its underlying mechanism(s). Rats that were randomly allocated to five groups: control, GdCl3, ISO, ISO + GdCl3, and ISO + verapamil. Serum levels of AA and cardiac markers, infarct area, and cell apoptosis in heart were measured by ELISA assay, TTC and TUNEL staining, respectively. Chemical interaction between AA and GdCl3 was evaluated by mass and UV spectrometry. The expressions and translocations of death receptor related molecules into lipid rafts were detected in neonatal rat ventricular myocytes by Western blots. Compared with ISO-administered rats, GdCl3 significantly ameliorated the myocardium injury, demonstrated by restoring serum cardiac troponin I, lactate dehydrogenase, creatine kinase MB and AA to near normal levels, and decreasing infarct area and cell apoptosis. In addition, an activation of AA-Fas pathway was found in ISO-induced myocardial injury, which was abrogated by GdCl3. Furthermore, AA induced cell apoptosis through clustering and activating death receptor related molecules TNFR1, Fas and FADD in lipid rafts, a process significantly prevented by the pretreatment with GdCl3. Finally, GdCl3 at the molar ratio of 1/3 (GdCl3/AA) was mostly effective in abolishing AA-induced Ca(2+) response and cell apoptosis, because an obvious change in the chemical identity of AA was obtained by GdCl3 according to this molar ratio. In conclusion, this study demonstrates for the first time that GdCl3 protects myocardium against ISO-induced cell apoptosis through, at least partly, serving as a scavenger of AA, therefore abolishing its downstream

  7. Chloride Test

    MedlinePlus

    ... Addison disease, or increased salt intake. If both chloride and sodium levels are high in a person on a ... anything else I should know? Drugs that affect sodium blood levels will also cause changes in chloride. In addition, swallowing large amounts of baking soda ...

  8. Association between Anger and Mental Stress-Induced Myocardial Ischemia

    PubMed Central

    Pimple, Pratik; Shah, Amit; Rooks, Cherie; Bremner, J. Douglas; Nye, Jonathon; Ibeanu, Ijeoma; Murrah, Nancy; Shallenberger, Lucy; Kelley, Mary; Raggi, Paolo; Vaccarino, Viola

    2014-01-01

    Background Mental stress-induced myocardial ischemia is associated with adverse prognosis in coronary artery disease patients. Anger is thought to be a trigger of acute coronary syndromes and is associated with increased cardiovascular risk; however, little direct evidence exists for a link between anger and myocardial ischemia. Methods [99mTc]sestamibi single-photon emission tomography was performed at rest, after mental stress (a social stressor with a speech task), and after exercise/pharmacological stress. Summed scores of perfusion abnormalities were obtained by observer-independent software. A summed difference score, the difference between stress and rest scores, was used to quantify myocardial ischemia under both stress conditions. The Spielberger's State-Trait Anger Expression Inventory was used to assess different anger dimensions. Results The mean age was 50 years, 50% were female and 60% were non-white. After adjusting for demographic factors, smoking, coronary artery disease severity, depressive and anxiety symptoms, each interquartile range increment in state-anger score was associated with 0.36 units adjusted increase in ischemia as measured by the summed difference score (95% CI: 0.14-0.59); the corresponding association for trait-anger was 0.95 (95% CI: 0.21-1.69). Anger expression scales were not associated ischemia. None of the anger dimensions were related to ischemia during exercise/pharmacological stress. Conclusion Anger, both as an emotional state and as a personality trait, is significantly associated with propensity to develop myocardial ischemia during mental stress, but not during exercise/pharmacological stress. Patients with this psychological profile may be at increased risk for silent ischemia induced by emotional stress and this may translate into worse prognosis. PMID:25497256

  9. On the function and fate of chloride ions in amyloidogenic self-assembly of insulin in an acidic environment: salt-induced condensation of fibrils.

    PubMed

    Babenko, Viktoria; Surmacz-Chwedoruk, Weronika; Dzwolak, Wojciech

    2015-02-24

    Formation of amyloid fibrils is often facilitated in the presence of specific charge-compensating ions. Dissolved sodium chloride is known to accelerate insulin fibrillation at low pH that has been attributed to the shielding of electrostatic repulsion between positively charged insulin molecules by chloride ions. However, the subsequent fate of Cl(-) anions; that is, possible entrapment within elongating fibrils or escape into the bulk solvent, remains unclear. Here, we show that, while the presence of NaCl at the onset of insulin aggregation induces structural variants of amyloid with distinct fingerprint infrared features, a delayed addition of salt to fibrils that have been already formed in its absence and under quiescent conditions triggers a "condensation effect": amyloid superstructures with strong chiroptical properties are formed. Chloride ions appear to stabilize these superstructures in a manner similar to stabilization of DNA condensates by polyvalent cations. The concentration of residual chloride ions trapped within bovine insulin fibrils grown in 0.1 M NaCl, at pD 1.9, and rinsed extensively with water afterward is less than 1 anion per 16 insulin monomers (as estimated using ion chromatography) implying absence of defined solvent-sequestered nesting sites for chloride counterions. Our results have been discussed in the context of mechanisms of insulin aggregation.

  10. Resveratrol reverses cadmium chloride-induced testicular damage and subfertility by downregulating p53 and Bax and upregulating gonadotropins and Bcl-2 gene expression.

    PubMed

    Eleawa, Samy M; Alkhateeb, Mahmoud A; Alhashem, Fahaid H; Bin-Jaliah, Ismaeel; Sakr, Hussein F; Elrefaey, Hesham M; Elkarib, Abbas O; Alessa, Riyad M; Haidara, Mohammad A; Shatoor, Abdullah S; Khalil, Mohammad A

    2014-04-24

    This study was performed to investigate the protective and therapeutic effects of resveratrol (RES) against CdCl2-induced toxicity in rat testes. Seven experimental groups of adult male rats were formulated as follows: A) controls+NS, B) control+vehicle (saline solution of hydroxypropyl cyclodextrin), C) RES treated, D) CdCl2+NS, E) CdCl2+vehicle, F) RES followed by CdCl2 and M) CdCl2 followed by RES. At the end of the protocol, serum levels of FSH, LH and testosterone were measured in all groups, and testicular levels of TBARS and superoxide dismutase (SOD) activity were measured. Epididymal semen analysis was performed, and testicular expression of Bcl-2, p53 and Bax was assessed by RT-PCR. Also, histopathological changes of the testes were examined microscopically. Administration of RES before or after cadmium chloride in rats improved semen parameters including count, motility, daily sperm production and morphology, increased serum concentrations of gonadotropins and testosterone, decreased testicular lipid peroxidation and increased SOD activity. RES not only attenuated cadmium chloride-induced testicular histopathology but was also able to protect against the onset of cadmium chloride testicular toxicity. Cadmium chloride downregulated the anti-apoptotic gene Bcl2 and upregulated the expression of pro-apoptotic genes p53 and Bax. Resveratrol protected against and partially reversed cadmium chloride testicular toxicity via upregulation of Bcl2 and downregulation of p53 and Bax gene expression. The antioxidant activity of RES protects against cadmium chloride testicular toxicity and partially reverses its effect via upregulation of BCl2 and downregulation of p53 and Bax expression. PMID:24492640

  11. Resveratrol Reverses Cadmium Chloride-induced Testicular Damage and Subfertility by Downregulating p53 and Bax and Upregulating Gonadotropins and Bcl-2 gene Expression

    PubMed Central

    ELEAWA, Samy M; ALKHATEEB, Mahmoud A; ALHASHEM, Fahaid H; BIN-JALIAH, Ismaeel; SAKR, Hussein F; ELREFAEY, Hesham M; ELKARIB, Abbas O; ALESSA, Riyad M; HAIDARA, Mohammad A; SHATOOR, Abdullah S.; KHALIL, Mohammad A

    2014-01-01

    This study was performed to investigate the protective and therapeutic effects of resveratrol (RES) against CdCl2-induced toxicity in rat testes. Seven experimental groups of adult male rats were formulated as follows: A) controls+NS, B) control+vehicle (saline solution of hydroxypropyl cyclodextrin), C) RES treated, D) CdCl2+NS, E) CdCl2+vehicle, F) RES followed by CdCl2 and M) CdCl2 followed by RES. At the end of the protocol, serum levels of FSH, LH and testosterone were measured in all groups, and testicular levels of TBARS and superoxide dismutase (SOD) activity were measured. Epididymal semen analysis was performed, and testicular expression of Bcl-2, p53 and Bax was assessed by RT-PCR. Also, histopathological changes of the testes were examined microscopically. Administration of RES before or after cadmium chloride in rats improved semen parameters including count, motility, daily sperm production and morphology, increased serum concentrations of gonadotropins and testosterone, decreased testicular lipid peroxidation and increased SOD activity. RES not only attenuated cadmium chloride-induced testicular histopathology but was also able to protect against the onset of cadmium chloride testicular toxicity. Cadmium chloride downregulated the anti-apoptotic gene Bcl2 and upregulated the expression of pro-apoptotic genes p53 and Bax. Resveratrol protected against and partially reversed cadmium chloride testicular toxicity via upregulation of Bcl2 and downregulation of p53 and Bax gene expression. The antioxidant activity of RES protects against cadmium chloride testicular toxicity and partially reverses its effect via upregulation of BCl2 and downregulation of p53 and Bax expression. PMID:24492640

  12. Resveratrol reverses cadmium chloride-induced testicular damage and subfertility by downregulating p53 and Bax and upregulating gonadotropins and Bcl-2 gene expression.

    PubMed

    Eleawa, Samy M; Alkhateeb, Mahmoud A; Alhashem, Fahaid H; Bin-Jaliah, Ismaeel; Sakr, Hussein F; Elrefaey, Hesham M; Elkarib, Abbas O; Alessa, Riyad M; Haidara, Mohammad A; Shatoor, Abdullah S; Khalil, Mohammad A

    2014-04-24

    This study was performed to investigate the protective and therapeutic effects of resveratrol (RES) against CdCl2-induced toxicity in rat testes. Seven experimental groups of adult male rats were formulated as follows: A) controls+NS, B) control+vehicle (saline solution of hydroxypropyl cyclodextrin), C) RES treated, D) CdCl2+NS, E) CdCl2+vehicle, F) RES followed by CdCl2 and M) CdCl2 followed by RES. At the end of the protocol, serum levels of FSH, LH and testosterone were measured in all groups, and testicular levels of TBARS and superoxide dismutase (SOD) activity were measured. Epididymal semen analysis was performed, and testicular expression of Bcl-2, p53 and Bax was assessed by RT-PCR. Also, histopathological changes of the testes were examined microscopically. Administration of RES before or after cadmium chloride in rats improved semen parameters including count, motility, daily sperm production and morphology, increased serum concentrations of gonadotropins and testosterone, decreased testicular lipid peroxidation and increased SOD activity. RES not only attenuated cadmium chloride-induced testicular histopathology but was also able to protect against the onset of cadmium chloride testicular toxicity. Cadmium chloride downregulated the anti-apoptotic gene Bcl2 and upregulated the expression of pro-apoptotic genes p53 and Bax. Resveratrol protected against and partially reversed cadmium chloride testicular toxicity via upregulation of Bcl2 and downregulation of p53 and Bax gene expression. The antioxidant activity of RES protects against cadmium chloride testicular toxicity and partially reverses its effect via upregulation of BCl2 and downregulation of p53 and Bax expression.

  13. Aluminium induced oxidative stress and DNA damage in root cells of Allium cepa L.

    PubMed

    Achary, V Mohan Murali; Jena, Suprava; Panda, Kamal K; Panda, Brahma B

    2008-06-01

    Aluminium (Al) was evaluated for induction of oxidative stress and DNA damage employing the growing roots of Allium cepa L. as the assay system. Intact roots of A. cepa were treated with different concentrations, 0, 1, 10, 50, 100, or 200 microM of aluminium chloride, at pH 4.5 for 4 h (or 2 h for comet assay) at room temperature, 25+/-1 degrees C. Following treatment the parameters investigated in root tissue were Al-uptake, cell death, extra cellular generation of reactive oxygen intermediates (ROI), viz. O(2)(*-), H(2)O(2) and (*)OH, lipid peroxidation, protein oxidation, activities of antioxidant enzymes namely catalase (CAT), superoxide dismutase (SOD), guaiacol peroxidase (GPX), ascorbate peroxidase (APX); and DNA damage, assessed by comet assay. The findings indicated that Al triggered generation of extra-cellular ROI following a dose-response. Through application of specific enzyme inhibitors it was demonstrated that extra-cellular generation of ROI was primarily due to the activity of cell wall bound NADH-PX. Generation of ROI in root tissue as well as cell death was better correlated to the levels of root Al-uptake rather than to the concentrations of Al in ambient experimental solutions. Induction of lipid peroxidation and protein oxidation by Al were statistically significant. Whereas Al inhibited CAT activity, enhanced SOD, GPX and APX activities significantly; that followed dose-response. Comet assay provided evidence that Al induced DNA damage in a range of concentrations 50-200 microM, which was comparable to that induced by ethylmethane sulfonate (EMS), an alkylating mutagen served as the positive control. The findings provided evidence that Al comparable to biotic stress induced oxidative burst at the cell surface through up- or down-regulation of some of the key enzymes of oxidative metabolism ultimately resulting in oxidative stress leading to DNA damage and cell death in root cells of A. cepa. PMID:18068230

  14. Oxidative stress induces mitochondrial fragmentation in frataxin-deficient cells

    SciTech Connect

    Lefevre, Sophie; Sliwa, Dominika; Rustin, Pierre; Camadro, Jean-Michel; Santos, Renata

    2012-02-10

    Highlights: Black-Right-Pointing-Pointer Yeast frataxin-deficiency leads to increased proportion of fragmented mitochondria. Black-Right-Pointing-Pointer Oxidative stress induces complete mitochondrial fragmentation in {Delta}yfh1 cells. Black-Right-Pointing-Pointer Oxidative stress increases mitochondrial fragmentation in patient fibroblasts. Black-Right-Pointing-Pointer Inhibition of mitochondrial fission in {Delta}yfh1 induces oxidative stress resistance. -- Abstract: Friedreich ataxia (FA) is the most common recessive neurodegenerative disease. It is caused by deficiency in mitochondrial frataxin, which participates in iron-sulfur cluster assembly. Yeast cells lacking frataxin ({Delta}yfh1 mutant) showed an increased proportion of fragmented mitochondria compared to wild-type. In addition, oxidative stress induced complete fragmentation of mitochondria in {Delta}yfh1 cells. Genetically controlled inhibition of mitochondrial fission in these cells led to increased resistance to oxidative stress. Here we present evidence that in yeast frataxin-deficiency interferes with mitochondrial dynamics, which might therefore be relevant for the pathophysiology of FA.

  15. Fluid Production Induced Stress Analysis Surrounding an Elliptic Fracture

    NASA Astrophysics Data System (ADS)

    Pandit, Harshad Rajendra

    Hydraulic fracturing is an effective technique used in well stimulation to increase petroleum well production. A combination of multi-stage hydraulic fracturing and horizontal drilling has led to the recent boom in shale gas production which has changed the energy landscape of North America. During the fracking process, highly pressurized mixture of water and proppants (sand and chemicals) is injected into to a crack, which fractures the surrounding rock structure and proppants help in keeping the fracture open. Over a longer period, however, these fractures tend to close due to the difference between the compressive stress exerted by the reservoir on the fracture and the fluid pressure inside the fracture. During production, fluid pressure inside the fracture is reduced further which can accelerate the closure of a fracture. In this thesis, we study the stress distribution around a hydraulic fracture caused by fluid production. It is shown that fluid flow can induce a very high hoop stress near the fracture tip. As the pressure gradient increases stress concentration increases. If a fracture is very thin, the flow induced stress along the fracture decreases, but the stress concentration at the fracture tip increases and become unbounded for an infinitely thin fracture. The result from the present study can be used for studying the fracture closure problem, and ultimately this in turn can lead to the development of better proppants so that prolific well production can be sustained for a long period of time.

  16. TRIB2 regulates normal and stress-induced thymocyte proliferation

    PubMed Central

    Liang, Kai Ling; O’Connor, Caitriona; Veiga, J Pedro; McCarthy, Tommie V; Keeshan, Karen

    2016-01-01

    TRIB2, a serine/threonine pseudokinase identified as an oncogene, is expressed at high levels in the T-cell compartment of hematopoiesis. The proliferation of developing thymocytes is tightly controlled to prevent leukemic transformation of T cells. Here we examine Trib2 loss in murine hematopoiesis under steady state and proliferative stress conditions, including genotoxic and oncogenic stress. Trib2−/− developing thymocytes show increased proliferation, and Trib2−/− mice have significantly higher thymic cellularity at steady state. During stress hematopoiesis, Trib2−/− developing thymocytes undergo accelerated proliferation and demonstrate hypersensitivity to 5-fluorouracil (5-FU)-induced cell death. Despite the increased cell death post 5-FU-induced proliferative stress, Trib2−/− mice exhibit accelerated thymopoietic recovery post treatment due to increased cell division kinetics of developing thymocytes. The increased proliferation in Trib2−/− thymocytes was exacerbated under oncogenic stress. In an experimental murine T-cell acute lymphoblastic leukemia (T-ALL) model, Trib2−/− mice had reduced latency in vivo, which associated with impaired MAP kinase (MAPK) activation. High and low expression levels of Trib2 correlate with immature and mature subtypes of human T-ALL, respectively, and associate with MAPK. Thus, TRIB2 emerges as a novel regulator of thymocyte cellular proliferation, important for the thymopoietic response to genotoxic and oncogenic stress, and possessing tumor suppressor function. PMID:27462446

  17. Shear stress induces osteogenic differentiation of human mesenchymal stem cells

    PubMed Central

    Yourek, Gregory; McCormick, Susan M; Mao, Jeremy J; Reilly, Gwendolen C

    2014-01-01

    Aim To determine whether fluid flow-induced shear stress affects the differentiation of bone marrow-derived human mesenchymal stem cells (hMSCs) into osteogenic cells. Materials & methods hMSCs cultured with or without osteogenic differentiation medium were exposed to fluid flow-induced shear stress and analyzed for alkaline phosphatase activity and expression of osteogenic genes. Results Immediately following shear stress, alkaline phosphatase activity in osteogenic medium was significantly increased. At days 4 and 8 of culture the mRNA expression of bone morphogenetic protein-2 and osteopontin was significantly higher in hMSCs subjected to shear stress than those cultured in static conditions. However, hMSCs cultured in osteogenic differentiation medium were less responsive in gene expression of alkaline phosphatase and bone morphogenetic protein-2. Conclusion These data demonstrate that shear stress stimulates hMSCs towards an osteoblastic phenotype in the absence of chemical induction, suggesting that certain mechanical stresses may serve as an alternative to chemical stimulation of stem cell differentiation. PMID:20868327

  18. Activation of the hypothalamic-pituitary-adrenal stress axis induces cellular oxidative stress

    PubMed Central

    Spiers, Jereme G.; Chen, Hsiao-Jou Cortina; Sernia, Conrad; Lavidis, Nickolas A.

    2015-01-01

    Glucocorticoids released from the adrenal gland in response to stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis induce activity in the cellular reduction-oxidation (redox) system. The redox system is a ubiquitous chemical mechanism allowing the transfer of electrons between donor/acceptors and target molecules during oxidative phosphorylation while simultaneously maintaining the overall cellular environment in a reduced state. The objective of this review is to present an overview of the current literature discussing the link between HPA axis-derived glucocorticoids and increased oxidative stress, particularly focussing on the redox changes observed in the hippocampus following glucocorticoid exposure. PMID:25646076

  19. Ovariectomy exacerbates oxidative stress and cardiopathy induced by adriamycin.

    PubMed

    Muñoz-Castañeda, Juan Rafael; Muntané, Jordi; Herencia, Carmen; Muñoz, Maria C; Bujalance, Inmaculada; Montilla, Pedro; Túnez, Issac

    2006-02-01

    Ovarian hormone depletion in ovariectomized experimental animals is a useful model with which to study the physiopathological consequences of menopause in women. It has been suggested that menopause is a risk factor for the induction of several cardiovascular disorders. In the present study we analyzed the effects of ovarian hormone depletion by ovariectomy (OVX) in a model of oxidative stress and cardiopathy induced by adriamycin (AD). To evaluate these effects, we measured parameters related to cardiac damage (creatinine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase) and oxidative stress (malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, reduced glutathione, nitric oxide and carbonyl proteins) in cardiac tissue and erythrocytes. OVX was found to alter all markers of oxidative stress and cell damage in cardiac tissue. Similarly, the OVX-derived loss of ovarian hormones enhanced cardiac damage and oxidative stress induced by AD. Our results suggest that antioxidant status in cardiac tissue and erythrocytes is seriously compromised by OVX during the cardiomyopathy induced by AD in experimental animals. In conclusion, the absence of hormones caused by OVX or menopause may induce or accelerate pre-existing cardiovascular dysfunctions.

  20. Neuromodulator and Emotion Biomarker for Stress Induced Mental Disorders.

    PubMed

    Gu, Simeng; Wang, Wei; Wang, Fushun; Huang, Jason H

    2016-01-01

    Affective disorders are a leading cause of disabilities worldwide, and the etiology of these many affective disorders such as depression and posttraumatic stress disorder is due to hormone changes, which includes hypothalamus-pituitary-adrenal axis in the peripheral nervous system and neuromodulators in the central nervous system. Consistent with pharmacological studies indicating that medical treatment acts by increasing the concentration of catecholamine, the locus coeruleus (LC)/norepinephrine (NE) system is regarded as a critical part of the central "stress circuitry," whose major function is to induce "fight or flight" behavior and fear and anger emotion. Despite the intensive studies, there is still controversy about NE with fear and anger. For example, the rats with LC ablation were more reluctant to leave a familiar place and took longer to consume the food pellets in an unfamiliar place (neophobia, i.e., fear in response to novelty). The reason for this discrepancy might be that NE is not only for flight (fear), but also for fight (anger). Here, we try to review recent literatures about NE with stress induced emotions and their relations with mental disorders. We propose that stress induced NE release can induce both fear and anger. "Adrenaline rush or norepinephrine rush" and fear and anger emotion might act as biomarkers for mental disorders.

  1. Neuromodulator and Emotion Biomarker for Stress Induced Mental Disorders.

    PubMed

    Gu, Simeng; Wang, Wei; Wang, Fushun; Huang, Jason H

    2016-01-01

    Affective disorders are a leading cause of disabilities worldwide, and the etiology of these many affective disorders such as depression and posttraumatic stress disorder is due to hormone changes, which includes hypothalamus-pituitary-adrenal axis in the peripheral nervous system and neuromodulators in the central nervous system. Consistent with pharmacological studies indicating that medical treatment acts by increasing the concentration of catecholamine, the locus coeruleus (LC)/norepinephrine (NE) system is regarded as a critical part of the central "stress circuitry," whose major function is to induce "fight or flight" behavior and fear and anger emotion. Despite the intensive studies, there is still controversy about NE with fear and anger. For example, the rats with LC ablation were more reluctant to leave a familiar place and took longer to consume the food pellets in an unfamiliar place (neophobia, i.e., fear in response to novelty). The reason for this discrepancy might be that NE is not only for flight (fear), but also for fight (anger). Here, we try to review recent literatures about NE with stress induced emotions and their relations with mental disorders. We propose that stress induced NE release can induce both fear and anger. "Adrenaline rush or norepinephrine rush" and fear and anger emotion might act as biomarkers for mental disorders. PMID:27051536

  2. Neuromodulator and Emotion Biomarker for Stress Induced Mental Disorders

    PubMed Central

    Gu, Simeng; Wang, Wei; Huang, Jason H.

    2016-01-01

    Affective disorders are a leading cause of disabilities worldwide, and the etiology of these many affective disorders such as depression and posttraumatic stress disorder is due to hormone changes, which includes hypothalamus-pituitary-adrenal axis in the peripheral nervous system and neuromodulators in the central nervous system. Consistent with pharmacological studies indicating that medical treatment acts by increasing the concentration of catecholamine, the locus coeruleus (LC)/norepinephrine (NE) system is regarded as a critical part of the central “stress circuitry,” whose major function is to induce “fight or flight” behavior and fear and anger emotion. Despite the intensive studies, there is still controversy about NE with fear and anger. For example, the rats with LC ablation were more reluctant to leave a familiar place and took longer to consume the food pellets in an unfamiliar place (neophobia, i.e., fear in response to novelty). The reason for this discrepancy might be that NE is not only for flight (fear), but also for fight (anger). Here, we try to review recent literatures about NE with stress induced emotions and their relations with mental disorders. We propose that stress induced NE release can induce both fear and anger. “Adrenaline rush or norepinephrine rush” and fear and anger emotion might act as biomarkers for mental disorders. PMID:27051536

  3. Tributyltin chloride increases phenylephrine-induced contraction and vascular stiffness in mesenteric resistance arteries from female rats.

    PubMed

    Ribeiro Júnior, Rogério Faustino; Marques, Vinicius Bermond; Nunes, Dieli Oliveira; Ronconi, Karoline de Sousa; de Araújo, Julia F P; Rodrigues, Paula Lopes; Padilha, Alessandra Simão; Vassallo, Dalton Valentim; Graceli, Jones B; Stefanon, Ivanita

    2016-03-15

    Tributyltin chloride (TBT) is an organotin compound that reduces estrogen levels in female rats. We aimed to investigate the effects of TBT exposure on vascular tonus and vascular remodelling in the resistance arteries of female rats. Rats were treated daily with TBT (500 ng/kg) for 15 days. TBT did not change arterial blood pressure but did modify some morpho-physiological parameters of third-order mesenteric resistance arteries in the following ways: (1) decreased lumen and external diameters; (2) increased wall/lm ratio and wall thickness; (3) decreased distensibility and increased stiffness; (4) increased collagen deposition; and (5) increased pulse wave velocity. TBT exposure increased the phenylephrine-induced contractile response in mesenteric resistance arteries. However, vasodilatation responses induced by acetylcholine and sodium nitroprusside were not modified by TBT. It is suggested that TBT exposure reduces vascular nitric oxide (NO) production, because:(1) L-NAME incubation did not cause a leftward shift in the concentration-response curve for phenylephrine; (2) both eNOS protein expression; (3) in situ NO production were reduced. Incubation with L-NAME; and (4) SOD shifted the phenylephrine response curve to the left in TBT rats. Tiron, catalase, ML-171 and VAS2870 decreased vascular reactivity to phenylephrine only in TBT rats. Moreover, increased superoxide anion production was observed in the mesenteric resistance arteries of TBT rats accompanied by an increase in gp91phox, catalase, AT1 receptor and total ERK1/2 protein expression. In conclusion, these findings show that TBT induced alterations are most likely due to a reduction of NO production combined with increased O2(-) production derived from NADPH oxidase and ERK1/2 activation. These findings offer further evidence that TBT is an environmental risk factor for cardiovascular disease.

  4. Dietary flavonoid fisetin regulates aluminium chloride-induced neuronal apoptosis in cortex and hippocampus of mice brain.

    PubMed

    Prakash, Dharmalingam; Sudhandiran, Ganapasam

    2015-12-01

    Dietary flavonoids have been suggested to promote brain health by protecting brain parenchymal cells. Recently, understanding the possible mechanism underlying neuroprotective efficacy of flavonoids is of great interest. Given that fisetin exerts neuroprotection, we have examined the mechanisms underlying fisetin in regulating Aβ aggregation and neuronal apoptosis induced by aluminium chloride (AlCl3) administration in vivo. Male Swiss albino mice were induced orally with AlCl3 (200 mg/kg. b.wt./day/8 weeks). Fisetin (15 mg/Kg. b.wt. orally) was administered for 4 weeks before AlCl3-induction and administered simultaneously for 8 weeks during AlCl3-induction. We found aggregation of Amyloid beta (Aβ 40-42), elevated expressions of Apoptosis stimulating kinase (ASK-1), p-JNK (c-Jun N-terminal Kinase), p53, cytochrome c, caspases-9 and 3, with altered Bax/Bcl-2 ratio in favour of apoptosis in cortex and hippocampus of AlCl3-administered mice. Furthermore, TUNEL and fluoro-jade C staining demonstrate neurodegeneration in cortex and hippocampus. Notably, treatment with fisetin significantly (P<0.05) reduced Aβ aggregation, ASK-1, p-JNK, p53, cytochrome c, caspase-9 and 3 protein expressions and modulated Bax/Bcl-2 ratio. TUNEL-positive and fluoro-jade C stained cells were also significantly reduced upon fisetin treatment. We have identified the involvement of fisetin in regulating ASK-1 and p-JNK as possible mediator of Aβ aggregation and subsequent neuronal apoptosis during AlCl3-induced neurodegeneration. These findings define the possibility that fisetin may slow or prevent neurodegneration and can be utilised as neuroprotective agent against Alzheimer's and Parkinson's disease.

  5. Does aspirin-induced oxidative stress cause asthma exacerbation?

    PubMed

    Kacprzak, Dorota; Pawliczak, Rafał

    2015-06-19

    Aspirin-induced asthma (AIA) is a distinct clinical syndrome characterized by severe asthma exacerbations after ingestion of aspirin or other non-steroidal anti-inflammatory drugs. The exact pathomechanism of AIA remains unknown, though ongoing research has shed some light. Recently, more and more attention has been focused on the role of aspirin in the induction of oxidative stress, especially in cancer cell systems. However, it has not excluded the similar action of aspirin in other inflammatory disorders such as asthma. Moreover, increased levels of 8-isoprostanes, reliable biomarkers of oxidative stress in expired breath condensate in steroid-naïve patients with AIA compared to AIA patients treated with steroids and healthy volunteers, has been observed. This review is an attempt to cover aspirin-induced oxidative stress action in AIA and to suggest a possible related pathomechanism.

  6. Wrinkling of Thin Films Induced by Viscous Stress

    NASA Astrophysics Data System (ADS)

    Chatterjee, Sourav; McDonald, Christina; Niu, Jiani; Huang, Rui; Velankar, Sachin

    2013-11-01

    Compression of thin films attached to compliant solid substrates can induce a variety of highly ordered and complex wrinkling patterns. We study an analogous problem of the wrinkling instability of a thin film floating on a viscous fluid. Uniaxial compression of the fluid induces a viscous stress which leads to the wrinkling of the film. We experimentally determine the effect of geometry and material properties on the wrinkle wavelength. A shear lag approach is used to determine the stress distribution prior to buckling. A linear stability analysis of the film under this stress distribution is used to determine the maximally growing wavelength in the system. Both experiments as well as stability analysis show that the wavelength depends significantly on film length and the ratio of the film and fluid layer thickness. Most importantly, unlike previous research on fluid-supported films, the wrinkle wavelength is rate-dependent, and reduces with increasing compression rate.

  7. FEM simulation of residual stresses induced by laser Peening

    NASA Astrophysics Data System (ADS)

    Peyre, P.; Sollier, A.; Chaieb, I.; Berthe, L.; Bartnicki, E.; Braham, C.; Fabbro, R.

    2003-08-01

    Benefits from laser Peening have been demonstrated several times in fields like fatigue, wear or stress corrosion cracking. However, in spite of recent work on the calculation of residual stresses, very few authors have considered a finite element method (FEM) approach to predict laser-induced mechanical effect. This comes mainly from the high strain rates involved during LP (10^6 s^{-1}), that necessitate the precise determination of dynamic properties, and also from the possible combination of thermal and mechanical loadings in the case of LP without protective coatings. In this paper, we aim at presenting a global approach of the problem, starting from the determination of loading conditions and dynamic yield strengths, to finish with FEM calculation of residual stress fields induced on a 12% Cr martensitic stainless steel and a 7075 aluminium alloy.

  8. Mono-2-Ethylhexyl Phthalate Induces Oxidative Stress Responses in Human Placental Cells In Vitro

    PubMed Central

    Tetz, Lauren M; Cheng, Adrienne A.; Korte, Cassandra S.; Giese, Roger W.; Wang, Poguang; Harris, Craig; Meeker, John D; Loch-Caruso, Rita

    2013-01-01

    Di-2-ethylhexyl phthalate (DEHP) is an environmental contaminant commonly used as a plasticizer in polyvinyl chloride products. Exposure to DEHP has been linked to adverse pregnancy outcomes in humans including preterm birth, low birth-weight, and pregnancy loss. Although oxidative stress is linked to the pathology of adverse pregnancy outcomes, effects of DEHP metabolites, including the active metabolite, mono-2-ethylhexyl phthalate (MEHP), on oxidative stress responses in placental cells have not been previously evaluated. The objective of the current study is to identify MEHP-stimulated oxidative stress responses in human placental cells. We treated a human placental cell line, HTR-8/SVneo, with MEHP and then measured reactive oxygen species (ROS) generation using the dichlorofluorescein assay, oxidized thymine with mass-spectrometry, redox-sensitive gene expression with qRT-PCR, and apoptosis using a luminescence assay for caspase 3/7 activity. Treatment of HTR-8 cells with 180 μM MEHP increased ROS generation, oxidative DNA damage, and caspase 3/7 activity, and resulted in differential expression of redox-sensitive genes. Notably, 90 and 180 μM MEHP significantly induced mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS2), an enzyme important for synthesis of prostaglandins implicated in initiation of labor. The results from the present study are the first to demonstrate that MEHP stimulates oxidative stress responses in placental cells. Furthermore, the MEHP concentrations used were within an order of magnitude of the highest concentrations measured previously in human umbilical cord or maternal serum. The findings from the current study warrant future mechanistic studies of oxidative stress, apoptosis, and prostaglandins as molecular mediators of DEHP/MEHP-associated adverse pregnancy outcomes. PMID:23360888

  9. Stereocontrolled synthesis of rosuvastatin calcium via iodine chloride-induced intramolecular cyclization.

    PubMed

    Xiong, Fangjun; Wang, Haifeng; Yan, Lingjie; Han, Sheng; Tao, Yuan; Wu, Yan; Chen, Fener

    2016-01-28

    A novel, stereoselective approach towards rosuvastatin calcium from the known (S)-homoallylic alcohol has been developed. The synthesis is highlighted by a regio- and stereocontrolled ICl-induced intramolecular cyclization of chiral homoallylic carbonate to deliver the C6-formyl statin side chain with a syn-1,3-diol moiety. An improved synthesis of the rosuvastatin pyrimidine core moiety is also included. Moreover, this methodology is useful in the asymmetric synthesis of structural variants of statins such as pitavastatin calcium and atorvastatin calcium and their related analogs.

  10. Chloride Cotransporters as a Molecular Mechanism underlying Spreading Depolarization-Induced Dendritic Beading

    PubMed Central

    Steffensen, Annette B.; Sword, Jeremy; Croom, Deborah

    2015-01-01

    Spreading depolarizations (SDs) are waves of sustained neuronal and glial depolarization that propagate massive disruptions of ion gradients through the brain. SD is associated with migraine aura and recently recognized as a novel mechanism of injury in stroke and brain trauma patients. SD leads to neuronal swelling as assessed in real time with two-photon laser scanning microscopy (2PLSM). Pyramidal neurons do not express aquaporins and thus display low inherent water permeability, yet SD rapidly induces focal swelling (beading) along the dendritic shaft by unidentified molecular mechanisms. To address this issue, we induced SD in murine hippocampal slices by focal KCl microinjection and visualized the ensuing beading of dendrites expressing EGFP by 2PLSM. We confirmed that dendritic beading failed to arise during large (100 mOsm) hyposmotic challenges, underscoring that neuronal swelling does not occur as a simple osmotic event. SD-induced dendritic beading was not prevented by pharmacological interference with the cytoskeleton, supporting the notion that dendritic beading may result entirely from excessive water influx. Dendritic beading was strictly dependent on the presence of Cl−, and, accordingly, combined blockade of Cl−-coupled transporters led to a significant reduction in dendritic beading without interfering with SD. Furthermore, our in vivo data showed a strong inhibition of dendritic beading during pharmacological blockage of these cotransporters. We propose that SD-induced dendritic beading takes place as a consequence of the altered driving forces and thus activity for these cotransporters, which by transport of water during their translocation mechanism may generate dendritic beading independently of osmotic forces. SIGNIFICANCE STATEMENT Spreading depolarization occurs during pathological conditions such as stroke, brain injury, and migraine and is characterized as a wave of massive ion translocation between intracellular and extracellular

  11. Anoctamin 1 induces calcium-activated chloride secretion and proliferation of renal cyst-forming epithelial cells.

    PubMed

    Buchholz, Bjoern; Faria, Diana; Schley, Gunnar; Schreiber, Rainer; Eckardt, Kai-Uwe; Kunzelmann, Karl

    2014-05-01

    Polycystic kidney diseases are characterized by multiple bilateral renal cysts that gradually enlarge and lead to a decline in renal function. Cyst enlargement is driven by transepithelial chloride secretion, stimulated by enhanced levels of cyclic adenosine monophosphate, which activates apical cystic fibrosis transmembrane conductance regulator chloride channels. However, chloride secretion by calcium-dependent chloride channels, activated through stimulation of purinergic receptors, also has a major impact. To identify the molecular basis of calcium-dependent chloride secretion in cyst expansion, we determined the role of anoctamin 1 and 6, two recently discovered calcium-activated chloride channels both of which are expressed in epithelial cells. We found that anoctamin 1, which plays a role in epithelial fluid secretion and proliferation, is strongly expressed in principal-like MDCK cells (PLCs) forming cysts within a collagen matrix, in an embryonic kidney cyst model, and in human autosomal dominant polycystic kidney disease tissue. Knockdown of anoctamin 1 but not anoctamin 6 strongly diminished the calcium-dependent chloride secretion of PLCs. Moreover, two inhibitors of anoctamin ion channels, tannic acid and a more selective inhibitor of anoctamin 1, significantly inhibited PLC cyst growth and cyst enlargement in an embryonic kidney cyst model. Knockdown of ANO1 by morpholino analogs also attenuated embryonic cyst growth. Thus, calcium-activated chloride secretion by anoctamin 1 appears to be a crucial component of renal cyst growth.

  12. Hypoxic-induced stress protein expression in rat cardiac myocytes

    SciTech Connect

    Howard, G.; Geoghegan, T.E.

    1986-05-01

    Mammalian stress proteins can be induced in cells and tissues exposed to a variety of conditions including hyperthermia and diminished O/sub 2/ supply. The authors have previously shown that the expression of three stress proteins (71, 85, and 95 kDa) was induced in cardiac tissue from mice exposed to hypoxic conditions. The expression of mRNAs coding for the 85 and 95 kDa proteins increase with time of exposure to hypoxia, while the mRNA coding for the 71 kDa protein is transiently induced. The authors extended these studies to investigate the expression of stress proteins in isolated rat cardiac myocytes. Freshly prepared myocytes were exposed to control, hypoxic, anoxic, or heat-shock environments for up to 16 h. The proteins were then labeled for 6 hours with (/sup 35/S)methionine. Analysis of the solubilized proteins by SDS-PAGE and autoradiography showed that there was a 6-fold increase in synthesis of the 85 kDa protein upon exposure to hypoxia but not heat-shock conditions. The 71 kDa protein was present at high levels in both control and treated myocyte protein preparations, and presumably had been induced during the isolation procedure. Total RNA isolated from intact rat heart and isolated myocytes was compared by cell-free translation analysis and showed induction of RNAs coding for several stress proteins in the myocyte preparation. The induced proteins at 85 and 95 kDa have molecular weights similar to reported cell stress and/or glucose-regulated proteins.

  13. Microsecond molecular dynamics simulation of guanidinium chloride induced unfolding of ubiquitin.

    PubMed

    Mandal, Manoj; Mukhopadhyay, Chaitali

    2014-10-21

    An all atom molecular dynamics simulation was used to explore the atomic detail mechanism of guanidinium induced unfolding of the protein ubiquitin. Ubiquitin unfolds through pre-unfolded (intermediate) states, i.e. guanidinium induced unfolding of ubiquitin appears to be a multi-step process, and loss of hydrophobic contacts of C-terminal residues is crucial for ubiquitin unfolding. Free-energy landscapes show that barrier separation between folded and unfolded basins is ∼5.0 kcal mol(-1), and both the basins are of comparable energy. It was observed that guanidinium ions interact directly with ubiquitin. Favorable electrostatic interaction is the main driving force for such accumulation of guanidinium ions near protein, but van der Waals energy also contributes. RDF plots show that accumulation of guanidinium ions near specific residues is the main cause for destabilization of intra-residue interactions crucial to maintain the three-dimensional fold of the protein. One salt-bridge interaction between Lys11 and Glu34 appears to be important to maintain the crystal structure of ubiquitin and this salt-bridge can map the unfolding process of ubiquitin. PMID:25197836

  14. Aluminum chloride induces neuroinflammation, loss of neuronal dendritic spine and cognition impairment in developing rat.

    PubMed

    Cao, Zheng; Yang, Xu; Zhang, Haiyang; Wang, Haoran; Huang, Wanyue; Xu, Feibo; Zhuang, Cuicui; Wang, Xiaoguang; Li, Yanfei

    2016-05-01

    Aluminum (Al) is present in the daily life of humans, and the incidence of Al contamination increased in recent years. Long-term excessive Al intake induces neuroinflammation and cognition impairment. Neuroinflammation alter density of dendritic spine, which, in turn, influence cognition function. However, it is unknown whether increased neuroinflammation is associated with altered density of dendritic spine in Al-treated rats. In the present study, AlCl3 was orally administrated to rat at 50, 150 and 450 mg/kg for 90d. We examined the effects of AlCl3 on the cognition function, density of dendritic spine in hippocampus of CA1 and DG region and the mRNA levels of IL-1β, IL-6, TNF-α, MHC II, CX3CL1 and BNDF in developing rat. These results showed exposure to AlCl3 lead to increased mRNA levels of IL-1β, IL-6, TNF-α and MCH II, decreased mRNA levels of CX3CL1 and BDNF, decreased density of dendritic spine and impaired learning and memory in developing rat. Our results suggest AlCl3 can induce neuroinflammation that may result in loss of spine, and thereby leads to learning and memory deficits. PMID:26946116

  15. The role of <100> edge dislocations in nucleating radiation-induced colloid particles in sodium chloride

    SciTech Connect

    Teutonico, L.J.

    1982-09-01

    A theoretical program to investigate the role of dislocations in the nucleation of sodium colloids in irradiated rock salt has been outlined. As the first study in the investigation the interaction of radiation-produced defects with the <001> edge dislocation in rock salt, i.e., the edge dislocation in the principal slip system of NaCl, has been considered. The interaction potential between a symmetric defect and the <001> edge dislocation has been determined on the basis of anisotropic elasticity theory. The potential arises from the interaction between the long-range stress field of the dislocation and the displacements around the point defect. The corresponding flow lines, i.e., the lines along which the defects flow to the dislocation, have also been determined. In general, the flow lines are closed loops passing through the center of the dislocation. One of the novel features introduced by anisotropy is the possibility of open flow lines for certain elastic constant values. Along some of these open flow lines defects are attracted to the dislocation, whereas long others defects are repelled from the dislocation of common plane. 33 refs., 17 figs.

  16. [Exercise-induced shear stress: Physiological basis and clinical impact].

    PubMed

    Rodríguez-Núñez, Iván; Romero, Fernando; Saavedra, María Javiera

    2016-01-01

    The physiological regulation of vascular function is essential for cardiovascular health and depends on adequate control of molecular mechanisms triggered by endothelial cells in response to mechanical and chemical stimuli induced by blood flow. Endothelial dysfunction is one of the major risk factors for cardiovascular disease, where an imbalance between synthesis of vasodilator and vasoconstrictor molecules is one of its main mechanisms. In this context, the shear stress is one of the most important mechanical stimuli to improve vascular function, due to endothelial mechanotransduction, triggered by stimulation of various endothelial mechanosensors, induce signaling pathways culminating in increased bioavailability of vasodilators molecules such as nitric oxide, that finally trigger the angiogenic mechanisms. These mechanisms allow providing the physiological basis for the effects of exercise on vascular health. In this review it is discussed the molecular mechanisms involved in the vascular response induced by shear stress and its impact in reversing vascular injury associated with the most prevalent cardiovascular disease in our population. PMID:27118039

  17. Role of Oxidative Stress in Transformation Induced by Metal Mixture

    PubMed Central

    Martín, Silva-Aguilar; Emilio, Rojas; Mahara, Valverde

    2011-01-01

    Metals are ubiquitous pollutants present as mixtures. In particular, mixture of arsenic-cadmium-lead is among the leading toxic agents detected in the environment. These metals have carcinogenic and cell-transforming potential. In this study, we used a two step cell transformation model, to determine the role of oxidative stress in transformation induced by a mixture of arsenic-cadmium-lead. Oxidative damage and antioxidant response were determined. Metal mixture treatment induces the increase of damage markers and the antioxidant response. Loss of cell viability and increased transforming potential were observed during the promotion phase. This finding correlated significantly with generation of reactive oxygen species. Cotreatment with N-acetyl-cysteine induces effect on the transforming capacity; while a diminution was found in initiation, in promotion phase a total block of the transforming capacity was observed. Our results suggest that oxidative stress generated by metal mixture plays an important role only in promotion phase promoting transforming capacity. PMID:22191014

  18. [Exercise-induced shear stress: Physiological basis and clinical impact].

    PubMed

    Rodríguez-Núñez, Iván; Romero, Fernando; Saavedra, María Javiera

    2016-01-01

    The physiological regulation of vascular function is essential for cardiovascular health and depends on adequate control of molecular mechanisms triggered by endothelial cells in response to mechanical and chemical stimuli induced by blood flow. Endothelial dysfunction is one of the major risk factors for cardiovascular disease, where an imbalance between synthesis of vasodilator and vasoconstrictor molecules is one of its main mechanisms. In this context, the shear stress is one of the most important mechanical stimuli to improve vascular function, due to endothelial mechanotransduction, triggered by stimulation of various endothelial mechanosensors, induce signaling pathways culminating in increased bioavailability of vasodilators molecules such as nitric oxide, that finally trigger the angiogenic mechanisms. These mechanisms allow providing the physiological basis for the effects of exercise on vascular health. In this review it is discussed the molecular mechanisms involved in the vascular response induced by shear stress and its impact in reversing vascular injury associated with the most prevalent cardiovascular disease in our population.

  19. Vinyl chloride monomer (VCM) induces high occurrence of neural tube defects in embryonic mouse brain during neurulation.

    PubMed

    Quan, Hongyu; Ma, Teng; Zhao, Xianxian; Zhao, Baixiong; Liu, Yunlai; Li, Hongli

    2014-05-01

    The aim of this study was to explore the direct embryonic teratogenicity of vinyl chloride monomer (VCM), especially the toxic effects on the early development of the nervous system and its underlying mechanisms. Pregnant mice at embryonic day 6.5 (E6.5) were injected with different doses of VCM (200, 400 and 600 mg/kg) and embryos were harvested at E10.5. Our results showed that doses higher than 400 mg/kg of VCM increased the incidence of malformed embryos, especially the neural tube defects (NTDs). In addition, high-dose of VCM decreased mitotic figure counts in the neuroepithelium and enhanced the percentage of cells in G0/G1 phase, while they were reduced in S phase. The more VCM was injected into mice, the fewer positive PCNA cells were seen and the more positive TUNEL cells were observed in the neuroepithelium. Moreover, significant increases in the levels of caspase-3 protein were observed in NTD embryos. Our results demonstrate that during early pregnancy, exposure to doses higher than 400 mg/kg of VCM increases the incidence of malformations and particularly the rate of NTDs. High-dose of VCM inhibits the proliferation of neural cells and induces cell apoptosis, leading to an imbalance in the ratio of proliferation and apoptosis. Meanwhile, the apoptosis of neuroepithelial cells might be accelerated by the activation of the caspase-3 pathway, and it might be a reason for NTDs.

  20. Protective effect of magnesium chloride on sodium fluoride induced alterations in various hydroxyproline fractions in rat lungs.

    PubMed

    Siddiqi, N J

    2011-02-12

    Frequent absorption of the fluoride causes tooth decay, damage of kidneys, bones, nerves and muscles. The present study was carried out to study the reported protective effect of magnesium chloride on sodium fluoride (NaF) induced alterations in rat lung hydroxyproline/ collagen content. To study the dose response of NaF following groups were studied: (i) normal rats (ii) placebo group, (iii) rats treated with two different doses of NaF. To study the protective effect of MgCl2 the following groups of rats were studied (i) normal rats (ii) rats injected with MgCl2 (iii) rats injected with NaF (iv) rats injected with MgCl2 followed by NaF. Sodium fluoride doses of 10 and 20 mg/kg body weight of rats caused a significant increase (p < 0. 001) increase in peptide- bound and total Hyp content in rat lungs. Administration of MgCl2 alone to rats also caused significant increase in peptide- bound, protein- bound and total Hyp fractions in rat lungs (p < 0. 001). Administration of MgCl2 thirty minutes before NaF restored the altered protein bound Hyp fraction to almost normal levels. The present study concludes that although MgCl2 has been reported to be protective against toxic effects of NaF, it exerts an independent effect on hydroxyproline and collagen content in rat lungs.

  1. Stress-induced analgesia and endogenous opioid peptides: the importance of stress duration.

    PubMed

    Parikh, Drupad; Hamid, Abdul; Friedman, Theodore C; Nguyen, Khanh; Tseng, Andy; Marquez, Paul; Lutfy, Kabirullah

    2011-01-15

    Stress is known to elicit pain relief, a phenomenon referred to as stress-induced analgesia. Based on stress parameters, opioid and non-opioid intrinsic pain inhibitory systems can be activated. In the present study, we assessed whether changing the duration of stress would affect the involvement of endogenous opioids in antinociception elicited by swim in warm water (32 °C), known to be opioid-mediated. Using mice lacking beta-endorphin, enkephalins or dynorphins and their respective wild-type littermates, we assessed the role of each opioid peptide in antinociception induced by a short (3 min) vs. long (15 min) swim. Mice were tested for baseline hot plate latency, exposed to swim (3 or 15 min) in warm water (32 °C) and then tested for antinociception at 5, 15 and 30 min. Our results revealed that both swim paradigms induced significant antinociception in wild-type mice. However, the short swim failed to induce antinociception in beta-endorphin-deficient mice, illustrating that beta-endorphin is important in this form of stress-induced antinociception. On the other hand, antinociception elicited by the long swim was only slightly reduced in beta-endorphin-deficient mice despite pretreatment with naloxone, a non-selective opioid receptor antagonist, significantly attenuated the antinociception elicited by the long swim. Nevertheless, a delayed hyperalgesic response developed in mice lacking beta-endorphin following exposure to either swim paradigm. On the other hand, mice lacking enkephalins or dynorphins and their respective wild-type littermates expressed a comparable antinociceptive response and did not exhibit the delayed hyperalgesic response. Together, our results suggest that the endogenous opioid peptide beta-endorphin not only mediates antinociception induced by the short swim but also prevents the delayed hyperalgesic response elicited by either swim paradigm. PMID:21044625

  2. Stress-induced analgesia and endogenous opioid peptides: the importance of stress duration

    PubMed Central

    Parikh, Drupad; Hamid, Abdul; Friedman, Theodore C.; Nguyen, Khanh; Tseng, Andy; Marquez, Paul; Lutfy, Kabirullah

    2010-01-01

    Stress is known to elicit pain relief, a phenomenon referred to as stress-induced analgesia. Based on stress parameters, opioid and non-opioid intrinsic pain inhibitory systems can be activated. In the present study, we assessed whether changing the duration of stress would affect the involvement of endogenous opioids in antinociception elicited by swim in warm water (32°C), known to be opioid-mediated. Using mice lacking beta-endorphin, enkephalins or dynorphins and their respective wild-type littermates, we assessed the role of each opioid peptide in antinociception induced by a short (3 min) vs. long (15 min) swim. Mice were tested for baseline hot plate latency, exposed to swim (3 or 15 min) in warm water (32°C) and then tested for antinociception at 5, 15 and 30 min. Our results revealed that both swim paradigms induced significant antinociception in wild-type mice. However, the short swim failed to induce antinociception in beta-endorphin-deficient mice, illustrating that beta-endorphin is important in this form of stress-induced antinociception. On the other hand, antinociception elicited by the long swim was only slightly reduced in beta-endorphin-deficient mice despite pretreatment with naloxone, a non-selective opioid receptor antagonist, significantly attenuated the antinociception elicited by the long swim. Nevertheless, a delayed hyperalgesic response developed in mice lacking beta-endorphin following exposure to either swim paradigm. On the other hand, mice lacking enkephalins or dynorphins and their respective wild-type littermates expressed a comparable antinociceptive response and did not exhibit the delayed hyperalgesic response. Together, our results suggest that the endogenous opioid peptide beta-endorphin not only mediates antinociception induced by the short swim but also prevents the delayed hyperalgesic response elicited by either swim paradigm. PMID:21044625

  3. Hydrochlorothiazide attenuates lithium-induced nephrogenic diabetes insipidus independently of the sodium-chloride cotransporter.

    PubMed

    Sinke, Anne P; Kortenoeven, Marleen L A; de Groot, Theun; Baumgarten, Ruben; Devuyst, Olivier; Wetzels, Jack F M; Loffing, Johannes; Deen, Peter M T

    2014-03-01

    Lithium is the most common cause of nephrogenic diabetes insipidus (Li-NDI). Hydrochlorothiazide (HCTZ) combined with amiloride is the mainstay treatment in Li-NDI. The paradoxical antidiuretic action of HCTZ in Li-NDI is generally attributed to increased sodium and water uptake in proximal tubules as a compensation for increased volume loss due to HCTZ inhibition of the Na-Cl cotransporter (NCC), but alternative actions for HCTZ have been suggested. Here, we investigated whether HCTZ exerted an NCC-independent effect in Li-NDI. In polarized mouse cortical collecting duct (mpkCCD) cells, HCTZ treatment attenuated the Li-induced downregulation of aquaporin-2 (AQP2) water channel abundance. In these cells, amiloride reduces cellular Li influx through the epithelial sodium channel (ENaC). HCTZ also reduced Li influx, but to a lower extent. HCTZ increased AQP2 abundance on top of that of amiloride and did not affect the ENaC-mediated transcellular voltage. MpkCCD cells did not express NCC mRNA or protein. These data indicated that in mpkCCD cells, HCTZ attenuated lithium-induced downregulation of AQP2 independently of NCC and ENaC. Treatment of Li-NDI NCC knockout mice with HCTZ revealed a significantly reduced urine volume, unchanged urine osmolality, and increased cortical AQP2 abundance compared with Li-treated NCC knockout mice. HCTZ treatment further resulted in reduced blood Li levels, creatinine clearance, and alkalinized urinary pH. Our in vitro and in vivo data indicate that part of the antidiuretic effect of HCTZ in Li-NDI is NCC independent and may involve a tubuloglomerular feedback response-mediated reduction in glomerular filtration rate due to proximal tubular carbonic anhydrase inhibition.

  4. Capsaicin induces apoptosis in PC12 cells through ER stress.

    PubMed

    Krizanova, Olga; Steliarova, Iveta; Csaderova, Lucia; Pastorek, Michal; Hudecova, Sona

    2014-02-01

    Capsaicin, the pungent agent in chili peppers, has been shown to act as a tumor-suppressor in cancer. In our previous study, capsaicin was shown to induce apoptosis in the rat pheochromocytoma cell line (PC12 cells). Thus, the aim of the present study was to determine the potential mechanism by which capsaicin induces apoptosis. We treated PC12 cells with 50, 100 and 500 µM capsaicin and measured the reticular calcium content and expression of the reticular calcium transport systems. These results were correlated with endoplasmic reticulum (ER) stress markers CHOP, ATF4 and X-box binding protein 1 (XBP1), as well as with apoptosis induction. We observed that capsaicin decreased reticular calcium in a concentration-dependent manner. Simultaneously, expression levels of the sarco/endoplasmic reticulum pump and ryanodin receptor of type 2 were modified. These changes were accompanied by increased ER stress, as documented by increased stress markers. Thus, from these results we propose that in PC12 cells capsaicin induces apoptosis through increased ER stress. PMID:24337105

  5. Naltrexone attenuates endoplasmic reticulum stress induced hepatic injury in mice.

    PubMed

    Moslehi, A; Nabavizadeh, F; Nabavizadeh, Fatemeh; Dehpour, A R; Dehpou, A R; Tavanga, S M; Hassanzadeh, G; Zekri, A; Nahrevanian, H; Sohanaki, H

    2014-09-01

    Endoplasmic reticulum (ER) stress provides abnormalities in insulin action, inflammatory responses, lipoprotein B100 degradation and hepatic lipogenesis. Excess accumulation of triglyceride in hepatocytes may also lead to disorders such as non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Opioid peptides are involved in triglyceride and cholesterol dysregulation, inflammation and cell death. In this study, we evaluated Naltrexone effects on ER stress induced liver injury. To do so, C57/BL6 mice received saline, DMSO and Naltrexone, as control groups. ER stress was induced by tunicamycin (TM) injection. Naltrexone was given before TM administration. Liver blood flow and biochemical serum analysis were measured. Histopathological evaluations, TNF-α measurement and Real-time RT-PCR were also performed. TM challenge provokes steatosis, cellular ballooning and lobular inflammation which significantly reduced in Naltrexone treated animals. ALT, AST and TNF-α increased in the TM group and improved in the Naltrexone plus TM group. Triglyceride and cholesterol levels decreased in TM treated mice with no increase in Naltrexone treated animals. In the Naltrexone plus TM group, gene expression of Bax/Bcl-2 ratio and caspase3 significantly lowered compared with the TM group. In this study, we found that Naltrexone had a notable alleviating role in ER stress induced steatosis and liver injury.

  6. Stress induced reversible crystal transition in poly(butylene succinate)

    NASA Astrophysics Data System (ADS)

    Liu, Guoming; Zheng, Liuchun; Zhang, Xiuqin; Li, Chuncheng; Wang, Dujin

    2015-03-01

    The plastic deformation mechanism of semi-crystalline polymers is a long-studied topic, which is crucial for establishing structure/property relationships. For polymers with stress induced crystal transition, some open questions still need to be answered, such as on which stage of plastic deformation does the crystal transition take place, and more importantly, what happens on the lamellar structure during crystal transition. In this talk, stress-induced reversible crystal transition in poly(butylene succinate) was systematically investigated by in-situ WAXS and SAXS. A ``lamellar thickening'' phenomenon was observed during stretching, which was shown to mainly originated from the reversible crystal transition. This mechanism was shown to be valid in poly(ethylene succinate). The critical stress for the transition was measured in a series of PBS-based crystalline-amorphous multi-block copolymers. Interestingly, these PBS copolymers exhibited identical critical stress independent of amorphous blocks. The universal critical stress for crystal transition was interpreted through a single-microfibril-stretching mechanism. The work is financially supported by the National Natural Science Foundation of China (Grant No. 51203170).

  7. Spatially discriminating Russian wheat aphid induced plant stress from other wheat stressing factors

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The Russian wheat aphid (RWA) Diuraphis noxia (Mordvilko) is a major pest of winter wheat and barley in the United States. RWA induces stress to the wheat crop by damaging plant foliage, lowering the greenness of plants, and affecting productivity. Multispectral remote sensing is effective at dete...

  8. Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler's Bursa of Fabricius.

    PubMed

    Yin, Shuang; Guo, Hongrui; Cui, Hengmin; Peng, Xi; Fang, Jing; Zuo, Zhicai; Deng, Junliang; Wang, Xun; Tang, Kun; Li, Jian

    2016-05-01

    The purpose of this study was to investigate the histopathological lesions, oxidative damage, changes of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) contents in the bursa of Fabricius and serum immunoglobulins (IgG, IgM, IgA) induced by dietary nickel chloride (NiCl2). Two hundred and eighty-one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Lesions were observed in the NiCl2-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae. Concurrently, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxyl radical and glutathione (GSH) contents were significantly (p < 0.05 or p < 0.01) decreased, while malondialdehyde (MDA) contents were increased in the NiCl2-treated groups. The serum IgG, IgM, and bursa IgG and IgM contents were significantly (p < 0.05 or p < 0.01) lower in the NiCl2-treated groups than those in the control group. The above-mentioned results show that dietary NiCl2 in excess of 300 mg/kg can cause histopathological lesions via oxidative damage, which finally impairs the function of the bursa of Fabricius and reduces IgG and IgM contents of the serum and the bursa of Fabricius. The study is aimed to provide helpful materials for studies on Ni- or Ni compounds-induced B cell toxicity in both human and other animals in the future. PMID:26440478

  9. Acute pulmonary toxicity and inflammation induced by combined exposure to didecyldimethylammonium chloride and ethylene glycol in rats.

    PubMed

    Kwon, Do Young; Kim, Hyun-Mi; Kim, Eunji; Lim, Yeon-Mi; Kim, Pilje; Choi, Kyunghee; Kwon, Jung-Taek

    2016-02-01

    Didecyldimethylammonium chloride (DDAC), an antimicrobial agent, has been reported to induce pulmonary toxicity in animal studies. DDAC is frequently used in spray-form household products in combination with ethylene glycol (EG). The purpose of this study was to evaluate the toxic interaction between DDAC and EG in the lung. DDAC at a sub-toxic dose (100 μg/kg body weight) was mixed with a non-toxic dose of EG (100 or 200 μg/kg body weight), and was administrated to rats via intratracheal instillation. Lactate dehydrogenase activity and total protein content in the bronchoalveolar lavage fluid (BALF) were not changed by singly treated DDAC or EG, but significantly enhanced at 1 d after treatment with the mixture, with the effect dependent on the dose of EG. Total cell count in BALF was largely increased and polymorphonuclear leukocytes were predominantly recruited to the lung in rats administrated with the mixture. Inflammatory cytokines, tumor necrosis factor-alpha and interleukin-6 also appeared to be increased by the mixture of DDAC and EG (200 μg/kg body weight) at 1 d post-exposure, which might be associated with the increase in inflammatory cells in lung. BALF protein content and inflammatory cell recruitment in the lung still remained elevated at 7 d after the administration of DDAC with the higher dose of EG. These results suggest that the combination of DDAC and EG can synergistically induce pulmonary cytotoxicity and inflammation, and EG appears to amplify the harmful effects of DDAC on the lung. Therefore pulmonary exposure to these two chemicals commonly found in commercial products can be a potential hazard to human health. PMID:26763389

  10. Curcumin attenuates gastric cancer induced by N-methyl-N-nitrosourea and saturated sodium chloride in rats.

    PubMed

    Sintara, Kawiya; Thong-Ngam, Duangporn; Patumraj, Suthiluk; Klaikeaw, Naruemon

    2012-01-01

    To determine effects of curcumin on N-methyl-N-nitrosourea (MNU) and saturated sodium chloride (s-NaCl)-induced gastric cancer in rats. Male Wistar rats were divided into 5 groups: control (CO), control supplemented with 200 mg/kg curcumin (CC), MNU + s-NaCl, MNU + s-NaCl supplemented with 200 mg/kg curcumin daily for the first 3 weeks (MNU + s-NaCl + C3W), and MNU + s-NaCl supplemented with curcumin for 20 weeks (MNU + s-NaCl + C20W). To induce stomach cancer, rats except for CO and CC were orally treated with 100 mg/kg MNU on day 0 and 14, and s-NaCl twice-a-week for the first 3 weeks. The experiment was finished and rats were sacrificed at the end of 20 weeks. Cancers were found in forestomachs of all rats in MNU + s-NaCl. The expressions of phosphorylated inhibitor kappaB alpha (phospho-IκBα), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and cyclin D1 significantly increased in MNU + s-NaCl compared with CO. Curcumin treatments for 3 and 20 weeks reduced the cancer incidence resulting in a decrease of phospho-IκBα expression in benign tumor-bearing rats compared with MNU + s-NaCl. Curcumin treatment for 20 weeks also decreased 8-OHdG expression in benign tumor-bearing rats compared with MNU + s-NaCl. Curcumin can attenuate cancer via a reduction of phospho-IκBα and 8-OHdG expressions, which may play a promising role in gastric carcinogenesis.

  11. Berberine chloride pretreatment exhibits neuroprotective effect against 6-hydroxydopamine-induced neuronal insult in rat

    PubMed Central

    Negahdar, Feraidoon; Mehdizadeh, Mehdi; Joghataei, Mohammad Taghi; Roghani, Mehrdad; Mehraeen, Fereshteh; Poorghayoomi, Ehsan

    2015-01-01

    Parkinson’s disease (PD) is a rather common movement disorder as a result of the degeneration of dopaminergic neurons within the substantianigra. Current treatments for PD afford symptomatic relief with no prevention of disease progression. Due to the neuroprotective and anti-apoptotic potential of the isoquinoline alkaloid berberine (BBR), this study was conducted to assess whether BBR pretreatment could attenuate behavioral and neuronal derangement in 6-hydroxydopamine (6-OHDA)-induced model of PD in the rat. Unilateral intrastriatal 6-OHDA-lesioned rats received BBR at doses of 25 and/or 50 mg/kg (i.p.) three times at an interval of 24 h, started 2 days before the surgery. After 1 week, apomorphine caused significant contralateral rotations and a significant reduction in the number of Nissl-stained and tyrosine-hydroxylase (TH)-positive neurons on the left side of the substantianigra. BBR pretreatment at a dose of 50 mg/kg significantly reduced rotations and prevented loss of TH-positive neurons. These results indicate pre-lesion administration of BBR could protect against 6-OHDA toxicity and this may be of benefit besides other available therapies in PD. PMID:26664381

  12. Stress-induced phase transformation in nanocrystalline UO2

    SciTech Connect

    Uberuaga, Blas Pedro; Desai, Tapan

    2009-01-01

    We report a stress-induced phase transfonnation in stoichiometric UO{sub 2} from fluorite to the {alpha}-PbO{sub 2} structure using molecular dynamics (MD) simulations and density functional theory (DFT) calculations. MD simulations, performed on nanocrystalline microstructure under constant-stress tensile loading conditions, reveal a heterogeneous nucleation of the {alpha}-PbO{sub 2} phase at the grain boundaries followed by the growth of this phase towards the interior of the grain. The DFT calculations confinn the existence of the {alpha}-PbO{sub 2} structure, showing that it is energetically favored under tensile loading conditions.

  13. Stress Induced Branching of Growing Crystals on Curved Surfaces

    NASA Astrophysics Data System (ADS)

    Köhler, Christian; Backofen, Rainer; Voigt, Axel

    2016-04-01

    If two-dimensional crystals grow on a curved surface, the Gaussian curvature of the surface induces elastic stress and affects the growth pathway. The elastic stress can be alleviated by incorporating defects or, if this is energetically unfavorable, via an elastic instability which leads to anisotropic growth with branched ribbonlike structures. This instability provides a generic route to grow defect-free crystals on curved surfaces. Depending on the elastic properties of the crystal and the geometric properties of the surface, different growth morphologies with two-, four-, and sixfold symmetry develop. Using a phase field crystal type modeling approach, we provide a microscopic understanding of the morphology selection.

  14. Physiological changes induced by chromium stress in plants: an overview.

    PubMed

    Hayat, Shamsul; Khalique, Gulshan; Irfan, Mohammad; Wani, Arif Shafi; Tripathi, Bhumi Nath; Ahmad, Aqil

    2012-07-01

    This article presents an overview of the mechanism of chromium (Cr) stress in plants. Toxic effects of Cr on plant growth and development depend primarily on its valence state. Cr(VI) is highly toxic and mobile whereas Cr(III) is less toxic. Cr-induced oxidative stress involves induction of lipid peroxidation in plants that cause severe damage to cell membranes which includes degradation of photosynthetic pigments causing deterioration in growth. The potential of plants with the adequacy to accumulate or to stabilize Cr compounds for bioremediation of Cr contamination has gained engrossment in recent years.

  15. Stress Induced Branching of Growing Crystals on Curved Surfaces.

    PubMed

    Köhler, Christian; Backofen, Rainer; Voigt, Axel

    2016-04-01

    If two-dimensional crystals grow on a curved surface, the Gaussian curvature of the surface induces elastic stress and affects the growth pathway. The elastic stress can be alleviated by incorporating defects or, if this is energetically unfavorable, via an elastic instability which leads to anisotropic growth with branched ribbonlike structures. This instability provides a generic route to grow defect-free crystals on curved surfaces. Depending on the elastic properties of the crystal and the geometric properties of the surface, different growth morphologies with two-, four-, and sixfold symmetry develop. Using a phase field crystal type modeling approach, we provide a microscopic understanding of the morphology selection.

  16. Neural circuit for psychological stress-induced hyperthermia

    PubMed Central

    Nakamura, Kazuhiro

    2015-01-01

    Psychological stress-induced hyperthermia (PSH) is a basic physiological stress response to increase physical performances to defend homeostasis and life from stressors, such as natural enemies. However, excessive and long-lasting stressors can lead to chronic hyperthermia, particularly recognized in humans as a psychosomatic symptom called “psychogenic fever.” The sympathetic and neuroendocrine responses that can contribute to PSH include brown adipose tissue (BAT) thermogenesis, cutaneous vasoconstriction, tachycardia and glucocorticoid secretion. Research on the central circuits underlying these stress responses has recently revealed several fundamental circuit mechanisms including hypothalamomedullary pathways driving the sympathetic stress responses. Psychological stress activates a monosynaptic glutamatergic excitatory neurotransmission from the dorsomedial hypothalamus (DMH) to sympathetic premotor neurons in the rostral medullary raphe region (rMR) to drive BAT thermogenesis and tachycardia, leading to the development of PSH. This glutamatergic neurotransmission could be potentiated by orexin neurons in the lateral hypothalamus through their projections to the rMR. Psychological stress also activates another monosynaptic pathway from the DMH to the paraventricular hypothalamic nucleus to stimulate the hypothalamo-pituitary-adrenal axis for the secretion of glucocorticoids. PSH is independent from the prostaglandin-mediated trigger mechanism for inflammation-induced fever, and several forebrain regions are considered to provide stress-driven inputs to the DMH to activate the sympathetic- and neuroendocrine-driving neurons. The circuit mechanism of PSH based on animal experiments would be relevant to understandings of the etiology of psychogenic fever in humans. This review describes the current understandings of the central circuit mechanism of PSH with recent important progress in research. PMID:27227049

  17. Neural circuit for psychological stress-induced hyperthermia.

    PubMed

    Nakamura, Kazuhiro

    2015-01-01

    Psychological stress-induced hyperthermia (PSH) is a basic physiological stress response to increase physical performances to defend homeostasis and life from stressors, such as natural enemies. However, excessive and long-lasting stressors can lead to chronic hyperthermia, particularly recognized in humans as a psychosomatic symptom called "psychogenic fever." The sympathetic and neuroendocrine responses that can contribute to PSH include brown adipose tissue (BAT) thermogenesis, cutaneous vasoconstriction, tachycardia and glucocorticoid secretion. Research on the central circuits underlying these stress responses has recently revealed several fundamental circuit mechanisms including hypothalamomedullary pathways driving the sympathetic stress responses. Psychological stress activates a monosynaptic glutamatergic excitatory neurotransmission from the dorsomedial hypothalamus (DMH) to sympathetic premotor neurons in the rostral medullary raphe region (rMR) to drive BAT thermogenesis and tachycardia, leading to the development of PSH. This glutamatergic neurotransmission could be potentiated by orexin neurons in the lateral hypothalamus through their projections to the rMR. Psychological stress also activates another monosynaptic pathway from the DMH to the paraventricular hypothalamic nucleus to stimulate the hypothalamo-pituitary-adrenal axis for the secretion of glucocorticoids. PSH is independent from the prostaglandin-mediated trigger mechanism for inflammation-induced fever, and several forebrain regions are considered to provide stress-driven inputs to the DMH to activate the sympathetic- and neuroendocrine-driving neurons. The circuit mechanism of PSH based on animal experiments would be relevant to understandings of the etiology of psychogenic fever in humans. This review describes the current understandings of the central circuit mechanism of PSH with recent important progress in research.

  18. Stress-induced core temperature changes in pigeons (Columba livia).

    PubMed

    Bittencourt, Myla de Aguiar; Melleu, Fernando Falkenburger; Marino-Neto, José

    2015-02-01

    Changes in body temperature are significant physiological consequences of stressful stimuli in mammals and birds. Pigeons (Columba livia) prosper in (potentially) stressful urban environments and are common subjects in neurobehavioral studies; however, the thermal responses to stress stimuli by pigeons are poorly known. Here, we describe acute changes in the telemetrically recorded celomatic (core) temperature (Tc) in pigeons given a variety of potentially stressful stimuli, including transfer to a novel cage (ExC) leading to visual isolation from conspecifics, the presence of the experimenter (ExpR), gentle handling (H), sham intracelomatic injections (SI), and the induction of the tonic immobility (TI) response. Transfer to the ExC cage provoked short-lived hyperthermia (10-20 min) followed by a long-lasting and substantial decrease in Tc, which returned to baseline levels 2 h after the start of the test. After a 2-hour stay in the ExC, the other potentially stressful stimuli evoked only weak, marginally significant hyperthermic (ExpR, IT) or hypothermic (SI) responses. Stimuli delivered 26 h after transfer to the ExC induced definite and intense increases in Tc (ExpR, H) or hypothermic responses (SI). These Tc changes appear to be unrelated to modifications in general activity (as measured via telemetrically recorded actimetric data). Repeated testing failed to affect the hypothermic responses to the transference to the ExC, even after nine trials and at 1- or 8-day intervals, suggesting that the social (visual) isolation from conspecifics may be a strong and poorly controllable stimulus in this species. The present data indicated that stress-induced changes in Tc may be a consistent and reliable physiological parameter of stress but that they may also show stressor type-, direction- and species-specific attributes.

  19. Stress-induced core temperature changes in pigeons (Columba livia).

    PubMed

    Bittencourt, Myla de Aguiar; Melleu, Fernando Falkenburger; Marino-Neto, José

    2015-02-01

    Changes in body temperature are significant physiological consequences of stressful stimuli in mammals and birds. Pigeons (Columba livia) prosper in (potentially) stressful urban environments and are common subjects in neurobehavioral studies; however, the thermal responses to stress stimuli by pigeons are poorly known. Here, we describe acute changes in the telemetrically recorded celomatic (core) temperature (Tc) in pigeons given a variety of potentially stressful stimuli, including transfer to a novel cage (ExC) leading to visual isolation from conspecifics, the presence of the experimenter (ExpR), gentle handling (H), sham intracelomatic injections (SI), and the induction of the tonic immobility (TI) response. Transfer to the ExC cage provoked short-lived hyperthermia (10-20 min) followed by a long-lasting and substantial decrease in Tc, which returned to baseline levels 2 h after the start of the test. After a 2-hour stay in the ExC, the other potentially stressful stimuli evoked only weak, marginally significant hyperthermic (ExpR, IT) or hypothermic (SI) responses. Stimuli delivered 26 h after transfer to the ExC induced definite and intense increases in Tc (ExpR, H) or hypothermic responses (SI). These Tc changes appear to be unrelated to modifications in general activity (as measured via telemetrically recorded actimetric data). Repeated testing failed to affect the hypothermic responses to the transference to the ExC, even after nine trials and at 1- or 8-day intervals, suggesting that the social (visual) isolation from conspecifics may be a strong and poorly controllable stimulus in this species. The present data indicated that stress-induced changes in Tc may be a consistent and reliable physiological parameter of stress but that they may also show stressor type-, direction- and species-specific attributes. PMID:25479572

  20. Oxidative stress-induced calcium signalling in Aspergillus nidulans.

    PubMed

    Greene, Vilma; Cao, Hong; Schanne, Francis A X; Bartelt, Diana C

    2002-05-01

    The effects of oxidative stress on levels of calcium ion (Ca(2+)) in Aspergillus nidulans were measured using strains expressing aequorin in the cytoplasm (Aeq(cyt)) and mitochondria (Aeq(mt)). When oxidative stress was induced by exposure to 10-mM H(2)O(2), the mitochondrial calcium response (Ca(mt)(2+)) was greater than the change in cytoplasmic calcium (Ca(c)(2+)). The Ca(mt)(2+) response to H(2)O(2) was dose dependent, while the increase in [Ca(c)(2+)] did not change with increasing H(2)O(2). The increase in both [Ca(c)(2+)] and [Ca(mt)(2+)] in response to oxidative stress was enhanced by exposure of cells to Ca(2+). The presence of chelator in the external medium only partially inhibited the Ca(mt)(2+) and Ca(c)(2+) responses to oxidative stress. Reagents that alter calcium fluxes had varied effects on the Ca(mt)(2+) response to peroxide. Ruthenium red blocked the increase in [Ca(mt)(2+)], while neomycin caused an even greater increase in [Ca(mt)(2+)]. Treatment with ruthenium red and neomycin had no effect on the Ca(c)(2+) response. Bafilomycin A and oligomycin had no effect on either the mitochondrial or cytoplasmic response. Inhibitors of both voltage-regulated calcium channels and intracellular calcium release channels inhibited the Ca(2+)-dependent component of the Ca(mt)(2+) response to oxidative stress. We conclude that the more significant Ca(2+) response to oxidative stress occurs in the mitochondria and that both intracellular and extracellular calcium pools can contribute to the increases in [Ca(c)(2+)] and [Ca(mt)(2+)] induced by oxidative stress.

  1. Oxidative Stress Induces Senescence in Cultured RPE Cells

    PubMed Central

    Aryan, Nona; Betts-Obregon, Brandi S.; Perry, George; Tsin, Andrew T.

    2016-01-01

    The aim of this research is to determine whether oxidative stress induces cellular senescence in human retinal pigment epithelial cells. Cultured ARPE19 cells were subjected to different concentrations of hydrogen peroxide to induce oxidative stress. Cells were seeded into 24-well plates with hydrogen peroxide added to cell medium and incubated at 37°C + 5% CO2 for a 90-minute period [at 0, 300, 400 and 800 micromolar (MCM) hydrogen peroxide]. The number of viable ARPE19 cells were recorded using the Trypan Blue Dye Exclusion Method and cell senescence was measured by positive staining for senescence-associated beta-galactosidase (SA-beta-Gal) protein. Without hydrogen peroxide treatment, the number of viable ARPE19 cells increased significantly from 50,000 cells/well to 197,000 within 72 hours. Treatment with hydrogen peroxide reduced this level of cell proliferation significantly (to 52,167 cells at 400 MCM; to 49,263 cells at 800 MCM). Meanwhile, cells with a high level of positive senescence-indicator SA-Beta-Gal-positive staining was induced by hydrogen peroxide treatment (from a baseline level of 12% to 80% at 400 MCM and at 800 MCM). Our data suggests that oxidative stress from hydrogen peroxide treatment inhibited ARPE19 cell proliferation and induced cellular senescence. PMID:27651846

  2. Oxidative Stress Induces Senescence in Cultured RPE Cells.

    PubMed

    Aryan, Nona; Betts-Obregon, Brandi S; Perry, George; Tsin, Andrew T

    2016-01-01

    The aim of this research is to determine whether oxidative stress induces cellular senescence in human retinal pigment epithelial cells. Cultured ARPE19 cells were subjected to different concentrations of hydrogen peroxide to induce oxidative stress. Cells were seeded into 24-well plates with hydrogen peroxide added to cell medium and incubated at 37°C + 5% CO2 for a 90-minute period [at 0, 300, 400 and 800 micromolar (MCM) hydrogen peroxide]. The number of viable ARPE19 cells were recorded using the Trypan Blue Dye Exclusion Method and cell senescence was measured by positive staining for senescence-associated beta-galactosidase (SA-beta-Gal) protein. Without hydrogen peroxide treatment, the number of viable ARPE19 cells increased significantly from 50,000 cells/well to 197,000 within 72 hours. Treatment with hydrogen peroxide reduced this level of cell proliferation significantly (to 52,167 cells at 400 MCM; to 49,263 cells at 800 MCM). Meanwhile, cells with a high level of positive senescence-indicator SA-Beta-Gal-positive staining was induced by hydrogen peroxide treatment (from a baseline level of 12% to 80% at 400 MCM and at 800 MCM). Our data suggests that oxidative stress from hydrogen peroxide treatment inhibited ARPE19 cell proliferation and induced cellular senescence. PMID:27651846

  3. Oxidative Stress Induces Senescence in Cultured RPE Cells

    PubMed Central

    Aryan, Nona; Betts-Obregon, Brandi S.; Perry, George; Tsin, Andrew T.

    2016-01-01

    The aim of this research is to determine whether oxidative stress induces cellular senescence in human retinal pigment epithelial cells. Cultured ARPE19 cells were subjected to different concentrations of hydrogen peroxide to induce oxidative stress. Cells were seeded into 24-well plates with hydrogen peroxide added to cell medium and incubated at 37°C + 5% CO2 for a 90-minute period [at 0, 300, 400 and 800 micromolar (MCM) hydrogen peroxide]. The number of viable ARPE19 cells were recorded using the Trypan Blue Dye Exclusion Method and cell senescence was measured by positive staining for senescence-associated beta-galactosidase (SA-beta-Gal) protein. Without hydrogen peroxide treatment, the number of viable ARPE19 cells increased significantly from 50,000 cells/well to 197,000 within 72 hours. Treatment with hydrogen peroxide reduced this level of cell proliferation significantly (to 52,167 cells at 400 MCM; to 49,263 cells at 800 MCM). Meanwhile, cells with a high level of positive senescence-indicator SA-Beta-Gal-positive staining was induced by hydrogen peroxide treatment (from a baseline level of 12% to 80% at 400 MCM and at 800 MCM). Our data suggests that oxidative stress from hydrogen peroxide treatment inhibited ARPE19 cell proliferation and induced cellular senescence.

  4. Oxidative stress in MeHg-induced neurotoxicity

    SciTech Connect

    Farina, Marcelo; Aschner, Michael; Rocha, Joao B.T.

    2011-11-15

    Methylmercury (MeHg) is an environmental toxicant that leads to long-lasting neurological and developmental deficits in animals and humans. Although the molecular mechanisms mediating MeHg-induced neurotoxicity are not completely understood, several lines of evidence indicate that oxidative stress represents a critical event related to the neurotoxic effects elicited by this toxicant. The objective of this review is to summarize and discuss data from experimental and epidemiological studies that have been important in clarifying the molecular events which mediate MeHg-induced oxidative damage and, consequently, toxicity. Although unanswered questions remain, the electrophilic properties of MeHg and its ability to oxidize thiols have been reported to play decisive roles to the oxidative consequences observed after MeHg exposure. However, a close examination of the relationship between low levels of MeHg necessary to induce oxidative stress and the high amounts of sulfhydryl-containing antioxidants in mammalian cells (e.g., glutathione) have led to the hypothesis that nucleophilic groups with extremely high affinities for MeHg (e.g., selenols) might represent primary targets in MeHg-induced oxidative stress. Indeed, the inhibition of antioxidant selenoproteins during MeHg poisoning in experimental animals has corroborated this hypothesis. The levels of different reactive species (superoxide anion, hydrogen peroxide and nitric oxide) have been reported to be increased in MeHg-exposed systems, and the mechanisms concerning these increments seem to involve a complex sequence of cascading molecular events, such as mitochondrial dysfunction, excitotoxicity, intracellular calcium dyshomeostasis and decreased antioxidant capacity. This review also discusses potential therapeutic strategies to counteract MeHg-induced toxicity and oxidative stress, emphasizing the use of organic selenocompounds, which generally present higher affinity for MeHg when compared to the classically

  5. Oxidative stress induces senescence in human mesenchymal stem cells

    SciTech Connect

    Brandl, Anita; Meyer, Matthias; Bechmann, Volker; Nerlich, Michael; Angele, Peter

    2011-07-01

    Mesenchymal stem cells (MSCs) contribute to tissue repair in vivo and form an attractive cell source for tissue engineering. Their regenerative potential is impaired by cellular senescence. The effects of oxidative stress on MSCs are still unknown. Our studies were to investigate into the proliferation potential, cytological features and the telomere linked stress response system of MSCs, subject to acute or prolonged oxidant challenge with hydrogen peroxide. Telomere length was measured using the telomere restriction fragment assay, gene expression was determined by rtPCR. Sub-lethal doses of oxidative stress reduced proliferation rates and induced senescent-morphological features and senescence-associated {beta}-galactosidase positivity. Prolonged low dose treatment with hydrogen peroxide had no effects on cell proliferation or morphology. Sub-lethal and prolonged low doses of oxidative stress considerably accelerated telomere attrition. Following acute oxidant insult p21 was up-regulated prior to returning to initial levels. TRF1 was significantly reduced, TRF2 showed a slight up-regulation. SIRT1 and XRCC5 were up-regulated after oxidant insult and expression levels increased in aging cells. Compared to fibroblasts and chondrocytes, MSCs showed an increased tolerance to oxidative stress regarding proliferation, telomere biology and gene expression with an impaired stress tolerance in aged cells.

  6. Osmotic Stress-Induced Polyamine Accumulation in Cereal Leaves 1

    PubMed Central

    Flores, Hector E.; Galston, Arthur W.

    1984-01-01

    Arginine decarboxylase activity increases 2- to 3-fold in osmotically stressed oat leaves in both light and dark, but putrescine accumulation in the dark is only one-third to one-half of that in light-stressed leaves. If arginine or ornithine are supplied to dark-stressed leaves, putrescine rises to levels comparable to those obtained by incubation under light. Thus, precursor amino acid availability is limiting to the stress response. Amino acid levels change rapidly upon osmotic treatment; notably, glutamic acid decreases with a corresponding rise in glutamine. Difluoromethylarginine (0.01-0.1 millimolar), the enzyme-activated irreversible inhibitor of arginine decarboxylase, prevents the stress-induced putrescine rise, as well as the incorporation of label from [14C]arginine, with the expected accumulation of free arginine, but has no effect on the rest of the amino acid pool. The use of specific inhibitors such as α-difluoromethylarginine is suggested as probes for the physiological significance of stress responses by plant cells. PMID:16663552

  7. Chronic psychosocial stress induces visceral hyperalgesia in mice.

    PubMed

    Tramullas, Mónica; Dinan, Timothy G; Cryan, John F

    2012-05-01

    Experimental and clinical evidence has shown that chronic stress plays an important role in the onset and/or exacerbation of symptoms of functional gastrointestinal disorders. Here, we aimed to investigate whether exposure to a chronic and temporally unpredictable psychosocial stressor alters visceral and somatic nociception as well as anxiety-related behaviour. In male C57BL/6J mice, chronic stress was induced by repeated exposure to social defeat (SD, 2 h) and overcrowding (OC, 24 h) during 19 consecutive days. Visceral and somatic nociception was evaluated by colorectal distension and a hot plate, respectively. The social interaction test was used to assess social anxiety. Mice exposed to psychosocial stress developed visceral hyperalgesia and somatic hypoalgesia 24 h following the last stress session. SD/OC mice also exhibited social anxiety-like behaviour. All these changes were also associated with physiological alterations, measured as a decreased faecal pellet output and hypothalamic-pituitary-adrenal (HPA) axis disruption. Taken together, these data confirm that this mouse model of chronic psychosocial stress may be useful for studies on the pathophysiological mechanisms underlying such stress-associated disorders and to further test potential therapies.

  8. Antidiabetic and hypolipidaemic effects of a methanol/methylene-chloride extract of Laportea ovalifolia (Urticaceae), measured in rats with alloxan-induced diabetes.

    PubMed

    Momo, C E N; Oben, J E; Tazoo, D; Dongo, E

    2006-01-01

    A decoction of the leaves of Laportea ovalifolia is widely used in Cameroon for the treatment of several illnesses, including diabetes mellitus. The antidiabetic and hypolipidaemic effects of a methanol/methylene-chloride extract of the aerial parts of L. ovalifolia have now been investigated, in normal rats and rats with diabetes induced by the intraperitoneal injection of alloxan (at 150 mg/kg bodyweight). In the diabetic rats, 2 weeks of daily, intragastric treatment with the L. ovalifolia extract not only produced a significant reduction in the fasting serum glucose concentrations but also lowered the serum concentrations of total cholesterol, triglycerides, and low-density-lipoprotein cholesterol, lowered the ratio of total cholesterol to high-density-lipoprotein (HDL) cholesterol, and increased the serum concentration of HDL cholesterol. At least in rats with alloxan-induced diabetes, the methanol/methylene-chloride extract of L. ovalifolia therefore appears to possess antidiabetic and hypolipidaemic properties.

  9. Physiological responses of broiler chickens to heat stress and dietary electrolyte balance (sodium plus potassium minus chloride, milliequivalents per kilogram).

    PubMed

    Borges, S A; Fischer da Silva, A V; Majorka, A; Hooge, D M; Cummings, K R

    2004-09-01

    Individually caged male Cobb broilers (24), 44 d of age, were used to evaluate effects of heat stress (1 d of data collection) and dietary electrolyte balance (DEB; Na + K - Cl, mEq/kg from 1 d of age). During summer rearing, mortality was variable, but DEB 240 improved growth, feed conversion ratio, water intake, and water:feed ratio vs. DEB 0. The temperature sequence for heat stress was 24 to 32 degrees C in 30 min, 32 to 36 degrees C in 30 min, 36 to 37 degrees C in 15 min, and 37 to 41 degrees C in 45 min. Maximum temperature was held for 15, 60, 90, or 360 min for data collection (relative humidity averaged 42 +/- 7%). Results from the same room before and after heat stress were analyzed by DEB (1-factor ANOVA) and before vs. after heat stress compared across DEB (2-sample t-test). Heat stress decreased blood Na, K, and pCO2, and lymphocytes but increased heterophils. Blood HCO3 rose, Cl declined, and hematocrit gave a concave pattern (lowest at DEB 120) as DEB increased. After heat stress, DEB 0 decreased blood Na and K, and DEB 0 and 120 levels decreased blood HCO3. After heat stress blood pCO2 and hemoglobin decreased with DEB 240, but it had highest pCO2, a key factor. The DEB 120 gave longest times to panting and prostration with DEB 0 and 240 results lower but similar statistically. In heat stress, DEB 360 was excessive, DEB 120 and 240 were favorable, and DEB 0 was intermediate based on hematology, panting, and prostration responses.

  10. Vinyl chloride and polyvinyl chloride.

    PubMed

    Lewis, R

    1999-01-01

    Polyvinyl chloride (PVC) is an important plastic resin for construction, pipe and tubing, siding, and other uses. Exposures to vinyl chloride monomer during the early years of production resulted in an important sentinel health event: the recognition of an excess of a rare liver cancer, hepatic angiosarcoma, at facilities throughout the world. Several other syndromes, including acro-osteolysis, also have been associated with PVC, but less clearly with vinyl chloride. Extensive research ranging from large-scale epidemiologic studies to biomarker research into molecular mechanisms continues to provide valuable insight into the pathogenesis of occupational cancer.

  11. Inefficacy of osmotic backwash induced by sodium chloride salt solution in controlling SWRO membrane fouling

    NASA Astrophysics Data System (ADS)

    Farooque, A. Mohammed; Al-Jeshi, Subhi; Saeed, Mohamed O.; Alreweli, Ali

    2014-12-01

    A study was conducted to evaluate the efficacy of osmotic backwash induced by high salt (NaCl) concentration solution on feed side of seawater reverse osmosis (SWRO) membranes, online and offline, in controlling membrane fouling and therefore minimizing/eliminating the need for chemical cleaning. SWRO membranes were deliberately fouled by feeding seawater from an open intake located on the Arabian Gulf Coast without dosing chemicals. The fouled membranes were subjected to offline cleaning with the salt solution of up to 25 % concentration. Despite the partial removal of foulants from the membrane surface, SWRO membrane performance could not be restored, indicating the ineffectiveness of osmotic backwash in aiding offline salt cleaning. Similarly, online osmotic backwash was found to be not only ineffective in removing foulants from membrane surfaces but actually increased the fouling rate, as indicated by faster fouling rates compared to other cases. Although the driving force required for the osmotic backwash existed, the generated back flow proved to be insufficient to detach foulants from membrane surfaces. During the study period, the average SWRO membrane flux was maintained between 19 and 23 LMH, whereas the average generated back flow flux by high salt concentration solution was only 11 LMH, which was not adequate to remove foulants from membrane surfaces. Moreover, it seems that the membrane configuration as well as inherent microstructure of SWRO membrane places certain constraints on the osmotic backwash process and renders osmotic backwash ineffective in tackling SWRO membrane fouling. Hence, chemical cleaning is essential to restore SWRO membrane performance whenever fouling occurs, and the use of highly concentrated salt solution does not have any significant benefit. Membrane autopsy revealed only an insignificant accumulation of biofouling layer despite the absence of disinfection. However, it was shown that culturable biofilm bacteria species

  12. Biologically Synthesized Gold Nanoparticles Ameliorate Cold and Heat Stress-Induced Oxidative Stress in Escherichia coli.

    PubMed

    Zhang, Xi-Feng; Shen, Wei; Gurunathan, Sangiliyandi

    2016-01-01

    Due to their unique physical, chemical, and optical properties, gold nanoparticles (AuNPs) have recently attracted much interest in the field of nanomedicine, especially in the areas of cancer diagnosis and photothermal therapy. Because of the enormous potential of these nanoparticles, various physical, chemical, and biological methods have been adopted for their synthesis. Synthetic antioxidants are dangerous to human health. Thus, the search for effective, nontoxic natural compounds with effective antioxidative properties is essential. Although AuNPs have been studied for use in various biological applications, exploration of AuNPs as antioxidants capable of inhibiting oxidative stress induced by heat and cold stress is still warranted. Therefore, one goal of our study was to produce biocompatible AuNPs using biological methods that are simple, nontoxic, biocompatible, and environmentally friendly. Next, we aimed to assess the antioxidative effect of AuNPs against oxidative stress induced by cold and heat in Escherichia coli, which is a suitable model for stress responses involving AuNPs. The response of aerobically grown E. coli cells to cold and heat stress was found to be similar to the oxidative stress response. Upon exposure to cold and heat stress, the viability and metabolic activity of E. coli was significantly reduced compared to the control. In addition, levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and leakage of proteins and sugars were significantly elevated, and the levels of lactate dehydrogenase activity (LDH) and adenosine triphosphate (ATP) significantly lowered compared to in the control. Concomitantly, AuNPs ameliorated cold and heat-induced oxidative stress responses by increasing the expression of antioxidants, including glutathione (GSH), glutathione S-transferase (GST), super oxide dismutase (SOD), and catalase (CAT). These consistent physiology and biochemical data suggest that AuNPs can ameliorate cold and heat stress-induced

  13. Cyclooxygenase-2 inhibition reduces stress-induced affective pathology.

    PubMed

    Gamble-George, Joyonna Carrie; Baldi, Rita; Halladay, Lindsay; Kocharian, Adrina; Hartley, Nolan; Silva, Carolyn Grace; Roberts, Holly; Haymer, Andre; Marnett, Lawrence J; Holmes, Andrew; Patel, Sachin

    2016-01-01

    Mood and anxiety disorders are the most prevalent psychiatric conditions and are exacerbated by stress. Recent studies have suggested cyclooxygenase-2 (COX-2) inhibition could represent a novel treatment approach or augmentation strategy for affective disorders including anxiety disorders and major depression. We show that traditional COX-2 inhibitors and a newly developed substrate-selective COX-2 inhibitor (SSCI) reduce a variety of stress-induced behavioral pathologies in mice. We found that these behavioral effects were associated with a dampening of neuronal excitability in the basolateral amygdala (BLA) ex vivo and in vivo, and were mediated by small-conductance calcium-activated potassium (SK) channel and CB1 cannabinoid receptor activation. Taken together, these data provide further support for the potential utility of SSCIs, as well as traditional COX-2 inhibitors, as novel treatment approaches for stress-related psychiatric disorders. PMID:27162170

  14. Cyclooxygenase-2 inhibition reduces stress-induced affective pathology

    PubMed Central

    Gamble-George, Joyonna Carrie; Baldi, Rita; Halladay, Lindsay; Kocharian, Adrina; Hartley, Nolan; Silva, Carolyn Grace; Roberts, Holly; Haymer, Andre; Marnett, Lawrence J; Holmes, Andrew; Patel, Sachin

    2016-01-01

    Mood and anxiety disorders are the most prevalent psychiatric conditions and are exacerbated by stress. Recent studies have suggested cyclooxygenase-2 (COX-2) inhibition could represent a novel treatment approach or augmentation strategy for affective disorders including anxiety disorders and major depression. We show that traditional COX-2 inhibitors and a newly developed substrate-selective COX-2 inhibitor (SSCI) reduce a variety of stress-induced behavioral pathologies in mice. We found that these behavioral effects were associated with a dampening of neuronal excitability in the basolateral amygdala (BLA) ex vivo and in vivo, and were mediated by small-conductance calcium-activated potassium (SK) channel and CB1 cannabinoid receptor activation. Taken together, these data provide further support for the potential utility of SSCIs, as well as traditional COX-2 inhibitors, as novel treatment approaches for stress-related psychiatric disorders. DOI: http://dx.doi.org/10.7554/eLife.14137.001 PMID:27162170

  15. High shear stress induces atherosclerotic vulnerable plaque formation through angiogenesis

    PubMed Central

    Wang, Yi; Qiu, Juhui; Luo, Shisui; Xie, Xiang; Zheng, Yiming; Zhang, Kang; Ye, Zhiyi; Liu, Wanqian; Gregersen, Hans; Wang, Guixue

    2016-01-01

    Rupture of atherosclerotic plaques causing thrombosis is the main cause of acute coronary syndrome and ischemic strokes. Inhibition of thrombosis is one of the important tasks developing biomedical materials such as intravascular stents and vascular grafts. Shear stress (SS) influences the formation and development of atherosclerosis. The current review focuses on the vulnerable plaques observed in the high shear stress (HSS) regions, which localizes at the proximal region of the plaque intruding into the lumen. The vascular outward remodelling occurs in the HSS region for vascular compensation and that angiogenesis is a critical factor for HSS which induces atherosclerotic vulnerable plaque formation. These results greatly challenge the established belief that low shear stress is important for expansive remodelling, which provides a new perspective for preventing the transition of stable plaques to high-risk atherosclerotic lesions. PMID:27482467

  16. Beneficial effect of zinc chloride and zinc ionophore pyrithione on attenuated cardioprotective potential of preconditioning phenomenon in STZ-induced diabetic rat heart.

    PubMed

    Jamwal, Sumit; Kumar, Kushal; Reddy, B V Krishna

    2016-05-01

    Ischemic preconditioning (IPC) is well demonstrated to produce cardioprotection by phosphorylation and subsequent inactivation of glycogen synthase kinase-3β (GSk-3β) in the normal rat heart, but its effect is attenuated in the diabetic rat heart. This study was designed to investigate the effect of zinc chloride and zinc ionophore pyrithione (ZIP) on the attenuated cardioprotective potential of IPC in the diabetic rat heart. Diabetes mellitus (DM) was induced by a single intraperitoneal administration of streptozotocin (STZ) (50 mg/kg; i.p). The isolated perfused rat heart was subjected to 30 minutes of ischemia followed by 120 minutes of reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining and cardiac injury was measured by estimating lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) in the coronary effluent. Also, GSK-3β was measured and neutrophil accumulation was measured by estimating myeloperoxidase (MPO) levels. IPC significantly decreased the myocardial infarct size, the release of LDH and CK-MB, the GSK-3β levels and the MPO levels in the normal rat heart. Pre- and post-ischemic treatment with zinc chloride and zinc ionophore pyrithione (ZIP) in the normal and diabetic rat hearts significantly decreased the myocardial infarct size, the level of CK-MB and LDH in the coronary effluent and GSK-3β and MPO levels. Our results suggest that pharmacological preconditioning with zinc chloride and ZIP significantly restored the attenuated cardioprotective potential of IPC in the diabetic rat heart. PMID:26423303

  17. Modeling diffusion-induced stress in nanowire electrode structures

    NASA Astrophysics Data System (ADS)

    Deshpande, Rutooj; Cheng, Yang-Tse; Verbrugge, Mark W.

    There is an intense, worldwide effort to develop durable lithium ion batteries with high energy and power densities for a wide range of applications, including electric and hybrid electric vehicles. One of the critical challenges in advancing lithium ion battery technologies is fracture and decrepitation of the electrodes as a result of lithium diffusion during charging and discharging operations. When lithium is inserted in either the positive or negative electrode, a large volume change on the order of a few to several hundred percent, can occur. Diffusion-induced stresses (DISs) can therefore cause the nucleation and growth of cracks, leading to mechanical degradation of the active electrode materials. Our work is aimed at developing a mathematical model relating surface energy with diffusion-induced stresses in nanowire electrodes. With decreasing size of the electrode, the ratio of surface area to volume increases. Thus, surface energy and surface stress can play an important role in mitigating DISs in nanostructured electrodes. In this work, we establish relationships between the surface energy, surface stress, and the magnitude of DISs in nanowires. We find that DISs, especially the tensile stresses, can decrease significantly due to the surface effects. Our model also establishes a relationship between stress and the nanowire radius. We show that, with decreasing size, the electrode material will be less prone to mechanical degradation, leading to an increase in the life of lithium ion batteries, provided other phenomena are unaffected by increased surface area (e.g., chemical degradation reactions). Also we show that, in the case of nanostructures, surface strain energy is significant in magnitude comparing with bulk strain energy. A mathematical tool to calculate total strain energy is developed that can be used to compare strain energy with the fracture energy of that material in electrode system.

  18. Stress does not inhibit induced vitellogenesis in juvenile rainbow trout

    USGS Publications Warehouse

    Schwindt, A.R.; Feist, G.W.; Schreck, C.B.

    2007-01-01

    Vitellogenin (Vtg) is a widely used biomarker for xenoestrogen exposure in male fishes. In female fishes Vtg can be negatively affected by stress independent of declines in estrogen. However, few data are available on the effect of stress in male fish abnormally producing Vtg, such as when exposed to xenoestrogens. The objective for these studies was to determine the effects of stress on fish forced to produce Vtg. Three weeks prior to the experiment immature juvenile rainbow trout, Oncorhynchus mykiss, were acclimated to the experimental tanks and fed a maintenance ration. We induced Vtg synthesis by injecting 17??-estradiol (E2) 7 days prior to experimentation. Treatments in duplicate tanks were: (1) no stressor; (2) stressor; (3) E 2; (4) E2 and stressor. Plasma was collected at time = 0 for baseline measurements from eight fish per tank and Vtg was significantly elevated in treated fish compared to uninjected controls. Water was drained from the stressor tanks then refilled to a level that just covered the backs of the fish. Eight fish were sampled again at 4 and 9 h, and 1, 7, and 14 days of continuous stress. Stressor tanks were refilled with water to pre-stress levels and the fish were sampled after another 2 weeks. Cortisol was significantly elevated from the unstressed fish at 4 h; however, plasma Vtg in the E 2-stimulated fish was not affected by the stressor at any timepoint. These results indicate that fish capture procedures employed in the field or caging experiments likely do not lead to false negative results when plasma Vtg is used as a biomarker for xenoestrogen exposure. It also suggests that the energetic load induced by stress is insufficient to cause a reduction in Vtg, during a continuous E2 administration, at least within the timepoints examined in this study. ?? 2006 Springer Science+Business Media, Inc.

  19. Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling

    SciTech Connect

    Lovelace, Erica S.; Wagoner, Jessica; MacDonald, James; Bammler, Theo; Bruckner, Jacob; Brownell, Jessica; Beyer, Richard; Zink, Erika M.; Kim, Young-Mo; Kyle, Jennifer E.; Webb-Robertson, Bobbie-Jo M.; Waters, Katrina M.; Metz, Thomas O.; Farin, Federico; Oberlies, Nicholas H.; Polyak, Steve

    2015-08-28

    Silymarin (SM), a natural product, is touted as a liver protectant and preventer of both chronic inflammation and diseases. To define how SM elicits these effects at a systems level, we performed transcriptional profiling, metabolomics, and signaling studies in human liver and T cell lines. Multiple pathways associated with cellular stress and metabolism were modulated by SM treatment within 0.5 to four hours: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed suppression of glycolytic, TCA cycle, and amino acid metabolism by SM treatment. Antiinflammatory effects arose with prolonged (i.e. 24 hours) SM exposure, with suppression of multiple proinflammatory mRNAs and nuclear factor kappa B (NF-κB) and forkhead box O (FOXO) signaling. Studies with murine knock out cells revealed that SM inhibition of both mTOR and NF-κB was partially AMPK dependent, while SM inhibition of the mTOR pathway in part required DDIT4. Thus, SM activates stress and repair responses that culminate in an anti-inflammatory phenotype. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Therefore, natural products like SM may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation.

  20. Electrically-induced stresses and deflection in multiple plates

    SciTech Connect

    Hu, Jih-Perng; Tichler, P.R.

    1992-05-01

    Thermohydraulic tests are being planned at the High Flux Beam Reactor of Brookhaven National Laboratory, in which direct electrical heating of metal plates will simulate decay heating in parallel plate-type fuel elements. The required currents are high if plates are made of metal with a low electrical resistance, such as aluminum. These high currents will induce either attractive or repulsive forces between adjacent current-carrying plates. Such forces, if strong enough, will cause the plates to deflect and so change the geometry of the coolant channel between the plates. Since this is undesirable, an analysis has been made to evaluate the magnitude of the deflection and related stresses. In contrast to earlier publications in which either a concentrated or a uniform load was assumed, in this paper an exact force distribution on the plate is analytically solved and then used for stress and deflection calculations, assuming each plate to be a simply supported beam. Results indicate that due to superposition of the induced forces between plates in a multiple-and-parallel plate array, the maximum deflection and bending stress occur at the midpoint of the outermost plate. The maximum shear stress, which is inversely proportional to plate thickness, occurs at both ends of the outermost plate.

  1. Electrically-induced stresses and deflection in multiple plates

    SciTech Connect

    Hu, Jih-Perng; Tichler, P.R.

    1992-01-01

    Thermohydraulic tests are being planned at the High Flux Beam Reactor of Brookhaven National Laboratory, in which direct electrical heating of metal plates will simulate decay heating in parallel plate-type fuel elements. The required currents are high if plates are made of metal with a low electrical resistance, such as aluminum. These high currents will induce either attractive or repulsive forces between adjacent current-carrying plates. Such forces, if strong enough, will cause the plates to deflect and so change the geometry of the coolant channel between the plates. Since this is undesirable, an analysis has been made to evaluate the magnitude of the deflection and related stresses. In contrast to earlier publications in which either a concentrated or a uniform load was assumed, in this paper an exact force distribution on the plate is analytically solved and then used for stress and deflection calculations, assuming each plate to be a simply supported beam. Results indicate that due to superposition of the induced forces between plates in a multiple-and-parallel plate array, the maximum deflection and bending stress occur at the midpoint of the outermost plate. The maximum shear stress, which is inversely proportional to plate thickness, occurs at both ends of the outermost plate.

  2. Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling

    PubMed Central

    Lovelace, Erica S.; Wagoner, Jessica; MacDonald, James; Bammler, Theo; Bruckner, Jacob; Brownell, Jessica; Beyer, Richard; Zink, Erika M.; Kim, Young-Mo; Kyle, Jennifer E.; Webb-Robertson, Bobbie-Jo; Waters, Katrina M.; Metz, Thomas O.; Farin, Federico; Oberlies, Nicholas H.; Polyak, Stephen J.

    2016-01-01

    Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e. 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-κB) and forkhead box O (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-κB was partially AMPK dependent, while silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation. PMID:26186142

  3. Gruneisen-stress induced ablation of biological tissue

    SciTech Connect

    Dingus, R.S.; Scammon, R.J.

    1991-01-01

    The objective of biomedical applications of lasers is frequently to remove tissue in a controlled manner. However, for ablation induced by thermal- or photo-decomposition, damage to surrounding tissue may be excessive in some instances. Tissue can also be ablated by a hydrodynamic process referred to as front surface spallation, in which a thin layer next to a free surface is heated to levels, below vaporization but, so rapidly that it cannot undergo thermal expansion during laser heating. This generates a stress pulse, which propagates away from the heated region, with an initial amplitude that can be calculated using the Grueneisen coefficient. As the pulse reflects from the free surface, a tensile tail can develop of sufficient amplitude, exceeding the material strength, that a layer will be spalled off, taking much of the laser-deposited energy with it. Because tissue is generally a low strength material, this process has the potential of producing controlled ablation with reduced damage to the remaining tissue. However, to achieve these conditions, the laser pulse length, absorption depth and fluence must be properly tailored. This paper presents hydrodynamic calculations and analytical modeling relating to both stress- and thermal-induced ablation as a function of laser and tissue properties to illustrate the potential benefits of stress induced ablation. Also, guidance is given for tailoring the exposure parameters to enhance front surface spallation. 8 refs., 6 figs.

  4. Modeling Diffusion Induced Stresses for Lithium-Ion Battery Materials

    NASA Astrophysics Data System (ADS)

    Chiu Huang, Cheng-Kai

    Advancing lithium-ion battery technology is of paramount importance for satisfying the energy storage needs in the U.S., especially for the application in the electric vehicle industry. To provide a better acceleration for electric vehicles, a fast and repeatable discharging rate is required. However, particle fractures and capacity loss have been reported under high current rate (C-rate) during charging/discharging and after a period of cycling. During charging and discharging, lithium ions extract from and intercalate into electrode materials accompanied with the volume change and phase transition between Li-rich phase and Li-poor phase. It is suggested that the diffusion-induced-stress is one of the main reasons causing capacity loss due to the mechanical degradation of electrode particles. Therefore, there is a fundamental need to provide a mechanistic understanding by considering the structure-mechanics-property interactions in lithium-ion battery materials. Among many cathode materials, the olivine-based lithium-iron-phosphate (LiFePO4) with an orthorhombic crystal structure is one of the promising cathode materials for the application in electric vehicles. In this research we first use a multiphysic approach to investigate the stress evolution, especially on the phase boundary during lithiation in single LiFePO4 particles. A diffusion-controlled finite element model accompanied with the experimentally observed phase boundary propagation is developed via a finite element package, ANSYS, in which lithium ion concentration-dependent anisotropic material properties and volume misfits are incorporated. The stress components on the phase boundary are used to explain the Mode I, Mode II, and Mode III fracture propensities in LiFePO4 particles. The elastic strain energy evolution is also discussed to explain why a layer-by-layer lithium insertion mechanism (i.e. first-order phase transformation) is energetically preferred. Another importation issue is how current

  5. Per capita interactions and stress tolerance drive stress-induced changes in biodiversity effects on ecosystem functions

    PubMed Central

    Baert, Jan M.; Janssen, Colin R.; Sabbe, Koen; De Laender, Frederik

    2016-01-01

    Environmental stress changes the relationship between biodiversity and ecosystem functions, but the underlying mechanisms are poorly understood. Because species interactions shape biodiversity–ecosystem functioning relationships, changes in per capita interactions under stress (as predicted by the stress gradient hypothesis) can be an important driver of stress-induced changes in these relationships. To test this hypothesis, we measure productivity in microalgae communities along a diversity and herbicide gradient. On the basis of additive partitioning and a mechanistic community model, we demonstrate that changes in per capita interactions do not explain effects of herbicide stress on the biodiversity–productivity relationship. Instead, assuming that the per capita interactions remain unaffected by stress, causing species densities to only change through differences in stress tolerance, suffices to predict the stress-induced changes in the biodiversity–productivity relationship and community composition. We discuss how our findings set the stage for developing theory on how environmental stress changes biodiversity effects on ecosystem functions. PMID:27534986

  6. Per capita interactions and stress tolerance drive stress-induced changes in biodiversity effects on ecosystem functions.

    PubMed

    Baert, Jan M; Janssen, Colin R; Sabbe, Koen; De Laender, Frederik

    2016-01-01

    Environmental stress changes the relationship between biodiversity and ecosystem functions, but the underlying mechanisms are poorly understood. Because species interactions shape biodiversity-ecosystem functioning relationships, changes in per capita interactions under stress (as predicted by the stress gradient hypothesis) can be an important driver of stress-induced changes in these relationships. To test this hypothesis, we measure productivity in microalgae communities along a diversity and herbicide gradient. On the basis of additive partitioning and a mechanistic community model, we demonstrate that changes in per capita interactions do not explain effects of herbicide stress on the biodiversity-productivity relationship. Instead, assuming that the per capita interactions remain unaffected by stress, causing species densities to only change through differences in stress tolerance, suffices to predict the stress-induced changes in the biodiversity-productivity relationship and community composition. We discuss how our findings set the stage for developing theory on how environmental stress changes biodiversity effects on ecosystem functions. PMID:27534986

  7. Per capita interactions and stress tolerance drive stress-induced changes in biodiversity effects on ecosystem functions.

    PubMed

    Baert, Jan M; Janssen, Colin R; Sabbe, Koen; De Laender, Frederik

    2016-08-18

    Environmental stress changes the relationship between biodiversity and ecosystem functions, but the underlying mechanisms are poorly understood. Because species interactions shape biodiversity-ecosystem functioning relationships, changes in per capita interactions under stress (as predicted by the stress gradient hypothesis) can be an important driver of stress-induced changes in these relationships. To test this hypothesis, we measure productivity in microalgae communities along a diversity and herbicide gradient. On the basis of additive partitioning and a mechanistic community model, we demonstrate that changes in per capita interactions do not explain effects of herbicide stress on the biodiversity-productivity relationship. Instead, assuming that the per capita interactions remain unaffected by stress, causing species densities to only change through differences in stress tolerance, suffices to predict the stress-induced changes in the biodiversity-productivity relationship and community composition. We discuss how our findings set the stage for developing theory on how environmental stress changes biodiversity effects on ecosystem functions.

  8. Losartan abolishes oxidative stress induced by intermittent hypoxia in humans.

    PubMed

    Pialoux, Vincent; Foster, Glen E; Ahmed, Sofia B; Beaudin, Andrew E; Hanly, Patrick J; Poulin, Marc J

    2011-11-15

    The aim of this study was to assess the role of the type 1 angiotensin II (AT(1)) receptor in the increase of oxidative stress and NO metabolism during a single 6 h exposure to intermittent hypoxia (IH). Nine healthy young men were exposed, while awake, to sham IH, IH with placebo medication, and IH with the AT(1) receptor antagonist, losartan, using a double-blind, placebo-controlled, randomized, crossover study design. In addition to blood pressure, oxidative stress, peroxynitrite activity, uric acid, global antioxidant status and the end-products of NO (NOx) metabolism were measured in plasma before and after 6 h of IH. Oxidative stress and peroxynitrite activity increased and NOx decreased during IH with placebo. In contrast, neither sham IH nor IH with losartan affected these parameters. With respect to each condition, blood pressure had the same profile as oxidative stress. These results demonstrate that blockade of AT(1) receptors prevented the increase in oxidative stress and peroxynitrite activity and the decrease in NO metabolism induced by IH. Finally, this study suggests that the renin-angiotensin system may participate in the overproduction of reactive oxygen species associated with IH by upregulation of the actions of angiotensin II.

  9. Somatic embryogenesis - Stress-induced remodeling of plant cell fate.

    PubMed

    Fehér, Attila

    2015-04-01

    Plants as sessile organisms have remarkable developmental plasticity ensuring heir continuous adaptation to the environment. An extreme example is somatic embryogenesis, the initiation of autonomous embryo development in somatic cells in response to exogenous and/or endogenous signals. In this review I briefly overview the various pathways that can lead to embryo development in plants in addition to the fertilization of the egg cell and highlight the importance of the interaction of stress- and hormone-regulated pathways during the induction of somatic embryogenesis. Somatic embryogenesis can be initiated in planta or in vitro, directly or indirectly, and the requirement for dedifferentiation as well as the way to achieve developmental totipotency in the various systems is discussed in light of our present knowledge. The initiation of all forms of the stress/hormone-induced in vitro as well as the genetically provoked in planta somatic embryogenesis requires extensive and coordinated genetic reprogramming that has to take place at the chromatin level, as the embryogenic program is under strong epigenetic repression in vegetative plant cells. Our present knowledge on chromatin-based mechanisms potentially involved in the somatic-to-embryogenic developmental transition is summarized emphasizing the potential role of the chromatin to integrate stress, hormonal, and developmental pathways leading to the activation of the embryogenic program. The role of stress-related chromatin reorganization in the genetic instability of in vitro cultures is also discussed. This article is part of a Special Issue entitled: Stress as a fundamental theme in cell plasticity.

  10. Injection-induced seismicity on basement faults including poroelastic stressing

    NASA Astrophysics Data System (ADS)

    Chang, K. W.; Segall, P.

    2016-04-01

    Most significant induced earthquakes occur on faults within the basement beneath sedimentary cover. In this two-dimensional plane strain numerical study, we examine the full poroelastic response of basement faults to fluid injection into overlying strata, considering both (1) the permeability of the fault zone and (2) the hydraulic connectivity of the faults to the target horizon. Given hydraulic and mechanical properties, we compute the spatiotemporal change in Coulomb stress, which we separate into (1) the change in poroelastic stresses Δτs+fΔσn, where Δτs and Δσn are changes in shear and normal stress (Δτs>0 and Δσn>0 both favor slip), and (2) the change in pore pressure fΔp. Pore pressure diffusion into hydraulically connected, permeable faults dominates their mechanical stability. For hydraulically isolated or low-permeability faults, however, poroelastic stresses transmitted to deeper basement levels can trigger slip, even without elevated pore pressure. The seismicity rate on basement fault zones is predicted using the model of Dieterich (1994). High seismicity rates can occur on permeable, hydraulically connected faults due to direct pore pressure diffusion. Lower rates are predicted on isolated steeply dipping normal faults, caused solely by poroelastic stressing. In contrast, seismicity on similarly oriented reverse faults is inhibited.

  11. Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress

    PubMed Central

    Ślusarczyk, Joanna; Trojan, Ewa; Głombik, Katarzyna; Chamera, Katarzyna; Roman, Adam; Budziszewska, Bogusława; Basta-Kaim, Agnieszka

    2016-01-01

    The potential contribution of inflammation to the development of neuropsychiatric diseases has recently received substantial attention. In the brain, the main immune cells are the microglia. As they are the main source of inflammatory factors, it is plausible that the regulation of their activation may be a potential therapeutic target. Fractalkine (CX3CL1) and its receptor CX3CR1 play a crucial role in the control of the biological activity of the microglia. In the present study, using microglial cultures we investigated whether fractalkine is able to reverse changes in microglia caused by a prenatal stress procedure. Our study found that the microglia do not express fractalkine. Prenatal stress decreases the expression of the fractalkine receptor, which in turn is enhanced by the administration of exogenous fractalkine. Moreover, treatment with fractalkine diminishes the prenatal stress-induced overproduction of proinflammatory factors such as IL-1β, IL-18, IL-6, TNF-α, CCL2, or NO in the microglial cells derived from prenatally stressed newborns. In conclusion, the present results revealed that the pathological activation of microglia in prenatally stressed newborns may be attenuated by fractalkine administration. Therefore, understanding of the role of the CX3CL1-CX3CR1 system may help to elucidate the mechanisms underlying the neuron-microglia interaction and its role in pathological conditions in the brain. PMID:27239349

  12. Enhanced Oxidative Stress Is Responsible for TRPV4-Induced Neurotoxicity

    PubMed Central

    Hong, Zhiwen; Tian, Yujing; Yuan, Yibiao; Qi, Mengwen; Li, Yingchun; Du, Yimei; Chen, Lei; Chen, Ling

    2016-01-01

    Transient receptor potential vanilloid 4 (TRPV4) has been reported to be responsible for neuronal injury in pathological conditions. Excessive oxidative stress can lead to neuronal damage, and activation of TRPV4 increases the production of reactive oxygen species (ROS) and nitric oxide (NO) in many types of cells. The present study explored whether TRPV4-induced neuronal injury is mediated through enhancing oxidative stress. We found that intracerebroventricular injection of the TRPV4 agonist GSK1016790A increased the content of methane dicarboxylic aldehyde (MDA) and NO in the hippocampus, which was blocked by administration of the TRPV4 specific antagonist HC-067047. The activities of catalase (CAT) and glutathione peroxidase (GSH-Px) were decreased by GSK1016790A, whereas the activity of superoxide dismutase (SOD) remained unchanged. Moreover, the protein level and activity of neuronal nitric oxide synthase (nNOS) were increased by GSK1016790A, and the GSK1016790A-induced increase in NO content was blocked by an nNOS specific antagonist ARL-17477. The GSK1016790A-induced modulations of CAT, GSH-Px and nNOS activities and the protein level of nNOS were significantly inhibited by HC-067047. Finally, GSK1016790A-induced neuronal death and apoptosis in the hippocampal CA1 area were markedly attenuated by administration of a ROS scavenger Trolox or ARL-17477. We conclude that activation of TRPV4 enhances oxidative stress by inhibiting CAT and GSH-Px and increasing nNOS, which is responsible, at least in part, for TRPV4-induced neurotoxicity. PMID:27799895

  13. Contaminant-induced oxidative stress in fish: a mechanistic approach.

    PubMed

    Lushchak, Volodymyr I

    2016-04-01

    The presence of reactive oxygen species (ROS) in living organisms was described more than 60 years ago and virtually immediately it was suggested that ROS were involved in various pathological processes and aging. The state when ROS generation exceeds elimination leading to an increased steady-state ROS level has been called "oxidative stress." Although ROS association with many pathological states in animals is well established, the question of ROS responsibility for the development of these states is still open. Fish represent the largest group of vertebrates and they inhabit a broad range of ecosystems where they are subjected to many different aquatic contaminants. In many cases, the deleterious effects of contaminants have been connected to induction of oxidative stress. Therefore, deciphering of molecular mechanisms leading to such contaminant effects and organisms' response may let prevent or minimize deleterious impacts of oxidative stress. This review describes general aspects of ROS homeostasis, in particular highlighting its basic aspects, modification of cellular constituents, operation of defense systems and ROS-based signaling with an emphasis on fish systems. A brief introduction to oxidative stress theory is accompanied by the description of a recently developed classification system for oxidative stress based on its intensity and time course. Specific information on contaminant-induced oxidative stress in fish is covered in sections devoted to such pollutants as metal ions (particularly iron, copper, chromium, mercury, arsenic, nickel, etc.), pesticides (insecticides, herbicides, and fungicides) and oil with accompanying pollutants. In the last section, certain problems and perspectives in studies of oxidative stress in fish are described.

  14. Contaminant-induced oxidative stress in fish: a mechanistic approach.

    PubMed

    Lushchak, Volodymyr I

    2016-04-01

    The presence of reactive oxygen species (ROS) in living organisms was described more than 60 years ago and virtually immediately it was suggested that ROS were involved in various pathological processes and aging. The state when ROS generation exceeds elimination leading to an increased steady-state ROS level has been called "oxidative stress." Although ROS association with many pathological states in animals is well established, the question of ROS responsibility for the development of these states is still open. Fish represent the largest group of vertebrates and they inhabit a broad range of ecosystems where they are subjected to many different aquatic contaminants. In many cases, the deleterious effects of contaminants have been connected to induction of oxidative stress. Therefore, deciphering of molecular mechanisms leading to such contaminant effects and organisms' response may let prevent or minimize deleterious impacts of oxidative stress. This review describes general aspects of ROS homeostasis, in particular highlighting its basic aspects, modification of cellular constituents, operation of defense systems and ROS-based signaling with an emphasis on fish systems. A brief introduction to oxidative stress theory is accompanied by the description of a recently developed classification system for oxidative stress based on its intensity and time course. Specific information on contaminant-induced oxidative stress in fish is covered in sections devoted to such pollutants as metal ions (particularly iron, copper, chromium, mercury, arsenic, nickel, etc.), pesticides (insecticides, herbicides, and fungicides) and oil with accompanying pollutants. In the last section, certain problems and perspectives in studies of oxidative stress in fish are described. PMID:26607273

  15. Aloin Protects Skin Fibroblasts from Heat Stress-Induced Oxidative Stress Damage by Regulating the Oxidative Defense System

    PubMed Central

    Wang, Yu-Ren; Tsai, Hsin-I; Yu, Huang-Ping

    2015-01-01

    Oxidative stress is commonly involved in the pathogenesis of skin damage induced by environmental factors, such as heat stress. Skin fibroblasts are responsible for the connective tissue regeneration and the skin recovery from injury. Aloin, a bioactive compound in Aloe vera, has been reported to have various pharmacological activities, such as anti-inflammatory effects. The aim of this study was to investigate the protective effect of aloin against heat stress-mediated oxidative stress in human skin fibroblast Hs68 cells. Hs68 cells were first incubated at 43°C for 30 min to mimic heat stress. The study was further examined if aloin has any effect on heat stress-induced oxidative stress. We found that aloin protected Hs68 cells against heat stress-induced damage, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay. Aloin protected Hs68 cells by regulating reactive oxygen species production and increasing the levels of glutathione, cytosolic and mitochondrial superoxide dismutase. Aloin also prevented the elevation of thiobarbituric acid reactive substances and the reduction of 8-OH-dG induced by heat stress. These results indicated that aloin protected human skin fibroblasts from heat stress-induced oxidative stress damage by regulating the oxidative defense system. PMID:26637174

  16. Aloin Protects Skin Fibroblasts from Heat Stress-Induced Oxidative Stress Damage by Regulating the Oxidative Defense System.

    PubMed

    Liu, Fu-Wei; Liu, Fu-Chao; Wang, Yu-Ren; Tsai, Hsin-I; Yu, Huang-Ping

    2015-01-01

    Oxidative stress is commonly involved in the pathogenesis of skin damage induced by environmental factors, such as heat stress. Skin fibroblasts are responsible for the connective tissue regeneration and the skin recovery from injury. Aloin, a bioactive compound in Aloe vera, has been reported to have various pharmacological activities, such as anti-inflammatory effects. The aim of this study was to investigate the protective effect of aloin against heat stress-mediated oxidative stress in human skin fibroblast Hs68 cells. Hs68 cells were first incubated at 43°C for 30 min to mimic heat stress. The study was further examined if aloin has any effect on heat stress-induced oxidative stress. We found that aloin protected Hs68 cells against heat stress-induced damage, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay. Aloin protected Hs68 cells by regulating reactive oxygen species production and increasing the levels of glutathione, cytosolic and mitochondrial superoxide dismutase. Aloin also prevented the elevation of thiobarbituric acid reactive substances and the reduction of 8-OH-dG induced by heat stress. These results indicated that aloin protected human skin fibroblasts from heat stress-induced oxidative stress damage by regulating the oxidative defense system. PMID:26637174

  17. The Effects of a Liquid Sulfate/Chloride Environment on Superalloy Stress Rupture Properties at 1300 °F (704 °C)

    NASA Astrophysics Data System (ADS)

    Whitlow, G. A.; Beck, C. G.; Viswanathan, R.; Crombie, E. A.

    1984-01-01

    Data from a stress rupture study on several nickel and cobalt base alloys in a corrosive sulfate/chloride melt at 1300 °F (704 °C) indicated that over the stress range 525 to 700 MPa (75 to 100 ksi), the presence of the environment resulted in considerable reductions in rupture life. Preferential intergranular attack was observed, associated with the diffusion of oxygen and sulfur down a grain boundary to form a sulfide spike, with the subsequent initiation of a crack leading to failure. In an attempt to prevent such effects, it has been found that the application of aluminide or aluminum-chromium diffusion coatings to, for example, a Udimet 710 alloy eliminates this effect, such that rupture life in the salt environment is essentially comparable to that for the uncoated Udimet 710 in air. Modification of the alloy composition with respect to boron and carbon contents, as for instance in a Udimet 720 alloy, has a similar effect. Both approaches are being used to insure the life and reliability of turbine components operating in the low temperature corrosion regime.

  18. Separating triggered and stress-change induced seismcity

    NASA Astrophysics Data System (ADS)

    Zhuang, J.

    2013-12-01

    Once a major earthquake occurs, it usually not only triggers a sequence of many aftershock, but also changes the tectonic stress field in the regions nearby. According to the rate and state law (Dieterich, 1994), such stress changes result in a permanent change of the seismicity rate, increment or decrement. However, since aftershock sequence lasts quite a long time before it decays off, it is hard tell whether the high level of seismicity after a big earthquake is the continuation of the aftershock activity or caused by the changes of stress due this big earthquake. In this study, by making use of the space-time ETAS model (Ogata, 1998) and the stochastic declustering method (Zhuang et al., 2002, 2004), I developed a method to separate the seismicity induced by stress-change from the aftershock activity in a probability manner. For example, it is found that the probabilities that Lushan earthquakes belong the background seismcity, aftershock of the Wenchuan earthquake, are stress-change induced seismcity are, respectively, 38% and 12%, 50%. References Dieterich, J.H. (1994) A constitutive law for rate of earthquake production and its application to earthquake clustering, J. Geophys. Res. , 99 , 2601-2618. Ogata, Y. (1998. Space-time point-process models for earthquake occur- rences, Ann. Inst. Stat. Math., 50, 379-402. Zhuang J., Ogata Y. and Vere-Jones D. (2004). Analyzing earthquake clustering features by using stochastic reconstruction. Journal of Geophysical Research, 109, No. B5, B05301, doi:10.1029/2003JB002879. Zhuang J., Ogata Y. and Vere-Jones D. (2002). Stochastic declustering of space-time earthquake occurrences. Journal of the American Statistical Association, 97: 369-380.

  19. Exercise-induced dehydration with and without environmental heat stress results in increased oxidative stress.

    PubMed

    Hillman, Angela R; Vince, Rebecca V; Taylor, Lee; McNaughton, Lars; Mitchell, Nigel; Siegler, Jason

    2011-10-01

    While in vitro work has revealed that dehydration and hyperthermia can elicit increased cellular and oxidative stress, in vivo research linking dehydration, hyperthermia, and oxidative stress is limited. The purpose of this study was to investigate the effects of exercise-induced dehydration with and without hyperthermia on oxidative stress. Seven healthy male, trained cyclists (power output (W) at lactate threshold (LT): 199 ± 19 W) completed 90 min of cycling exercise at 95% LT followed by a 5-km time trial (TT) in 4 trials: (i) euhydration in a warm environment (EU-W, control), (ii) dehydration in a warm environment (DE-W), (iii) euhydration in a thermoneutral environment (EU-T), and (iv) dehydration in a thermoneutral environment (DE-T) (W: 33.9 ± 0.9 °C; T: 23.0 ± 1.0 °C). Oxidized glutathione (GSSG) increased significantly postexercise in dehydration trials only (DE-W: p < 0.01, DE-T: p = 0.03), and while not significant, total glutathione (TGSH) and thiobarbituric acid reactive substances (TBARS) tended to increase postexercise in dehydration trials (p = 0.08 for both). Monocyte heat shock protein 72 (HSP72) concentration was increased (p = 0.01) while lymphocyte HSP32 concentration was decreased for all trials (p = 0.02). Exercise-induced dehydration led to an increase in GSSG concentration while maintenance of euhydration attenuated these increases regardless of environmental condition. Additionally, we found evidence of increased cellular stress (measured via HSP) during all trials independent of hydration status and environment. Finally, both 90-min and 5-km TT performances were reduced during only the DE-W trial, likely a result of combined cellular stress, hyperthermia, and dehydration. These findings highlight the importance of fluid consumption during exercise to attenuate thermal and oxidative stress during prolonged exercise in the heat.

  20. Cordycepin prevents oxidative stress-induced inhibition of osteogenesis.

    PubMed

    Wang, Feng; Yin, Peipei; Lu, Ye; Zhou, Zubin; Jiang, Chaolai; Liu, Yingjie; Yu, Xiaowei

    2015-11-01

    Oxidative stress is known to be involved in impairment of osteogenesis and age-related osteoporosis. Cordycepin is one of the major bioactive components of Cordyceps militaris that has been shown to exert antioxidant and anti-inflammatory activities. However, there are few reports available regarding the effects of cordycepin on osteogenesis and the underlying mechanism. In this study, we investigated the potential osteoprotective effects of cordycepin and its mechanism systematically using both in vitro model as well as in vivo mouse models. We discovered that hydrogen peroxide (H2O2)-induced inhibition of osteogenesis which was rescued by cordycepin treatment in human bone marrow mesenchymal stem cells (BM-MSCs). Cordycepin exerted its protective effects partially by increasing or decreasing expression of osteogenic and osteoclastogenesis marker genes. Treatment with cordycepin increased Wnt-related genes' expression whereas supplementation of Wnt pathway inhibitor reversed its protective effects. In addition, administration of cordycepin promoted osteogenic differentiation of BM-MSCs by reducing oxidative stress in both ovariectomized and aged animal models. Taken together, these results support the protective effects of cordycepin on oxidative stress induced inhibition of osteogenesis by activation of Wnt pathway. PMID:26462178

  1. Cordycepin prevents oxidative stress-induced inhibition of osteogenesis

    PubMed Central

    Wang, Feng; Yin, Peipei; Lu, Ye; Zhou, Zubin; Jiang, Chaolai; Liu, Yingjie; Yu, Xiaowei

    2015-01-01

    Oxidative stress is known to be involved in impairment of osteogenesis and age-related osteoporosis. Cordycepin is one of the major bioactive components of Cordyceps militaris that has been shown to exert antioxidant and anti-inflammatory activities. However, there are few reports available regarding the effects of cordycepin on osteogenesis and the underlying mechanism. In this study, we investigated the potential osteoprotective effects of cordycepin and its mechanism systematically using both in vitro model as well as in vivo mouse models. We discovered that hydrogen peroxide (H2O2) induced inhibition of osteogenesis which was rescued by cordycepin treatment in human bone marrow mesenchymal stem cells (BM-MSCs). Cordycepin exerted its protective effects partially by increasing or decreasing expression of osteogenic and osteoclastogenesis marker genes. Treatment with cordycepin increased Wnt-related genes' expression whereas supplementation of Wnt pathway inhibitor reversed its protective effects. In addition, administration of cordycepin promoted osteogenic differentiation of BM-MSCs by reducing oxidative stress in both ovariectomized and aged animal models. Taken together, these results support the protective effects of cordycepin on oxidative stress induced inhibition of osteogenesis by activation of Wnt pathway. PMID:26462178

  2. Cloning and Characterization of a Novel Drosophila Stress Induced DNase

    PubMed Central

    Seong, Chang-Soo; Varela-Ramirez, Armando; Tang, Xiaolei; Anchondo, Brenda; Magallanes, Diego; Aguilera, Renato J.

    2014-01-01

    Drosophila melanogaster flies mount an impressive immune response to a variety of pathogens with an efficient system comprised of both humoral and cellular responses. The fat body is the main producer of the anti-microbial peptides (AMPs) with anti-pathogen activity. During bacterial infection, an array of secreted peptidases, proteases and other enzymes are involved in the dissolution of debris generated by pathogen clearance. Although pathogen destruction should result in the release a large amount of nucleic acids, the mechanisms for its removal are still not known. In this report, we present the characterization of a nuclease gene that is induced not only by bacterial infection but also by oxidative stress. Expression of the identified protein has revealed that it encodes a potent nuclease that has been named Stress Induced DNase (SID). SID belongs to a family of evolutionarily conserved cation-dependent nucleases that degrade both single and double-stranded nucleic acids. Down-regulation of sid expression via RNA interference leads to significant reduction of fly viability after bacterial infection and oxidative stress. Our results indicate that SID protects flies from the toxic effects of excess DNA/RNA released by pathogen destruction and from oxidative damage. PMID:25083901

  3. The protective effect of melatonin against brain oxidative stress and hyperlocomotion in a rat model of mania induced by ouabain.

    PubMed

    Souza, Leandro C; Wilhelm, Ethel Antunes; Bortolatto, Cristiani Folharini; Nogueira, Cristina Wayne; Boeira, Silvana P; Jesse, Cristiano R

    2014-09-01

    This study was designed to investigate the protective effect of melatonin in a preclinical animal model of mania induced by ouabain (OUA). Male Wistar rats were pretreated with melatonin (5 or 20mg/kg; intraperitoneal, i.p.) for seven days or with the mood stabilizer lithium chloride (positive control) (45 mg/kg, per oral, p.o.). One day after the last dose, animals received an intracerebroventricular (i.c.v.) injection of OUA (5μl, 10(-5)M), a Na(+)K(+)ATPase-inhibiting compound. Locomotor activity was assessed in the open-field test (OFT). The levels of reactive species (RS), protein carbonyl (PC) and non-protein thiols (NPSH), as well as the activities of the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were measured in the cerebral cortex and hippocampus of rats. OUA markedly increased the locomotor activity in the OFT, and the pretreatment with melatonin or lithium chloride prevented this effect. Melatonin treatment (similar to lithium) was also effective in preventing the following alterations elicited by OUA: increase of RS and PC levels; depletion of NPSH levels; increase of SOD activity; and inhibition of CAT and GPx activities. Moreover, we found that brain oxidative stress and behavioural alterations elicited by OUA were significantly correlated. Our study showed that Melatonin, similarly to lithium, protected against OUA-induced brain oxidative stress and hyperlocomotion in rats. Thus, our findings reinforce the notion that oxidative stress may play an important role in the manic-like behavioural. Therefore, we indicate that melatonin has antimanic-like action, suggesting a potential role for this substance in the pharmacological management of Bipolar disorder.

  4. Indium and indium tin oxide induce endoplasmic reticulum stress and oxidative stress in zebrafish (Danio rerio).

    PubMed

    Brun, Nadja Rebecca; Christen, Verena; Furrer, Gerhard; Fent, Karl

    2014-10-01

    Indium and indium tin oxide (ITO) are extensively used in electronic technologies. They may be introduced into the environment during production, use, and leaching from electronic devices at the end of their life. At present, surprisingly little is known about potential ecotoxicological implications of indium contamination. Here, molecular effects of indium nitrate (In(NO3)3) and ITO nanoparticles were investigated in vitro in zebrafish liver cells (ZFL) cells and in zebrafish embryos and novel insights into their molecular effects are provided. In(NO3)3 led to induction of endoplasmic reticulum (ER) stress response, induction of reactive oxygen species (ROS) and induction of transcripts of pro-apoptotic genes and TNF-α in vitro at a concentration of 247 μg/L. In(NO3)3 induced the ER stress key gene BiP at mRNA and protein level, as well as atf6, which ultimately led to induction of the important pro-apoptotic marker gene chop. The activity of In(NO3)3 on ER stress induction was much stronger than that of ITO, which is explained by differences in soluble free indium ion concentrations. The effect was also stronger in ZFL cells than in zebrafish embryos. Our study provides first evidence of ER stress and oxidative stress induction by In(NO3)3 and ITO indicating a critical toxicological profile that needs further investigation.

  5. Stress-induced alterations in prefrontal dendritic spines: Implications for post-traumatic stress disorder.

    PubMed

    Moench, Kelly M; Wellman, Cara L

    2015-08-01

    The medial prefrontal cortex (mPFC) is involved in a variety of important functions including emotional regulation, HPA axis regulation, and working memory. It also demonstrates remarkable plasticity in an experience-dependent manner. There is extensive evidence that stressful experiences can produce profound changes in the morphology of neurons within mPFC with a variety of behavioral consequences. The deleterious behavioral outcomes associated with mPFC dysfunction have been implicated in multiple psychopathologies, including post-traumatic stress disorder (PTSD). Given the prevalence of these disorders, a deeper understanding of the cellular mechanisms underlying stress-induced morphological changes in mPFC is critical, and could lead to improved therapeutic treatments. Here we give a brief review of recent studies examining the mechanisms underlying changes in mPFC pyramidal neuron dendritic spines - the primary sites of excitatory input in cortical pyramidal neurons. We begin with an overview of the effects of chronic stress on mPFC dendritic spine density and morphology followed by proposed mechanisms for these changes. We then discuss the time course of stress effects on mPFC as well as potential intercellular influences. Given that many psychopathologies, including PTSD, have different prevalence rates among men and women, we end with a discussion of the sex differences that have been observed in morphological changes in mPFC. Future directions and implications for PTSD are discussed throughout.

  6. Stress-induced self-cannibalism: on the regulation of autophagy by endoplasmic reticulum stress.

    PubMed

    Deegan, Shane; Saveljeva, Svetlana; Gorman, Adrienne M; Samali, Afshin

    2013-07-01

    Macroautophagy (autophagy) is a cellular catabolic process which can be described as a self-cannibalism. It serves as an essential protective response during conditions of endoplasmic reticulum (ER) stress through the bulk removal and degradation of unfolded proteins and damaged organelles; in particular, mitochondria (mitophagy) and ER (reticulophagy). Autophagy is genetically regulated and the autophagic machinery facilitates removal of damaged cell components and proteins; however, if the cell stress is acute or irreversible, cell death ensues. Despite these advances in the field, very little is known about how autophagy is initiated and how the autophagy machinery is transcriptionally regulated in response to ER stress. Some three dozen autophagy genes have been shown to be required for the correct assembly and function of the autophagic machinery; however; very little is known about how these genes are regulated by cellular stress. Here, we will review current knowledge regarding how ER stress and the unfolded protein response (UPR) induce autophagy, including description of the different autophagy-related genes which are regulated by the UPR. PMID:23052213

  7. Chemical Detection Based on Adsorption-Induced and Photo-Induced Stresses in MEMS Devices

    SciTech Connect

    Datskos, P.G.

    1999-04-05

    Recently there has been an increasing demand to perform real-time in-situ chemical detection of hazardous materials, contraband chemicals, and explosive chemicals. Currently, real-time chemical detection requires rather large analytical instrumentation that are expensive and complicated to use. The advent of inexpensive mass produced MEMS (micro-electromechanical systems) devices opened-up new possibilities for chemical detection. For example, microcantilevers were found to respond to chemical stimuli by undergoing changes in their bending and resonance frequency even when a small number of molecules adsorb on their surface. In our present studies, we extended this concept by studying changes in both the adsorption-induced stress and photo-induced stress as target chemicals adsorb on the surface of microcantilevers. For example, microcantilevers that have adsorbed molecules will undergo photo-induced bending that depends on the number of absorbed molecules on the surface. However, microcantilevers that have undergone photo-induced bending will adsorb molecules on their surfaces in a distinctly different way. Depending on the photon wavelength and microcantilever material, the microcantilever can be made to bend by expanding or contracting the irradiated surface. This is important in cases where the photo-induced stresses can be used to counter any adsorption-induced stresses and increase the dynamic range. Coating the surface of the microstructure with a different material can provide chemical specificity for the target chemicals. However, by selecting appropriate photon wavelengths we can change the chemical selectivity due to the introduction of new surface states in the MEMS device. We will present and discuss our results on the use of adsorption-induced and photo-induced bending of microcantilevers for chemical detection.

  8. A chloride capturing system via proton-induced structure transformation between opened- and closed-forms of dodecavanadates.

    PubMed

    Inoue, Yoshitaka; Kikukawa, Yuji; Kuwajima, Sho; Hayashi, Yoshihito

    2016-05-01

    Chloride-incorporated dodecavanadates show two distinct structures of the monoprotonated-form [HV12O32(Cl)](4-) (closed-V12) with a spherical closed-structure and the opened-form [V12O32(Cl)](5-) (opened-V12). The reaction of closed-V12 with a stoichiometric amount of ethylenediamine drives the structure transformation reaction to opened-V12, quantitatively. From time dependent observations of (51)V NMR, a tube-type intermediate [V12O32(Cl)](5-) (tube-V12) was observed in the transformation process. Isolation of the intermediate was achieved by the deprotonation reaction of closed-V12 with diethylamine, and the structure transformation was confirmed by using the isolated intermediate. The reverse transformation from opened-V12 to closed-V12 was also achieved by addition of trifluoroacetic acid. The geometrical difference between closed-V12 and opened-V12 is reflected in the reactivity difference to the external reagents, and this was demonstrated by examining the chloride removal reaction by using a silver cation. The incorporated chloride was preserved in the closed-V12 cage even in the presence of a silver cation. In contrast, the chloride in opened-V12 was removed as AgCl by the silver cation. In addition, by the reaction of chloride-free opened-V12 with a quantitative amount of {Et4N}Cl retrieved opened-V12, showing the capability of opened-V12 to recapture a guest chloride in the cavity. This transformation between two isomeric dodecavanadate structures is regarded as the movement of a molecular mitt to catch a ball and secure it.

  9. Driving-induced stress in urban college students.

    PubMed

    Rasmussen, C; Knapp, T J; Garner, L

    2000-04-01

    Urban college student commuters (N = 407) were surveyed about their experiences with stress induced by driving. Of the participants 23.6% reported becoming angry at another driver more than once per day. They rated stress from other drivers as equal to the stress experienced during a college examination but gave slightly lower ratings to traffic congestion, road construction, and finding a parking place as sources of stress. Slow drivers, a child not restrained, and a vehicle following too closely were the highest rated annoying situations. Of participants, 21.6% had reported another driver to the police; nearly 22% said they carried a weapon for protection from other drivers (5.4% said a gun). Men were more than twice as likely as women to carry a weapon and three times as likely to carry a gun. Of the total sample, 19.1% feared being shot by another driver. Most participants (75.8%) said drivers were more aggressive and dangerous than they were five years ago.

  10. Cancer Evolution under Drug-Induced Stress-Gradients

    NASA Astrophysics Data System (ADS)

    Lambert, Guillaume; Austin, Robert H.

    2011-03-01

    The lack of long term success in eliminating cancer cells while avoiding the evolution of drug resistance indicates that our understanding of how cells evolve in response to stress is still incomplete. We interpret this not as a failure of the current approaches, but rather as an indication that new research venues should be undertaken, where conventional wisdom is challenged in order to drive forward our understanding of cancer. Of particular importance, we believe that the powerful role of evolution in the origin of drug resistance is ill-understood. We do not ask whether evolution occurs, but rather how. We do not describe molecular mechanisms underlying drug resistance at the single cell level, but rather ask how does resistance spread in cancerous tissues and metastatic lesions. We attempt to answer these questions by studying the population-wide dynamics of drug evolution and the collective stress response of cancer cells in a microfluidics device. We use microfluidics technologies to impose high levels of stress on cancer cell metapopulation by create smoothly varying gradients of either oxygen, chemotherapeutic drug, nutrient or pH. We present long-term studies of the adaptation of tumorigenic cancer cells to drug- induced stress gradients. Partially supported by and performance at NCI U54CA143803, CNF ECS-0335765, NSF PHY- 0750323, and NSERC.

  11. Early light-induced proteins protect Arabidopsis from photooxidative stress.

    PubMed

    Hutin, Claire; Nussaume, Laurent; Moise, Nicolae; Moya, Ismaël; Kloppstech, Klaus; Havaux, Michel

    2003-04-15

    The early light-induced proteins (ELIPs) belong to the multigenic family of light-harvesting complexes, which bind chlorophyll and absorb solar energy in green plants. ELIPs accumulate transiently in plants exposed to high light intensities. By using an Arabidopsis thaliana mutant (chaos) affected in the posttranslational targeting of light-harvesting complex-type proteins to the thylakoids, we succeeded in suppressing the rapid accumulation of ELIPs during high-light stress, resulting in leaf bleaching and extensive photooxidative damage. Constitutive expression of ELIP genes in chaos before light stress resulted in ELIP accumulation and restored the phototolerance of the plants to the wild-type level. Free chlorophyll, a generator of singlet oxygen in the light, was detected by chlorophyll fluorescence lifetime measurements in chaos leaves before the symptoms of oxidative stress appeared. Our findings indicate that ELIPs fulfill a photoprotective function that could involve either the binding of chlorophylls released during turnover of pigment-binding proteins or the stabilization of the proper assembly of those proteins during high-light stress. PMID:12676998

  12. Stress-induced Ageing of Lithium-Ion Batteries.

    PubMed

    Held, Marcel; Sennhauser, Urs

    2015-01-01

    Lithium-ion batteries are well established for use in portable consumer products and are increasingly used in high power electro-mobility and photovoltaic storage applications. In hybrid and plug-in electric vehicles degradation and useful lifetime at standard operation conditions are critical parameters in addition to performance and safety. Here stress-induced ageing of commercially available high power battery cells of the type A123 AHR32113M1 Ultra-B, consisting of a LiFePO(4) cathode and a graphite anode have been investigated. A usually accepted capacity loss for electric vehicles of 20% was reached after 8560 stress profiles corresponding to a driving distance of almost 200'000 km. Cycling with a stress profile applying constant power corresponding to the average power and energy of a full stress profile and starting at 60% state of charge showed a much faster capacity loss. Electric impedance measurements show the dependence of the capacity loss and constant phase element at low frequency, indicating Li-ion diffusion blocking in the cathode. Microscopic analysis of anode, separator, and cathode, shows defect formation in bulk material and at interfaces.

  13. Stress-induced Ageing of Lithium-Ion Batteries.

    PubMed

    Held, Marcel; Sennhauser, Urs

    2015-01-01

    Lithium-ion batteries are well established for use in portable consumer products and are increasingly used in high power electro-mobility and photovoltaic storage applications. In hybrid and plug-in electric vehicles degradation and useful lifetime at standard operation conditions are critical parameters in addition to performance and safety. Here stress-induced ageing of commercially available high power battery cells of the type A123 AHR32113M1 Ultra-B, consisting of a LiFePO(4) cathode and a graphite anode have been investigated. A usually accepted capacity loss for electric vehicles of 20% was reached after 8560 stress profiles corresponding to a driving distance of almost 200'000 km. Cycling with a stress profile applying constant power corresponding to the average power and energy of a full stress profile and starting at 60% state of charge showed a much faster capacity loss. Electric impedance measurements show the dependence of the capacity loss and constant phase element at low frequency, indicating Li-ion diffusion blocking in the cathode. Microscopic analysis of anode, separator, and cathode, shows defect formation in bulk material and at interfaces. PMID:26842322

  14. Dietary vanadium induces oxidative stress in the intestine of broilers.

    PubMed

    Deng, Yuanxin; Cui, Hengmin; Peng, Xi; Fang, Jing; Wang, Kangping; Cui, Wei; Liu, Xiaodong

    2012-01-01

    The purpose of this study was to examine oxidative stress induced by dietary vanadium in the mucosa of different parts of intestine including duodenum, jejunum, ileum, and cecal tonsil. A total of 420 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium as ammonium metavanadate. During the experimental period of 42 days, oxidative stress parameters were determined for both control and experimental groups. The results showed that malondialdehyde content was significantly higher (p < 0.05 or p < 0.01) in 30, 45, and 60 mg/kg groups than in control group. In contrast, the activities of superoxide dismutase, catalase, and glutathione peroxidase, and ability to inhibit hydroxyl radical, and glutathione hormone content were significantly decreased (p < 0.05 or p < 0.01) mainly in 45 and 60 mg/kg groups in comparison with those of control group. However, the abovementioned oxidative stress parameters were not significantly changed (p > 0.05) in 5 and 15 mg/kg groups. It was concluded that dietary vanadium in excess of 30 mg/kg could cause obvious oxidative stress in the intestinal mucosa, which could impact the antioxidant function of intestinal tract in broilers.

  15. Driving-induced stress in urban college students.

    PubMed

    Rasmussen, C; Knapp, T J; Garner, L

    2000-04-01

    Urban college student commuters (N = 407) were surveyed about their experiences with stress induced by driving. Of the participants 23.6% reported becoming angry at another driver more than once per day. They rated stress from other drivers as equal to the stress experienced during a college examination but gave slightly lower ratings to traffic congestion, road construction, and finding a parking place as sources of stress. Slow drivers, a child not restrained, and a vehicle following too closely were the highest rated annoying situations. Of participants, 21.6% had reported another driver to the police; nearly 22% said they carried a weapon for protection from other drivers (5.4% said a gun). Men were more than twice as likely as women to carry a weapon and three times as likely to carry a gun. Of the total sample, 19.1% feared being shot by another driver. Most participants (75.8%) said drivers were more aggressive and dangerous than they were five years ago. PMID:10833736

  16. Mepiquat chloride

    Integrated Risk Information System (IRIS)

    Mepiquat chloride ; CASRN 24307 - 26 - 4 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogen

  17. Methyl chloride

    Integrated Risk Information System (IRIS)

    Methyl chloride ; CASRN 74 - 87 - 3 ( 07 / 17 / 2001 ) Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for

  18. Ethyl chloride

    Integrated Risk Information System (IRIS)

    Ethyl chloride ; CASRN 75 - 00 - 3 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Eff

  19. Benzyl chloride

    Integrated Risk Information System (IRIS)

    Benzyl chloride ; CASRN 100 - 44 - 7 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic E

  20. Vinyl chloride

    Integrated Risk Information System (IRIS)

    Vinyl chloride ; CASRN 75 - 01 - 4 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Eff

  1. Acetyl chloride

    Integrated Risk Information System (IRIS)

    Acetyl chloride ; CASRN 75 - 36 - 5 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Ef

  2. Hydrogen chloride

    Integrated Risk Information System (IRIS)

    Hydrogen chloride ; CASRN 7647 - 01 - 0 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogeni

  3. Allyl chloride

    Integrated Risk Information System (IRIS)

    Allyl chloride ; CASRN 107 - 05 - 1 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I ( Health Hazard Assessments for Noncarcinogenic Ef

  4. Brain most susceptible to cadmium induced oxidative stress in mice.

    PubMed

    Agnihotri, Sandeep K; Agrawal, Usha; Ghosh, Ilora

    2015-04-01

    Accumulated evidence over the years indicate that cadmium (Cd) may be a possible etiological factor for neurodegenerative diseases. This may possibly be linked to excessive generation of free radicals that damages the organs in the body depending on their defence mechanism. Since Cd is a toxic agent that affect several cell types, the aim of this study was to shed light on the effect of Cd and its consequences on different organs of the mice body. To test the hypothesis of concentration dependent Reactive Oxygen Species (ROS) generation and DNA damage, observations were done in the serum of 4-5 weeks old male Swiss albino mice by treating with cadmium chloride (CdCl2) in drinking water for 30 days. The expression of Bcl-2-associated X protein (Bax) an apoptotic marker protein was two times higher in brain compared to liver at an exposure level of 0.5mgL(-1) CdCl2. Furthermore the correlation and linkage data analysis of antioxidant defence system revealed a rapid alteration in the brain, compared to any other organs considered in this study. We report that even at low dose of Cd, it impaired the brain due to lipid peroxidase sensitivity which favoured the Cd-induced oxidative injury in the brain.

  5. Asbestos-induced disruption of calcium homeostasis induces endoplasmic reticulum stress in macrophages.

    PubMed

    Ryan, Alan J; Larson-Casey, Jennifer L; He, Chao; Murthy, Shuhba; Carter, A Brent

    2014-11-28

    Although the mechanisms for fibrosis development remain largely unknown, recent evidence indicates that endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) may act as an important fibrotic stimulus in diseased lungs. ER stress is observed in lungs of patients with idiopathic pulmonary fibrosis. In this study we evaluated if ER stress and the UPR was present in macrophages exposed to chrysotile asbestos and if ER stress in macrophages was associated with asbestos-induced pulmonary fibrosis. Macrophages exposed to chrysotile had elevated transcript levels of several ER stress genes. Macrophages loaded with the Ca(2+)-sensitive dye Fura2-AM showed that cytosolic Ca(2+) increased significantly within minutes after chrysotile exposure and remained elevated for a prolonged time. Chrysotile-induced increases in cytosolic Ca(2+) were partially inhibited by either anisomycin, an inhibitor of passive Ca(2+) leak from the ER, or 1,2-bis(2-aminophenoxyl)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator known to deplete ER Ca(2+) stores. Anisomycin inhibited X-box-binding protein 1 (XBP1) mRNA splicing and reduced immunoglobulin-binding protein (BiP) levels, whereas BAPTA-AM increased XBP1 splicing and BiP expression, suggesting that ER calcium depletion may be one factor contributing to ER stress in cells exposed to chrysotile. To evaluate ER stress in vivo, asbestos-exposed mice showed fibrosis development, and alveolar macrophages from fibrotic mice showed increased expression of BiP. Bronchoalveolar macrophages from asbestosis patients showed increased expression of several ER stress genes compared with normal subjects. These findings suggest that alveolar macrophages undergo ER stress, which is associated with fibrosis development.

  6. Senescence-Induced Oxidative Stress Causes Endothelial Dysfunction.

    PubMed

    Bhayadia, Raj; Schmidt, Bernhard M W; Melk, Anette; Hömme, Meike

    2016-02-01

    Age is a risk factor for cardiovascular disease, suggesting a causal relationship between age-related changes and vascular damage. Endothelial dysfunction is an early pathophysiological hallmark in the development of cardiovascular disease. Senescence, the cellular equivalent of aging, was proposed to be involved in endothelial dysfunction, but functional data showing a causal relationship are missing.Endothelium-dependent vasodilation was measured in aortic rings ex vivo. We investigated aortas from aged C57Bl/6 mice (24-28 months), in which p16 (INK4a) and p19 (ARF) expression, markers of stress-induced senescence, were significantly induced compared to young controls (4-6 months). To reflect telomere shortening in human aging, we investigated aortas from telomerase deficient (Terc(-/-)) mice of generation 3 (G3). Endothelium-dependent vasodilation in aged wildtype and in Terc(-/-) G3 mice was impaired. A combination of the superoxide dismutase mimetic 1-Oxyl-2,2,6, 6-tetramethyl-4-hydroxypiperidine (TEMPOL) and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin significantly improved endothelium-dependent vasodilation in aged wildtype and Terc(-/-) G3 mice compared to untreated controls. We show that both, aging and senescence induced by telomere shortening, cause endothelial dysfunction that can be restored by antioxidants, indicating a role for oxidative stress. The observation that cellular senescence is a direct signalling event leading to endothelial dysfunction holds the potential to develop new targets for the prevention of cardiovascular disease.

  7. Hypoxia inducible factors and the response to hypoxic stress

    PubMed Central

    Majmundar, Amar J.; Wong, Waihay J.; Simon, M. Celeste

    2011-01-01

    Oxygen (O2) is an essential nutrient that serves as a key substrate in cellular metabolism and bioenergetics. In a variety of physiological and pathological states, organisms encounter insufficient O2 availability, or hypoxia. In order to cope with this stress, evolutionarily conserved responses are engaged. In mammals, the primary transcriptional response to hypoxic stress is mediated by the Hypoxia-inducible factors (HIFs). While canonically regulated by prolyl hydroxylase domain-containing enzymes (PHDs), the HIFα subunits are intricately responsive to numerous other factors including Factor Inhibiting HIF-1α (FIH1), sirtuins, and metabolites. These transcription factors function in normal tissue homeostasis and impinge on critical aspects of disease progression and recovery. Insights from basic HIF biology are being translated into pharmaceuticals targeting the HIF pathway. PMID:20965423

  8. Differential sensitivity to chloride and sodium ions in seedlings of Glycine max and G. soja under NaCl stress.

    PubMed

    Luo, Qingyun; Yu, Bingjun; Liu, Youliang

    2005-09-01

    High Na+ and Cl- concentrations in soil cause hyperionic and hyperosmotic stress effects, the consequence of which can be plant demise. Ion-specific stress effects of Na+ and Cl- on seedlings of cultivated (Glycine max (L.) Merr) and wild soybean (Glycine soja Sieb. Et Zucc.) were evaluated and compared in isoosmotic solutions of Cl-, Na+ and NaCl. Results showed that under NaCl stress, Cl- was more toxic than Na+ to seedlings of G. max. Injury of six G. max cultivars, including 'Jackson' (salt sensitive) and 'Lee 68' (salt tolerant), was positively correlated with the content of Cl- in the leaves, and negatively with that in the roots. In subsequent research, seedlings of two G. max cultivars (salt-tolerant Nannong 1138-2, and salt-sensitive Zhongzihuangdou-yi) and two G. soja populations (BB52 and N23232) were subjected to isoosmotic solutions of 150mM Na+, Cl- and NaCl, respectively. G. max cv. Nannong 1138-2 and Zhongzihuangdou-yi were damaged much more heavily in the solution of Cl- than in that of Na+. Their Leaves were found to be more sensitive to Cl- than to Na+, and salt tolerance of these two G. max cultivars was mainly due to successful withholding of Cl- in the roots and stems to decrease its content in the leaves. The reverse response to isoosmotic stress of 150 mM Na+ and Cl- was shown in G. soja populations of BB52 and N23232; their leaves were not as susceptible to toxicity of Cl- as that of Na+. Salt tolerance of BB52 and N23232 was mainly due to successful withholding of Na+ in the roots and stems to decrease its content in the leaves. These results indicate that G. soja have advantages over G. max in those traits associated with the mechanism of Cl-tolerance, such as its withholding in roots and vacuoles of leaves. It is possible to use G. soja to improve the salt tolerance of G. max.

  9. Hyperoside Induces Endogenous Antioxidant System to Alleviate Oxidative Stress

    PubMed Central

    Park, Ji Young; Han, Xia; Piao, Mei Jing; Oh, Min Chang; Fernando, Pattage Madushan Dilhara Jayatissa; Kang, Kyoung Ah; Ryu, Yea Seong; Jung, Uhee; Kim, In Gyu; Hyun, Jin Won

    2016-01-01

    Background: Hyperoside, a flavonoid which is mainly found in Hypericum perforatum L., has many biological effects. One of the most important effects is to prevent the oxidative stress induced by reactive oxygen species. However, the molecular mechanisms underlying its effect are not fully understood. Oxidative stress is implicated in the occurrence of various physical diseases. A wide array of enzymatic antioxidant defense systems include NADH: quinone oxidoreductase 1, superoxide dismutase, and heme oxygenase-1 (HO-1). In the present study, the protective effects of hyperoside against hydrogen peroxide-induced oxidative stress in human lens epithelial cells, HLE-B3, were investigated in terms of HO-1 induction. Methods: The protein and mRNA expressions of HO-1 were examined by Western blotting and reverse transcriptase-PCR assays, respectively. To evaluate the ability of hyperoside to activate nuclear factor erythroid 2-related factor 2 (Nrf2), Western blotting and electrophoretic mobility shift assay were performed with nuclear extracts prepared from HLE-B3 cells treated with hyperoside. The activation of extracellular signal-regulated kinase (ERK), the upstream kinase of Nrf2 signaling, was monitored by Western blot analysis. The protective effect of hyperoside in HLE-B3 cells against hydrogen peroxide was performed by MTT assay. Results: Hyperoside increased both the mRNA and protein expression of HO-1 in a time- and dose-dependent manner. In addition, hyperoside elevated the level of of Nrf2 and its antioxidant response element-binding activity, which was modulated by upstream of ERK. Moreover, it activated ERK and restored cell viability which was decreased by hydrogen peroxide. Conclusions: Hyperoside is an effective compound to protect cells against oxidative stress via HO-1 induction. PMID:27051648

  10. Therapeutic Effects of Sodium Hyaluronate on Ocular Surface Damage Induced by Benzalkonium Chloride Preserved Anti-glaucoma Medications

    PubMed Central

    Liu, Xing; Yu, Fen-Fen; Zhong, Yi-Min; Guo, Xin-Xing; Mao, Zhen

    2015-01-01

    Background: Long-term use of benzalkonium chloride (BAC)-preserved drugs is often associated with ocular surface toxicity. Ocular surface symptoms had a substantial impact on the glaucoma patients’ quality of life and compliance. This study aimed to investigate the effects of sodium hyaluronate (SH) on ocular surface toxicity induced by BAC-preserved anti-glaucoma medications treatment. Methods: Fifty-eight patients (101 eyes), who received topical BAC-preserved anti-glaucoma medications treatment and met the severe dry eye criteria, were included in the analysis. All patients were maintained the original topical anti-glaucoma treatment. In the SH-treated group (56 eyes), unpreserved 0.3% SH eye drops were administered with 3 times daily for 90 days. In the control group (55 eyes), phosphate-buffered saline were administered with 3 times daily for 90 days. Ocular Surface Disease Index (OSDI) questionnaire, break-up time (BUT) test, corneal fluorescein staining, corneal and conjunctival rose Bengal staining, Schirmer test, and conjunctiva impression cytology were performed sequentially on days 0 and 91. Results: Compared with the control group, SH-treated group showed decrease in OSDI scores (Kruskal-Wallis test: H = 38.668, P < 0.001), fluorescein and rose Bengal scores (Wilcoxon signed-ranks test: z = −3.843, P < 0.001, and z = −3.508, P < 0.001, respectively), increase in tear film BUT (t-test: t = −10.994, P < 0.001) and aqueous tear production (t-test: t = −10.328, P < 0.001) on day 91. The goblet cell density was increased (t-test: t = −9.981, P < 0.001), and the morphology of the conjunctival epithelium were also improved after SH treatment. Conclusions: SH significantly improved both symptoms and signs of ocular surface damage in patients with BAC-preserved anti-glaucoma medications treatment. SH could be proposed as a new attempt to reduce ocular surface toxicity, and alleviate symptoms of ocular surface damage in BAC-preserved anti

  11. A redox-silent analogue of tocotrienol inhibits cobalt(II) chloride-induced VEGF expression via Yes signaling in mesothelioma cells.

    PubMed

    Sato, Ayami; Virgona, Nantiga; Ando, Akira; Ota, Masako; Yano, Tomohiro

    2014-01-01

    Vascular endothelial growth factor (VEGF) plays a crucial role in tumor angiogenesis and represents an attractive anticancer target. We have previously demonstrated that a redox-silent analogue of α-tocotrienol, 6-O-carboxypropyl-α-tocotrienol (T3E) exhibits potent anti-carcinogenic property in human malignant mesothelioma (MM) cells. However, inhibition of tumor growth by targeting VEGF pathway remains undetermined. In this study, we explored the inhibitory effect of T3E on the paracrine secretion of VEGF in MM cells under mimicked hypoxia by cobalt chloride (CoCl2). In this study we examine whether T3E can suppress the secretion of VEGF in MM cells exposed to mimic hypoxia by cobalt chloride (CoCl2). We found that CoCl2-induced hypoxia treatment leads to increased up-regulated hypoxia-inducible factor-2α (HIF-2α) and subsequently induced the secretion of VEGF in MM cells. This up-regulation activation mainly depended on the activation of Yes, a member of the Src family of kinases. Treatment of hypoxic MM cells with T3E effectively inhibited the secretion of VEGF, On the other hand, T3E inhibited CoCl2-induced gene expression of VEGF due to the inactivation of Yes/HIF-2α signaling. These data suggest that Yes/HIF2-α/VEGF could be a promising therapeutic target of T3E in MM cells.

  12. Che-1-induced inhibition of mTOR pathway enables stress-induced autophagy

    PubMed Central

    Desantis, Agata; Bruno, Tiziana; Catena, Valeria; De Nicola, Francesca; Goeman, Frauke; Iezzi, Simona; Sorino, Cristina; Ponzoni, Maurilio; Bossi, Gianluca; Federico, Vincenzo; La Rosa, Francesca; Ricciardi, Maria Rosaria; Lesma, Elena; De Meo, Paolo D'Onorio; Castrignanò, Tiziana; Petrucci, Maria Teresa; Pisani, Francesco; Chesi, Marta; Bergsagel, P Leif; Floridi, Aristide; Tonon, Giovanni; Passananti, Claudio; Blandino, Giovanni; Fanciulli, Maurizio

    2015-01-01

    Mammalian target of rapamycin (mTOR) is a key protein kinase that regulates cell growth, metabolism, and autophagy to maintain cellular homeostasis. Its activity is inhibited by adverse conditions, including nutrient limitation, hypoxia, and DNA damage. In this study, we demonstrate that Che-1, a RNA polymerase II-binding protein activated by the DNA damage response, inhibits mTOR activity in response to stress conditions. We found that, under stress, Che-1 induces the expression of two important mTOR inhibitors, Redd1 and Deptor, and that this activity is required for sustaining stress-induced autophagy. Strikingly, Che-1 expression correlates with the progression of multiple myeloma and is required for cell growth and survival, a malignancy characterized by high autophagy response. PMID:25770584

  13. Secondhand smoke exposure induces acutely airway acidification and oxidative stress.

    PubMed

    Kostikas, Konstantinos; Minas, Markos; Nikolaou, Eftychia; Papaioannou, Andriana I; Liakos, Panagiotis; Gougoura, Sofia; Gourgoulianis, Konstantinos I; Dinas, Petros C; Metsios, Giorgos S; Jamurtas, Athanasios Z; Flouris, Andreas D; Koutedakis, Yiannis

    2013-02-01

    Previous studies have shown that secondhand smoke induces lung function impairment and increases proinflammatory cytokines. The aim of the present study was to evaluate the acute effects of secondhand smoke on airway acidification and airway oxidative stress in never-smokers. In a randomized controlled cross-over trial, 18 young healthy never-smokers were assessed at baseline and 0, 30, 60, 120, 180 and 240 min after one-hour secondhand smoke exposure at bar/restaurant levels. Exhaled NO and CO measurements, exhaled breath condensate collection (for pH, H(2)O(2) and NO(2)(-)/NO(3)(-) measurements) and spirometry were performed at all time-points. Secondhand smoke exposure induced increases in serum cotinine and exhaled CO that persisted until 240 min. Exhaled breath condensate pH decreased immediately after exposure (p < 0.001) and returned to baseline by 180 min, whereas H(2)O(2) increased at 120 min and remained increased at 240 min (p = 0.001). No changes in exhaled NO and NO(2)/NO(3) were observed, while decreases in FEV(1) (p < 0.001) and FEV(1)/FVC (p < 0.001) were observed after exposure and returned to baseline by 180 min. A 1-h exposure to secondhand smoke induced airway acidification and increased airway oxidative stress, accompanied by significant impairment of lung function. Despite the reversal in EBC pH and lung function, airway oxidative stress remained increased 4 h after the exposure. Clinical trial registration number (EudraCT): 2009-013545-28.

  14. Stress-Induced Antinociception in Fish Reversed by Naloxone

    PubMed Central

    Wolkers, Carla Patrícia Bejo; Barbosa Junior, Augusto; Menescal-de-Oliveira, Leda; Hoffmann, Anette

    2013-01-01

    Pain perception in non-mammalian vertebrates such as fish is a controversial issue. We demonstrate that, in the fish Leporinus macrocephalus, an imposed restraint can modulate the behavioral response to a noxious stimulus, specifically the subcutaneous injection of 3% formaldehyde. In the first experiment, formaldehyde was applied immediately after 3 or 5 min of the restraint. Inhibition of the increase in locomotor activity in response to formaldehyde was observed, which suggests a possible restraint-induced antinociception. In the second experiment, the noxious stimulus was applied 0, 5, 10 and 15 min after the restraint, and both 3 and 5 min of restraint promoted short-term antinociception of approximately 5 min. In experiments 3 and 4, an intraperitoneal injection of naloxone (30 mg.kg−1) was administered 30 min prior to the restraint. The 3- minute restraint-induced antinociception was blocked by pretreatment with naloxone, but the corresponding 5-minute response was not. One possible explanation for this result is that an opioid and a non-preferential μ–opioid and/or non-opioid mechanism participate in this response modulation. Furthermore, we observed that both the 3- and 5- minutes restraint were severely stressful events for the organism, promoting marked increases in serum cortisol levels. These data indicate that the response to a noxious stimulus can be modulated by an environmental stressor in fish, as is the case in mammals. To our knowledge, this study is the first evidence for the existence of an endogenous antinociceptive system that is activated by an acute standardized stress in fish. Additionally, it characterizes the antinociceptive response induced by stress in terms of its time course and the opioid mediation, providing information for understanding the evolution of nociception modulation. PMID:23936261

  15. Addition lens alleviates reading-induced ocular stress.

    PubMed

    Choy, Camus K; Siu, Andrew W; Lam, Frankie Y; Tse, Jesse T; Lau, Sylvania Y

    2000-01-01

    BACKGROUND: Near tasks have been associated with binocular stress to induce myopia. The aim of this study was to investigate the effects of accommodation on reading-induced near heterophoria. METHODS: We measured the near heterophoria of 22 young adults before and after 30 minutes of reading. The reading task comprised a column of local English newsletter studied monocularly at 33 cm. One of three addition lenses (that is, 0.00 D, +1.50 D and +3.00 D) was randomly incorporated into the optical prescription. The difference in near heterophoria between the pre- and post-reading task was recorded. The experiment was completed on separate days for the other lens powers. RESULTS: Reading for 30 minutes with a plano lens addition (control) increased the near heterophoria by 3.81 +/- 0.95 prism dioptres (SEM) toward exo-deviation (p < 0.002). Addition of a +3.00 D lens significantly decreased the reading-induced exophoric shift to 1.36 +/- 0.55 prism dioptres (SEM). Similarly, a +1.50 D lens reduced the exophoric shift to 3.14 +/- 0.85 prism dioptres (SEM) but the difference was not statistically significant when compared with the control. CONCLUSIONS: The results showed that close work might cause eye strain via the extraocular muscles. Incorporation of plus lens into the optical correction caused a power-dependent reduction in the stress, that is, smaller exophoric shift. Whether binocular stress contributes to myopia and its response to addition lens therapy deserve further investigation.

  16. Melatonin Attenuates Noise Stress-induced Gastrointestinal Motility Disorder and Gastric Stress Ulcer: Role of Gastrointestinal Hormones and Oxidative Stress in Rats

    PubMed Central

    Zhang, Lei; Gong, Ji T; Zhang, Hu Q; Song, Quan H; Xu, Guang H; Cai, Lei; Tang, Xiao D; Zhang, Hai F; Liu, Fang-E; Jia, Zhan S; Zhang, Hong W

    2015-01-01

    Background/Aims There are increasing evidences for gastrointestinal motility disorder (GIMD) and gastric stress ulcer induced by noise stress. The present study was to investigate the reversed effect of melatonin on GIMD and gastric stress ulcer induced by noise stress and potential mechanism. Methods Noise stress was induced on rats, and melatonin (15 mg/kg) was administered to rats by intraperitoneal injection. Differences were assessed in gastric residual rate (GRR), small intestine propulsion rate (SPR), Guth injury score, cortisol, gastrointestinal hormones (calcitonin-gene-related peptide and motilin) and oxidative stress markers (superoxide dismutase and malondialde hyde) in blood plasma as well as gastric mucosa homogenate with or without melatonin. The pathological examination of gastric mucosa was also performed. Results The GRR and SPR were improved by noise stress compared with control (P < 0.05). The pathological examination and Guth injury score revealed gastric stress ulcer. Moreover, the levels of cortisol, motilin and malondialdehyde in blood plasma and malondialdehyde in gastric mucosa homogenate were increased by noise stress (P < 0.05). CGRP and superoxide dismutase activity in both of blood plasma and gastric mucosa homogenate were significantly decreased (P< 0.05). Furthermore, melatonin reversed changes in GRR, SPR, pathological examination, Guth injury score, cortisol, motilin, CGRP, superoxide dismutase activity and malondialdehyde (P < 0.05). Conclusions Melatonin is effective in reversing the GIMD and gastric stress ulcer induced by noise stress. The underlying mechanism may be involved in oxidative stress and gastrointestinal hormones. PMID:25537679

  17. Laser-induced stress transients: aqueous pores of membranes

    NASA Astrophysics Data System (ADS)

    Flotte, Thomas J.; Lee, Shun; Zhang, Hong; McAuliffe, Daniel J., Sr.; Taitelbaum, Jeremy; Doukas, Apostolos G.

    1996-05-01

    Lasers can be used to enhance the delivery of a number of molecules. The model that best fits our data is for the formation of aqueous pores. These pores are present for up to 80 seconds. Our experiments have shown that laser-induced stress transients can be utilized as a vector for intracellular delivery of molecules that may or may not normally cross the cell membrane. These two conditions have been tested with Photofrin and DNA. This technology may have applications in cell and molecular biology, cancer therapy, gene therapy, and others.

  18. Advances in metal-induced oxidative stress and human disease.

    PubMed

    Jomova, Klaudia; Valko, Marian

    2011-05-10

    Detailed studies in the past two decades have shown that redox active metals like iron (Fe), copper (Cu), chromium (Cr), cobalt (Co) and other metals undergo redox cycling reactions and possess the ability to produce reactive radicals such as superoxide anion radical and nitric oxide in biological systems. Disruption of metal ion homeostasis may lead to oxidative stress, a state where increased formation of reactive oxygen species (ROS) overwhelms body antioxidant protection and subsequently induces DNA damage, lipid peroxidation, protein modification and other effects, all symptomatic for numerous diseases, involving cancer, cardiovascular disease, diabetes, atherosclerosis, neurological disorders (Alzheimer's disease, Parkinson's disease), chronic inflammation and others. The underlying mechanism of action for all these metals involves formation of the superoxide radical, hydroxyl radical (mainly via Fenton reaction) and other ROS, finally producing mutagenic and carcinogenic malondialdehyde (MDA), 4-hydroxynonenal (HNE) and other exocyclic DNA adducts. On the other hand, the redox inactive metals, such as cadmium (Cd), arsenic (As) and lead (Pb) show their toxic effects via bonding to sulphydryl groups of proteins and depletion of glutathione. Interestingly, for arsenic an alternative mechanism of action based on the formation of hydrogen peroxide under physiological conditions has been proposed. A special position among metals is occupied by the redox inert metal zinc (Zn). Zn is an essential component of numerous proteins involved in the defense against oxidative stress. It has been shown, that depletion of Zn may enhance DNA damage via impairments of DNA repair mechanisms. In addition, Zn has an impact on the immune system and possesses neuroprotective properties. The mechanism of metal-induced formation of free radicals is tightly influenced by the action of cellular antioxidants. Many low-molecular weight antioxidants (ascorbic acid (vitamin C), alpha

  19. Stress-relief displacements induced by drilling--applications to holographic measurements of in situ stress

    SciTech Connect

    Ahrens, T.J.; Smither, C.L.

    1992-04-24

    The holographic stressmeter is an instrument which has been developed at Caltech to allow determination of the complete stress tensor from in situ borehole measurements. The stressmeter uses double-exposure holographic interferometry to record the displacements induced by the drilling of a small sidehole into the borehole wall. The local stresses, which are the result of the far-field stresses, concentrated at the borehole, cause deformation of the surface of the borehole wall in the vicinity of the sidehole. The first part of this study uses a thin infinite elastic plate subjected to plane stress at infinity to model the displacements at the borehole wall. However, the existence of some holograms which were difficult to model closely led us to examine the validity of this model. In order to investigate the problem further, we performed a two-dimensional finite element analysis for an elastic box with a terminated hole. We varied the dimensions of the hole to see what effect the radius and depth of the hole might have on the displacements. The plate model predicts that the depth of the hole should have no effect on the horizontal components of displacement, but the finite element results show that the magnitude of both components of the displacement depends on the depth of the sidehole. After considering these results, we developed a new model for the analysis of stress-relief displacements, following the work of Youngdahl and Sternberg (1965). For holes with a depth-to-diameter ratio greater than unity, the simple plane stress elastic plate solution breaks down and does not adequately model the displacements at the surface of the body and near the hole. Since these are the areas most critical to calculate accurately with the holographic technique, the revised model does a better job of fitting the observed data.

  20. Chronic mild stress facilitates melanoma tumor growth in mouse lines selected for high and low stress-induced analgesia.

    PubMed

    Ragan, Agnieszka R; Lesniak, Anna; Bochynska-Czyz, Marta; Kosson, Anna; Szymanska, Hanna; Pysniak, Kazimiera; Gajewska, Marta; Lipkowski, Andrzej W; Sacharczuk, Mariusz

    2013-09-01

    Both chronic stress conditions and hyperergic reaction to environmental stress are known to enhance cancer susceptibility. We described two mouse lines that displayed high (HA) and low (LA) swim stress-induced analgesia (SSIA) to investigate the relationship between inherited differences in sensitivity to stress and proneness to an increased growth rate of subcutaneously inoculated melanoma. These lines display several genetic and physiological differences, among which distinct sensitivity to mutagens and susceptibility to cancer are especially noticeable. High analgesic mice display high proneness both to stress and a rapid local spread of B16F0 melanoma. However, stress-resistant LA mice do not develop melanoma tumors after inoculation, or if so, tumors regress spontaneously. We found that the chronic mild stress (CMS) procedure leads to enhanced interlinear differences in melanoma susceptibility. Tumors developed faster in stress conditions in both lines. However, LA mice still displayed a tendency for spontaneous regression, and 50% of LA mice did not develop a tumor, even under stressed conditions. Moreover, we showed that chronic stress, but not tumor progression, induces depressive behavior, which may be an important clue in cancer therapy. Our results clearly indicate how the interaction between genetic susceptibility to stress and environmental stress determine the risk and progression of melanoma. To our knowledge, HA/LA mouse lines are the first animal models of distinct melanoma progression mediated by inherited differences in stress reactivity.

  1. ER stress and ER stress-induced apoptosis are activated in gastric SMCs in diabetic rats

    PubMed Central

    Chen, Xia; Fu, Xiang-Sheng; Li, Chang-Ping; Zhao, Hong-Xian

    2014-01-01

    AIM: To investigate the gastric muscle injury caused by endoplasmic reticulum (ER) stress in rats with diabetic gastroparesis. METHODS: Forty rats were randomly divided into two groups: a control group and a diabetic group. Diabetes was induced by intraperitoneal injection of 60 mg/kg of streptozotocin. Gastric emptying was determined at the 4th and 12th week. The ultrastructural changes in gastric smooth muscle cells (SMCs) were investigated by transmission electron microscopy. TdT-mediated dUTP nick end labeling (TUNEL) assay was performed to assess apoptosis of SMCs. Expression of the ER stress marker, glucose-regulated protein 78 (GRP78), and the ER-specific apoptosis mediator, caspase-12 protein, was determined by immunohistochemistry. RESULTS: Gastric emptying was significantly lower in the diabetic rats than in the control rats at the 12th wk (40.71% ± 2.50%, control rats vs 54.65% ± 5.22%, diabetic rats; P < 0.05). Swollen and distended ER with an irregular shape was observed in gastric SMCs in diabetic rats. Apoptosis of gastric SMCs increased in the diabetic rats in addition to increased expression of GRP78 and caspase-12 proteins. CONCLUSION: ER stress and ER stress-mediated apoptosis are activated in gastric SMCs in diabetic rats with gastroparesis. PMID:25009401

  2. Hyperglycemia-induced diaphragm weakness is mediated by oxidative stress

    PubMed Central

    2014-01-01

    Introduction A major consequence of ICU-acquired weakness (ICUAW) is diaphragm weakness, which prolongs the duration of mechanical ventilation. Hyperglycemia (HG) is a risk factor for ICUAW. However, the mechanisms underlying HG-induced respiratory muscle weakness are not known. Excessive reactive oxygen species (ROS) injure multiple tissues during HG, but only one study suggests that excessive ROS generation may be linked to HG-induced diaphragm weakness. We hypothesized that HG-induced diaphragm dysfunction is mediated by excessive superoxide generation and that administration of a specific superoxide scavenger, polyethylene glycol superoxide dismutase (PEG-SOD), would ameliorate these effects. Methods HG was induced in rats using streptozotocin (60 mg/kg intravenously) and the following groups assessed at two weeks: controls, HG, HG + PEG-SOD (2,000U/kg/d intraperitoneally for seven days), and HG + denatured (dn)PEG-SOD (2000U/kg/d intraperitoneally for seven days). PEG-SOD and dnPEG-SOD were administered on day 8, we measured diaphragm specific force generation in muscle strips, force-pCa relationships in single permeabilized fibers, contractile protein content and indices of oxidative stress. Results HG reduced diaphragm specific force generation, altered single fiber force-pCa relationships, depleted troponin T, and increased oxidative stress. PEG-SOD prevented HG-induced reductions in diaphragm specific force generation (for example 80 Hz force was 26.4 ± 0.9, 15.4 ± 0.9, 24.0 ± 1.5 and 14.9 ± 0.9 N/cm2 for control, HG, HG + PEG-SOD, and HG + dnPEG-SOD groups, respectively, P <0.001). PEG-SOD also restored HG-induced reductions in diaphragm single fiber force generation (for example, Fmax was 182.9 ± 1.8, 85.7 ± 2.0, 148.6 ± 2.4 and 90.9 ± 1.5 kPa in control, HG, HG + PEG-SOD, and HG + dnPEG-SOD groups, respectively, P <0.001). HG-induced troponin T depletion, protein nitrotyrosine formation

  3. Increased Oxidative Stress Induces Apoptosis in Human Cystic Fibrosis Cells

    PubMed Central

    Rottner, Mathilde; Tual-Chalot, Simon; Mostefai, H. Ahmed; Andriantsitohaina, Ramaroson; Freyssinet, Jean-Marie; Martínez, María Carmen

    2011-01-01

    Oxidative stress results in deleterious cell function in pathologies associated with inflammation. Here, we investigated the generation of superoxide anion as well as the anti-oxidant defense systems related to the isoforms of superoxide dismutases (SOD) in cystic fibrosis (CF) cells. Pro-apoptotic agents induced apoptosis in CF but not in control cells that was reduced by treatment with SOD mimetic. These effects were associated with increased superoxide anion production, sensitive to the inhibition of IκB-α phosphorylation, in pancreatic but not tracheal CF cells, and reduced upon inhibition of either mitochondrial complex I or NADPH oxidase. CF cells exhibited reduced expression, but not activity, of both Mn-SOD and Cu/Zn-SOD when compared to control cells. Although, expression of EC-SOD was similar in normal and CF cells, its activity was reduced in CF cells. We provide evidence that high levels of oxidative stress are associated with increased apoptosis in CFTR-mutated cells, the sources being different depending on the cell type. These observations underscore a reduced anti-oxidant defense mechanism, at least in part, via diminished EC-SOD activity and regulation of Cu/Zn-SOD and Mn-SOD expressions. These data point to new therapeutic possibilities in targeting anti-oxidant pathways to reduce oxidative stress and apoptosis in CF cells. PMID:21931865

  4. Stress-induced voiding study in integrated circuit interconnects

    NASA Astrophysics Data System (ADS)

    Hou, Yuejin; Tan, Cher Ming

    2008-07-01

    An analytical equation for an ultralarge-scale integration interconnect lifetime due to stress-induced voiding (SIV) is derived from the energy perspective. It is shown that the SIV lifetime is strongly dependent on the passivation quality at the cap layer/interconnect interface, the confinement effect by the surrounding materials to the interconnects, and the available diffusion paths in the interconnects. Contrary to the traditional power-law creep model, we find that the temperature exponent in SIV lifetime formulation is determined by the available diffusion paths for the interconnect atoms and the interconnect geometries. The critical temperature for the SIV is found to be independent of passivation integrity and dielectric confinement effect. Actual stress-free temperature (SFT) during the SIV process is also found to be different from the dielectric/cap layer deposition temperature or the final annealing temperature of the metallization, and it can be evaluated analytically once the activation energy, temperature exponent and critical temperature are determined experimentally. The smaller actual SFT indicates that a strong stress relaxation occurs before the high temperature storage test. Our results show that our SIV lifetime model can be used to predict the SIV lifetime in nano-interconnects.

  5. Programming stress-induced altruistic death in engineered bacteria

    PubMed Central

    Tanouchi, Yu; Pai, Anand; Buchler, Nicolas E; You, Lingchong

    2012-01-01

    Programmed death is often associated with a bacterial stress response. This behavior appears paradoxical, as it offers no benefit to the individual. This paradox can be explained if the death is ‘altruistic': the killing of some cells can benefit the survivors through release of ‘public goods'. However, the conditions where bacterial programmed death becomes advantageous have not been unambiguously demonstrated experimentally. Here, we determined such conditions by engineering tunable, stress-induced altruistic death in the bacterium Escherichia coli. Using a mathematical model, we predicted the existence of an optimal programmed death rate that maximizes population growth under stress. We further predicted that altruistic death could generate the ‘Eagle effect', a counter-intuitive phenomenon where bacteria appear to grow better when treated with higher antibiotic concentrations. In support of these modeling insights, we experimentally demonstrated both the optimality in programmed death rate and the Eagle effect using our engineered system. Our findings fill a critical conceptual gap in the analysis of the evolution of bacterial programmed death, and have implications for a design of antibiotic treatment. PMID:23169002

  6. Carbofuran-induced oxidative stress in mammalian brain.

    PubMed

    Rai, Devendra K; Sharma, Bechan

    2007-09-01

    Chronic exposure to carbofuran, a carbamate pesticide, via oral administration has been reported to generate reactive oxygen species (ROS) in rat brain. However, information regarding the effect of short-term intraperitoneal (i.p.) carbofuran intoxication on oxidative stress is lacking. In the present study, the effect of carbofuran on oxidative indices in brain of Wistar rats has been determined by exposing the animals to three subacute concentrations (0.2, 0.4 and 0.8 mg/kg body weight) equivalent to 10, 20, and 40%, respectively, of its LD50 (i.p.) for 24 h. Rat liver has been used as a positive control. The results demonstrated that carbofuran treatment at the 3 concentrations tested caused significant increase in lipid peroxidation (LPO) by 12.50, 34.38, and 59.38%, respectively. The increased oxidative stress at same pesticide concentrations significantly induced activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase in rat brain; the impact on catalase being more marked only at high-pesticide doses (0.4 and 0.8 mg/kg body weight). Carbofuran also caused reduction in protein content of rat tissues tested. Rat brain was more severely affected by carbofuran than liver. The results clearly demonstrated that i.p. administration of carbofuran accelerated oxidative stress in rat brain in a dose-dependent manner.

  7. Exercise-Induced Oxidative Stress and Dietary Antioxidants

    PubMed Central

    Yavari, Abbas; Javadi, Maryam; Mirmiran, Parvin; Bahadoran, Zahra

    2015-01-01

    Context: Overproduction of reactive oxygen and nitrogen species during physical exercise, exercise induced oxidative stress and antioxidant supplementation is interesting and controversial concepts that have been considered during the past decades. Evidence Acquisition: In this review, we aimed to summarize current evidence in relation to antioxidant supplementation outcomes during exercise and physical activity. For this aim, we obtained relevant articles through searches of the Medline and PubMed databases between 1980 to 2013. Although major studies have indicated that antioxidants could attenuate biomarkers of exercise-induced oxidative stress and the use of antioxidant supplement is a common phenomenon among athletes and physically active people, there are some doubts regarding the benefits of these. Results: It seems that the best recommendations regarding antioxidants and exercise are having a balanced diet rich in natural antioxidants and phytochemicals. Conclusions: Regular consumption of various fresh fruits and vegetables, whole grains, legumes and beans, sprouts and seeds is an effective and safe way to meet all antioxidant requirements in physically active persons and athletes. PMID:25883776

  8. Countermeasures against space radiation induced oxidative stress in mice.

    PubMed

    Kennedy, A R; Guan, J; Ware, J H

    2007-06-01

    Of particular concern for the health of astronauts during space travel is radiation from protons and high atomic number (Z), high energy particles (HZE particles). Space radiation is known to induce oxidative stress in astronauts after extended space flight. In the present study, the total antioxidant status was used as a biomarker to evaluate oxidative stress induced by proton and HZE particle radiation in the plasma of CBA mice and the protective effect of dietary supplement agents. The results indicate that exposure to proton and HZE particle radiation significantly decreased the plasma level of total antioxidants in the irradiated CBA mice. Dietary supplementation with L: -selenomethionine (SeM) or a combination of selected antioxidant agents (which included SeM) could partially or completely prevent the decrease in the total antioxidant status in the plasma of animals exposed to proton or HZE particle radiation. These findings suggest that exposure to space radiation may compromise the capacity of the host antioxidant defense system; this adverse biological effect can be prevented at least partially by dietary supplementation with agents expected to have effects on antioxidant activities.

  9. The diagnosis and treatment of stress-induced anovulation.

    PubMed

    Berga, S L; Loucks, T L

    2005-02-01

    Behaviors that activate the hypothalamic-pituitary-adrenal (HPA) axis or suppress the hypothalamic-pituitary-thyroidal (HPT) axis can disrupt the hypothalamic-pituitary-gonadal (HPG) axis in women and men. Individuals with functional hypothalamic hypogonadism typically engage in a combination of behaviors that serve as psychogenic stressors and present metabolic challenges. Complete recovery of gonadal function depends upon restoration of the HPA and HPT axes. Hormone replacement strategies have limited benefit because they do not promote recovery from these allostatic endocrine adjustments in the HPA and HPT axes. Indeed, the rationale for the use of sex steroid replacement is based on the erroneous assumption that functional forms of hypothalamic hypogonadism represent only an alteration in the hypothalamic-pituitary-ovarian (HPO) axis. Further, use of sex hormones masks deficits that accrue from altered HPA and HPT function. Long-term deleterious consequences of stress-induced anovulation may include an increased risk of cardiovascular disease, osteoporosis, depression, other psychiatric conditions, and dementia. Although fertility can be restored with exogenous administration of gonadotropins or pulsatile GnRH, fertility management alone will not permit recovery of the HPA and HPT axes. Failure to reverse the hormonal milieu induced by stress may increase the likelihood of poor obstetrical, fetal, or neonatal outcomes. In contrast, behavioral and psychological interventions that address problematic behaviors and attitudes have the potential to permit resumption of ovarian function along with recovery of the HPT and HPA axes. Full endocrine recovery offers better individual, maternal, and child health.

  10. Vitiligo: How do oxidative stress-induced autoantigens trigger autoimmunity?

    PubMed

    Xie, Heng; Zhou, Fubo; Liu, Ling; Zhu, Guannan; Li, Qiang; Li, Chunying; Gao, Tianwen

    2016-01-01

    Vitiligo is a common depigmentation disorder characterized by a loss of functional melanocytes and melanin from epidermis, in which the autoantigens and subsequent autoimmunity caused by oxidative stress play significant roles according to hypotheses. Various factors lead to reactive oxygen species (ROS) overproduction in the melanocytes of vitiligo: the exogenous and endogenous stimuli that cause ROS production, low levels of enzymatic and non-enzymatic antioxidants, disturbed antioxidant pathways and polymorphisms of ROS-associated genes. These factors synergistically contribute to the accumulation of ROS in melanocytes, finally leading to melanocyte damage and the production of autoantigens through the following ways: apoptosis, accumulation of misfolded peptides and cytokines induced by endoplasmic reticulum stress as well as the sustained unfolded protein response, and an 'eat me' signal for phagocytic cells triggered by calreticulin. Subsequently, autoantigens presentation and dendritic cells maturation occurred mediated by the release of antigen-containing exosomes, adenosine triphosphate and melanosomal autophagy. With the involvement of inducible heat shock protein 70, cellular immunity targeting autoantigens takes the essential place in the destruction of melanocytes, which eventually results in vitiligo. Several treatments, such as narrow band ultraviolet, quercetin and α-melanophore-stimulating hormone, are reported to be able to lower ROS thereby achieving repigmentation in vitiligo. In therapies targeting autoimmunity, restore of regulatory T cells is absorbing attention, in which narrow band ultraviolet also plays a role.

  11. Vitiligo: How do oxidative stress-induced autoantigens trigger autoimmunity?

    PubMed

    Xie, Heng; Zhou, Fubo; Liu, Ling; Zhu, Guannan; Li, Qiang; Li, Chunying; Gao, Tianwen

    2016-01-01

    Vitiligo is a common depigmentation disorder characterized by a loss of functional melanocytes and melanin from epidermis, in which the autoantigens and subsequent autoimmunity caused by oxidative stress play significant roles according to hypotheses. Various factors lead to reactive oxygen species (ROS) overproduction in the melanocytes of vitiligo: the exogenous and endogenous stimuli that cause ROS production, low levels of enzymatic and non-enzymatic antioxidants, disturbed antioxidant pathways and polymorphisms of ROS-associated genes. These factors synergistically contribute to the accumulation of ROS in melanocytes, finally leading to melanocyte damage and the production of autoantigens through the following ways: apoptosis, accumulation of misfolded peptides and cytokines induced by endoplasmic reticulum stress as well as the sustained unfolded protein response, and an 'eat me' signal for phagocytic cells triggered by calreticulin. Subsequently, autoantigens presentation and dendritic cells maturation occurred mediated by the release of antigen-containing exosomes, adenosine triphosphate and melanosomal autophagy. With the involvement of inducible heat shock protein 70, cellular immunity targeting autoantigens takes the essential place in the destruction of melanocytes, which eventually results in vitiligo. Several treatments, such as narrow band ultraviolet, quercetin and α-melanophore-stimulating hormone, are reported to be able to lower ROS thereby achieving repigmentation in vitiligo. In therapies targeting autoimmunity, restore of regulatory T cells is absorbing attention, in which narrow band ultraviolet also plays a role. PMID:26387449

  12. Countermeasures against space radiation induced oxidative stress in mice.

    PubMed

    Kennedy, A R; Guan, J; Ware, J H

    2007-06-01

    Of particular concern for the health of astronauts during space travel is radiation from protons and high atomic number (Z), high energy particles (HZE particles). Space radiation is known to induce oxidative stress in astronauts after extended space flight. In the present study, the total antioxidant status was used as a biomarker to evaluate oxidative stress induced by proton and HZE particle radiation in the plasma of CBA mice and the protective effect of dietary supplement agents. The results indicate that exposure to proton and HZE particle radiation significantly decreased the plasma level of total antioxidants in the irradiated CBA mice. Dietary supplementation with L: -selenomethionine (SeM) or a combination of selected antioxidant agents (which included SeM) could partially or completely prevent the decrease in the total antioxidant status in the plasma of animals exposed to proton or HZE particle radiation. These findings suggest that exposure to space radiation may compromise the capacity of the host antioxidant defense system; this adverse biological effect can be prevented at least partially by dietary supplementation with agents expected to have effects on antioxidant activities. PMID:17387501

  13. Assessing Cd-induced stress from plant spectral response

    NASA Astrophysics Data System (ADS)

    Kancheva, Rumiana; Georgiev, Georgi

    2014-10-01

    Remote sensing plays a significant role in local, regional and global monitoring of land covers. Ecological concerns worldwide determine the importance of remote sensing applications for the assessment of soil conditions, vegetation health and identification of stress-induced changes. The extensive industrial growth and intensive agricultural land-use arise the serious ecological problem of environmental pollution associated with the increasing anthropogenic pressure on the environment. Soil contamination is a reason for degradation processes and temporary or permanent decrease of the productive capacity of land. Heavy metals are among the most dangerous pollutants because of their toxicity, persistent nature, easy up-take by plants and long biological half-life. This paper takes as its focus the study of crop species spectral response to Cd pollution. Ground-based experiments were performed, using alfalfa, spring barley and pea grown in Cd contaminated soils and in different hydroponic systems under varying concentrations of the heavy metal. Cd toxicity manifested itself by inhibition of plant growth and synthesis of photosynthetic pigments. Multispectral reflectance, absorbance and transmittance, as well as red and far red fluorescence were measured and examined for their suitability to detect differences in plant condition. Statistical analysis was performed and empirical relationships were established between Cd concentration, plant growth variables and spectral response Various spectral properties proved to be indicators of plant performance and quantitative estimators of the degree of the Cd-induced stress.

  14. Effects of Active Mastication on Chronic Stress-Induced Bone Loss in Mice

    PubMed Central

    Azuma, Kagaku; Furuzawa, Manabu; Fujiwara, Shu; Yamada, Kumiko; Kubo, Kin-ya

    2015-01-01

    Chronic psychologic stress increases corticosterone levels, which decreases bone density. Active mastication or chewing attenuates stress-induced increases in corticosterone. We evaluated whether active mastication attenuates chronic stress-induced bone loss in mice. Male C57BL/6 (B6) mice were randomly divided into control, stress, and stress/chewing groups. Stress was induced by placing mice in a ventilated restraint tube (60 min, 2x/day, 4 weeks). The stress/chewing group was given a wooden stick to chew during the experimental period. Quantitative micro-computed tomography, histologic analysis, and biochemical markers were used to evaluate the bone response. The stress/chewing group exhibited significantly attenuated stress-induced increases in serum corticosterone levels, suppressed bone formation, enhanced bone resorption, and decreased trabecular bone mass in the vertebrae and distal femurs, compared with mice in the stress group. Active mastication during exposure to chronic stress alleviated chronic stress-induced bone density loss in B6 mice. Active mastication during chronic psychologic stress may thus be an effective strategy to prevent and/or treat chronic stress-related osteopenia. PMID:26664256

  15. Genetic damage induced by lead chloride in different tissues of fresh water climbing perch Anabas testudineus (Bloch).

    PubMed

    Ahmed, Md Kawser; Parvin, Elora; Arif, Mohammad; Islam, Md Monirul; Akter, Mosammat Salma; Khan, Mohammad Shahneawz

    2011-11-01

    The present investigation was undertaken to study the induction of DNA damage by lead chloride (PbCl(2)) in freshwater climbing perch Anabas testudineus using alkaline single cell gel electrophoresis (comet assay). Based on the LC(50) values of lead chloride of A. testudineus three different concentrations viz., 0.1, 1.0 and 2.0 mg/L were selected to expose fish. The DNA damage was observed in the gill, kidney and liver tissue as the percentage of DNA in comet tails and comet heads in the tissue of the exposed fish. DNA damage at different concentrations showed sensitivity to particular tissue. The liver tissue exhibited significantly (p < 0.01) higher DNA damage, followed by kidney and gill. However, the DNA damage was found to be dose dependent; at 2 mg/L of PbCl(2) the tail and head DNA of liver tissue were 57.84% and 39.49%, in kidney tissue the values were 52.36% and 44.97% whereas in gill tissue the values were 48.86% and 48.96% respectively. The current study explored the utility of the comet assay for in vivo laboratory studies using A. testudineus species for screening the genotoxic potential of lead chloride.

  16. Catalase activity as a biomarker for mild-stress-induced robustness in Bacillus weihenstephanensis.

    PubMed

    den Besten, Heidy M W; Effraimidou, Styliani; Abee, Tjakko

    2013-01-01

    Microorganisms are able to survive and grow in changing environments by activating stress adaptation mechanisms which may enhance bacterial robustness. Stress-induced enhanced robustness complicates the predictability of microbial inactivation. Using psychrotolerant Bacillus weihenstephanensis strain KBAB4 as a model, we investigated the impact of the culturing temperature on mild-oxidative-stress-induced (cross-)protection toward multiple stresses, including severe oxidative, heat, and acid stresses. Culturing at a refrigeration temperature (7°C) compared to the optimal growth temperature (30°C) affected both the robustness level of B. weihenstephanensis and the oxidative stress adaptive response. Scavengers of reactive oxygen species have a crucial role in adaptation to oxidative stresses, and this points to a possible predictive role in mild-oxidative-stress-induced robustness. Therefore, the catalase activity was determined upon mild oxidative stress treatment and was demonstrated to be significantly correlated with the robustness level of mild-stress-treated cells toward severe oxidative and heat stresses but not toward severe acid stress for cells grown at both refrigeration and optimal temperatures. The quantified correlations supported the predictive quality of catalase activity as a biomarker and also underlined that the predictive quality is stress specific. Biomarkers that are able to predict stress-induced enhanced robustness can be used to better understand stress adaptation mechanisms and might allow the design of effective combinations of hurdles to control microbial behavior.

  17. Potentiation by sevoflurane of the gamma-aminobutyric acid-induced chloride current in acutely dissociated CA1 pyramidal neurones from rat hippocampus.

    PubMed Central

    Wu, J.; Harata, N.; Akaike, N.

    1996-01-01

    1. The effects of a new kind of volatile anaesthetic, sevoflurane (Sev), on gamma-aminobutyric acid (GABA)-gated chloride current (Icl) in single neurones dissociated from the rat hippocampal CA1 area were examined using the nystatin perforated patch recording configuration under the voltage-clamp condition. All drugs were applied with a rapid perfusion system, termed the "Y-tube' method. 2. When the concentrations were higher than 3 x 10(-4) M, Sev, itself, induced an inward current (ISev) at a holding potential (VH) of -40 mV. The concentration-response curve of ISev was bell-shaped, with a suppressed peak and plateau currents at high concentrations (above 2 x 10(-3) M). The reversal potential of ISev (ESev) was close to the theoretical Cl- equilibrium potential, indicating that ISev was carried mainly by Cl-. 3. ISev was reversibly blocked by bicuculline (Bic), an antagonist of the GABAA receptor, in a concentration-dependent manner with a half-inhibitory concentration (IC50) of 7.2 x 10(-7) M. But ISev was insensitive to strychnine (Str), an antagonist of the glycine receptor. 4. At low concentrations (between 3 x 10(-4) and 10(-3) M), Sev markedly enhanced the 10(-6) M GABA induced current (IGABA) but reduced the IGABA with accelerating desensitization accompanied by a "hump' current after washout at high concentrations (higher than 2 x 10(-3) M). 5. Sev, 10(-3) M potentiated the current induced by low concentrations of GABA (between 10(-7) and 3 x 10(-6) M) but reduced the current induced by high concentrations (higher than 10(-5) M) of GABA with a clear acceleration of IGABA desensitization. 6. Sev, like pentobarbitone (PB), pregnanolone (PGN) or diazepam (DZP), potentiated the 10(-6) M GABA-induced response without shifting the reversal potential of IGABA. 7. ISev was augmented by PB, PGN, or DZP at concentrations that maximally potentiated IGABA, suggesting that Sev enhanced IGABA at a binding site distinct from that for PB, PGN, or DZP. 8. It is concluded

  18. The application of neutron diffraction to stress mapping in pipeline steels: Measurement of residual, applied, and defect-induced stresses

    SciTech Connect

    Clapham, L.; Krause, T.W.; Olsen, H.; Atherton, D.L.; Holden, T.M.

    1996-12-31

    Gas pipelines are inspected for defects including generalized corrosion, localized corrosion and environmentally-induced cracking. The most common in-line corrosion inspection tools utilize the magnetic flux leakage (MFL) technique, which is also sensitive to the pipeline stress state. Accurate determination of the residual, applied (bulk) and local defect-induced stresses is therefore essential to understand how stress affects MFL signals. This paper summarizes the results of the following work: (1) Measurement of residual stresses in a section of X70 pipe, using neutron diffraction. (2) Examination with neutron diffraction of the local stresses surrounding a blind (i.e., 50% through-wall) hole defect in the X70 pipe wall section, when the section is subjected to a bending stress in the hoop direction.

  19. Prenatal stress induces a phase advance of circadian corticosterone rhythm in adult rats which is prevented by postnatal stress.

    PubMed

    Koehl, M; Barbazanges, A; Le Moal, M; Maccari, S

    1997-06-13

    Prenatal and postnatal stressors can have different long-term neuroendocrine effects including modifications of stress-induced corticosterone secretion. However, very little is known about the possible long-term effects of prenatal or postnatal stress on the rhythmicity of basal corticosterone secretion in adult offspring. Corticosterone levels were thus determined at six different time points over 24 h in adult rats whose mothers had undergone restraint stress manipulations. The results demonstrate that prenatal stress induces a phase advance in the evening increase of corticosterone levels, and that this change is prevented by postnatal stress. It thus appears that the circadian system governing the HPA axis is modifiable by a prenatal stress, and remains susceptible to compensatory changes during the postnatal period. PMID:9221956

  20. Protective Effects of Carvacrol against Oxidative Stress Induced by Chronic Stress in Rat's Brain, Liver, and Kidney

    PubMed Central

    Samarghandian, Saeed; Farkhondeh, Tahereh; Samini, Fariborz; Borji, Abasalt

    2016-01-01

    Restraint stress may be associated with elevated free radicals, and thus, chronic exposure to oxidative stress may cause tissue damage. Several studies have reported that carvacrol (CAR) has a protective effect against oxidative stress. The present study was designed to investigate the protective effects of CAR on restraint stress induced oxidative stress damage in the brain, liver, and kidney. For chronic restraint stress, rats were kept in the restrainers for 6 h every day, for 21 consecutive days. The animals received systemic administrations of CAR daily for 21 days. To evaluate the changes of the oxidative stress parameters following restraint stress, the levels of malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) activities were measured in the brain, liver, and kidney. In the stressed animals that received vehicle, the MDA level was significantly higher (P < 0.001) and the levels of GSH and antioxidant enzymes were significantly lower than the nonstressed animals (P < 0.001). CAR ameliorated the changes in the stressed animals as compared with the control group (P < 0.001). This study indicates that CAR can prevent restraint stress induced oxidative damage. PMID:26904286

  1. Glacially induced stresses in sedimentary rocks of northern Poland

    NASA Astrophysics Data System (ADS)

    Trzeciak, Maciej; Dąbrowski, Marcin

    2016-04-01

    During the Pleistocene large continental ice sheets developed in Scandinavia and North America. Ice-loading caused bending of the lithosphere and outward flow in the mantle. Glacial loading is one of the most prominent tectono-mechanical event in the geological history of northern Poland. The Pomeranian region was subjected several times to a load equivalent of more than 1 km of rocks, which led to severe increase in both vertical and horizontal stresses in the upper crustal rocks. During deglaciation a rapid decrease in vertical stress is observed, which leads to destabilization of the crust - most recent postglacial faults scarps in northern Sweden indicate glacially induced earthquakes of magnitude ~Mw8. The presence of the ice-sheet altered as well the near-surface thermal structure - thermal gradient inversion is still observable in NW Poland. The glacially related processes might have left an important mark in the sedimentary cover of northern Poland, especially with regard to fracture reopening, changes in stress state, and damage development. In the present study, we model lithospheric bending caused by glacial load, but our point of interest lies in the overlying sediments. Typical glacial isostatic studies model the response of (visco-) elastic lithosphere over viscoelastic or viscous asthenosphere subjected to external loads. In our model, we introduce viscoelastic sedimentary layers at the top of this stack and examine the stress relaxation patterns therein. As a case study for our modelling, we used geological profiles from northern Poland, near locality of Wejherowo, which are considered to have unconventional gas potential. The Paleozoic profile of this area is dominated by almost 1 km thick Silurian-Ordovician shale deposits, which are interbedded with thin and strong limestone layers. This sequence is underlain by Cambrian shales and sandstones, and finally at ~3 km depth - Precambrian crystalline rocks. Above the Silurian there are approximately

  2. Nondestructive Induced Residual Stress Assessment in Superalloy Turbine Engine Components Using Induced Positron Annihilation (IPA)

    SciTech Connect

    Rideout, C. A.; Ritchie, S. J.; Denison, A.

    2007-03-21

    Induced Positron Analysis (IPA) has demonstrated the ability to nondestructively quantify shot peening/surface treatments and relaxation effects in single crystal superalloys, steels, titanium and aluminum with a single measurement as part of a National Science Foundation SBIR program and in projects with commercial companies. IPA measurement of surface treatment effects provides a demonstrated ability to quantitatively measure initial treatment effectiveness along with the effect of operationally induced changes over the life of the treated component. Use of IPA to nondestructively quantify surface and subsurface residual stresses in turbine engine materials and components will lead to improvements in current engineering designs and maintenance procedures.

  3. Molecular Mechanisms of Stress-Induced Myocardial Injury in a Rat Model Simulating Posttraumatic Stress Disorder

    PubMed Central

    Liu, Mi; Xu, Feifei; Tao, Tianqi; Song, Dandan; Li, Dong; Li, Yuzhen; Guo, Yucheng; Liu, Xiuhua

    2016-01-01

    ABSTRACT Objective Posttraumatic stress disorder (PTSD) is an independent risk factor for cardiovascular diseases. This study investigated the molecular mechanisms underlying myocardial injury induced by simulated PTSD. Methods Sprague-Dawley rats were randomly divided into two groups: control group (n = 18) and PTSD group (n = 30). The PTSD model was replicated using the single prolonged stress (SPS) method. On the 14th day poststress, the apoptotic cells in myocardium were assessed using both TUNEL method and transmission electron microscopy; the protein levels of the endoplasmic reticulum stress (ERS) molecules were measured by using Western blotting analysis. Results Exposure to SPS resulted in characteristic morphologic changes of apoptosis in cardiomyocytes assessed by transmission electron microscopy. Moreover, TUNEL staining was also indicative of the elevated apoptosis rate of cardiomyocytes from the SPS rats (30.69% versus 7.26%, p < .001). Simulated PTSD also induced ERS in myocardium, demonstrated by up-regulation of protein levels of glucose-regulated protein 78 (0.64 versus 0.26, p = .017), calreticulin (p = .040), and CCAAT/enhancer-binding protein-homologous protein (0.95 versus 0.43, p = .047), phosphorylation of protein kinase RNA–like ER kinase (p = .003), and caspase 12 activation (0.30 versus 0.06, p < .001) in myocardium from the SPS rats. The ratio of Bcl-2 to Bax decreased significantly in myocardium from the SPS rats (p = .005). Conclusions The ERS-related apoptosis mediated by the protein kinase RNA–like ER kinase/CCAAT/enhancer-binding protein-homologous protein and caspase 12 pathways may be associated with myocardial injury in a rat model simulating PTSD. This study may advance our understanding of how PTSD contributes to myocardial injury on a molecular level. PMID:27359173

  4. Contribution of calcium-activated chloride channel to elevated pulmonary artery pressure in pulmonary arterial hypertension induced by high pulmonary blood flow

    PubMed Central

    Wang, Kai; Chen, Chuansi; Ma, Jianfa; Lao, Jinquan; Pang, Yusheng

    2015-01-01

    The correlation between calcium-activated chloride channel (CaCC) and pulmonary arterial hypertension (PAH) induced by high pulmonary blood flow remains uncertain. In this study, we investigated the possible role and effects of CaCC in this disease. Sixty rats were randomly assigned to normal, sham, and shunt groups. Rats in the shunt group underwent abdominal aorta and inferior vena cava shunt surgery. The pulmonary artery pressure was measured by catheterization. Pathological changes, right ventricle hypertrophy index (RVHI), arterial wall area/vessel area (W/V), and arterial wall thickness/vessel external diameter (T/D) were analyzed by optical microscopy. Electrophysiological characteristics of pulmonary arterial smooth muscle cells (PASMCs) were investigated using patch clamp technology. After 11 weeks of shunting, PAH and pulmonary vascular structural remodeling (PVSR) developed, accompanied by increased pulmonary pressure and pathological interstitial pulmonary changes. Compared with normal and sham groups, pulmonary artery pressure, RVHI, W/V, and T/D of the shunt group rats increased significantly. Electrophysiological results showed primary CaCC characteristics. Compared with normal and sham groups, membrane capacitance and current density of PASMCs in the shunt group increased significantly, which were subsequently attenuated following chloride channel blocker niflumic acid (NFA) treatment. To conclude, CaCC contributed to PAH induced by high pulmonary blood flow and may represent a potential target for treatment of PAH. PMID:25755701

  5. Contribution of calcium-activated chloride channel to elevated pulmonary artery pressure in pulmonary arterial hypertension induced by high pulmonary blood flow.

    PubMed

    Wang, Kai; Chen, Chuansi; Ma, Jianfa; Lao, Jinquan; Pang, Yusheng

    2015-01-01

    The correlation between calcium-activated chloride channel (CaCC) and pulmonary arterial hypertension (PAH) induced by high pulmonary blood flow remains uncertain. In this study, we investigated the possible role and effects of CaCC in this disease. Sixty rats were randomly assigned to normal, sham, and shunt groups. Rats in the shunt group underwent abdominal aorta and inferior vena cava shunt surgery. The pulmonary artery pressure was measured by catheterization. Pathological changes, right ventricle hypertrophy index (RVHI), arterial wall area/vessel area (W/V), and arterial wall thickness/vessel external diameter (T/D) were analyzed by optical microscopy. Electrophysiological characteristics of pulmonary arterial smooth muscle cells (PASMCs) were investigated using patch clamp technology. After 11 weeks of shunting, PAH and pulmonary vascular structural remodeling (PVSR) developed, accompanied by increased pulmonary pressure and pathological interstitial pulmonary changes. Compared with normal and sham groups, pulmonary artery pressure, RVHI, W/V, and T/D of the shunt group rats increased significantly. Electrophysiological results showed primary CaCC characteristics. Compared with normal and sham groups, membrane capacitance and current density of PASMCs in the shunt group increased significantly, which were subsequently attenuated following chloride channel blocker niflumic acid (NFA) treatment. To conclude, CaCC contributed to PAH induced by high pulmonary blood flow and may represent a potential target for treatment of PAH.

  6. High affinity (/sup 3/H). beta. -Alanine uptake by scar margins of ferric chloride-induced epileptogenic foci in rat isocortex

    SciTech Connect

    Robitaille, Y.; Sherwin, A.

    1984-07-01

    Cortical astrocytes of normal mammalian brain are endowed with a high affinity uptake system for ..beta..-Alanine which is competitively inhibited by gamma aminobutyric acid (GABA), a neurotransmitter strongly implicated in epileptogenesis. The authors evaluated (/sup 3/H) ..beta..-Alanine uptake by reactive astrocytes proliferating within scar of epileptogenic foci induced in rat motor cortex by microinjections of 100 mM ferric chloride. Following in vitro incubation of scar tissue with (/sup 3/H) ..beta..-Alanine, ultrastructural morphometry of grain patterns at 5, 30 and 120 days post injection revealed early and significant grain count increases over astroglial processes, predominantly those related to perivascular glial end-feet. Astrocytic cell body and endothelial cell counts showed a more gradual and stepwise increase. Similar data were obtained by comparing visual and edited mean astrocytic grain counts. These results suggest that the enhanced uptake of reactive astrocytes may reflect a marked decrease of inhibitory GABAergic neurons within ferric chloride-induced scars. 7 figures, 1 table.

  7. Physical Exercise Counteracts Stress-induced Upregulation of Melanin-concentrating Hormone in the Brain and Stress-induced Persisting Anxiety-like Behaviors

    PubMed Central

    Kim, Tae-Kyung

    2016-01-01

    Chronic stress induces anxiety disorders, whereas physical exercise is believed to help people with clinical anxiety. In the present study, we investigated the mechanisms underlying stress-induced anxiety and its counteraction by exercise using an established animal model of anxiety. Mice treated with restraint for 2 h daily for 14 days exhibited anxiety-like behaviors, including social and nonsocial behavioral symptoms, and these behavioral impairments lasted for more than 12 weeks after the stress treatment was removed. Despite these lasting behavioral changes, wheel-running exercise treatment for 1 h daily from post-stress days 1 - 21 counteracted anxiety-like behaviors, and these anxiolytic effects of exercise persisted for more than 2 months, suggesting that anxiolytic effects of exercise stably induced. Repeated restraint treatment up-regulated the expression of the neuropeptide, melanin-concentrating hormone (MCH), in the lateral hypothalamus, hippocampus, and basolateral amygdala, the brain regions important for emotional behaviors. In an in vitro study, treatment of HT22 hippocampal cells with glucocorticoid increased MCH expression, suggesting that MCH upregulation can be initially triggered by the stress hormone, corticosterone. In contrast, post-stress treatment with wheel-running exercise reduced the stress-induced increase in MCH expression to control levels in the lateral hypothalamus, hippocampus and basolateral amygdala. Administration of an MCH receptor antagonist (SNAP94847) to stress-treated mice was therapeutic against stress-induced anxiety-like behaviors. These results suggest that repeated stress produces long-lasting anxiety-like behaviors and upregulates MCH in the brain, while exercise counteracts stress-induced MCH expression and persisting anxiety-like behaviors. PMID:27574483

  8. Physical Exercise Counteracts Stress-induced Upregulation of Melanin-concentrating Hormone in the Brain and Stress-induced Persisting Anxiety-like Behaviors.

    PubMed

    Kim, Tae-Kyung; Han, Pyung-Lim

    2016-08-01

    Chronic stress induces anxiety disorders, whereas physical exercise is believed to help people with clinical anxiety. In the present study, we investigated the mechanisms underlying stress-induced anxiety and its counteraction by exercise using an established animal model of anxiety. Mice treated with restraint for 2 h daily for 14 days exhibited anxiety-like behaviors, including social and nonsocial behavioral symptoms, and these behavioral impairments lasted for more than 12 weeks after the stress treatment was removed. Despite these lasting behavioral changes, wheel-running exercise treatment for 1 h daily from post-stress days 1 - 21 counteracted anxiety-like behaviors, and these anxiolytic effects of exercise persisted for more than 2 months, suggesting that anxiolytic effects of exercise stably induced. Repeated restraint treatment up-regulated the expression of the neuropeptide, melanin-concentrating hormone (MCH), in the lateral hypothalamus, hippocampus, and basolateral amygdala, the brain regions important for emotional behaviors. In an in vitro study, treatment of HT22 hippocampal cells with glucocorticoid increased MCH expression, suggesting that MCH upregulation can be initially triggered by the stress hormone, corticosterone. In contrast, post-stress treatment with wheel-running exercise reduced the stress-induced increase in MCH expression to control levels in the lateral hypothalamus, hippocampus and basolateral amygdala. Administration of an MCH receptor antagonist (SNAP94847) to stress-treated mice was therapeutic against stress-induced anxiety-like behaviors. These results suggest that repeated stress produces long-lasting anxiety-like behaviors and upregulates MCH in the brain, while exercise counteracts stress-induced MCH expression and persisting anxiety-like behaviors. PMID:27574483

  9. Physical Exercise Counteracts Stress-induced Upregulation of Melanin-concentrating Hormone in the Brain and Stress-induced Persisting Anxiety-like Behaviors.

    PubMed

    Kim, Tae-Kyung; Han, Pyung-Lim

    2016-08-01

    Chronic stress induces anxiety disorders, whereas physical exercise is believed to help people with clinical anxiety. In the present study, we investigated the mechanisms underlying stress-induced anxiety and its counteraction by exercise using an established animal model of anxiety. Mice treated with restraint for 2 h daily for 14 days exhibited anxiety-like behaviors, including social and nonsocial behavioral symptoms, and these behavioral impairments lasted for more than 12 weeks after the stress treatment was removed. Despite these lasting behavioral changes, wheel-running exercise treatment for 1 h daily from post-stress days 1 - 21 counteracted anxiety-like behaviors, and these anxiolytic effects of exercise persisted for more than 2 months, suggesting that anxiolytic effects of exercise stably induced. Repeated restraint treatment up-regulated the expression of the neuropeptide, melanin-concentrating hormone (MCH), in the lateral hypothalamus, hippocampus, and basolateral amygdala, the brain regions important for emotional behaviors. In an in vitro study, treatment of HT22 hippocampal cells with glucocorticoid increased MCH expression, suggesting that MCH upregulation can be initially triggered by the stress hormone, corticosterone. In contrast, post-stress treatment with wheel-running exercise reduced the stress-induced increase in MCH expression to control levels in the lateral hypothalamus, hippocampus and basolateral amygdala. Administration of an MCH receptor antagonist (SNAP94847) to stress-treated mice was therapeutic against stress-induced anxiety-like behaviors. These results suggest that repeated stress produces long-lasting anxiety-like behaviors and upregulates MCH in the brain, while exercise counteracts stress-induced MCH expression and persisting anxiety-like behaviors.

  10. Laser-induced stress transients: applications for molecular delivery

    NASA Astrophysics Data System (ADS)

    Flotte, Thomas J.; Lee, Shun; Zhang, Hong; McAuliffe, Daniel J.; Douki, Tina; Doukas, Apostolos G.

    1995-05-01

    Lasers can be used to enhance the delivery of a number of molecules. Other investigators have demonstrated local release of molecules from liposomes following laser irradiation, microbeam disruption of the cell membrane to increase cell transport, microbeam ablation of the zona pellucida surrounding the ovum to increase the chances of fertilization, and increased transcutaneous transport following ablation of the stratum corneum. Our experiments have shown that laser-induced stress transients can be utilized as a vector for intracellular delivery of molecules that may or may not normally cross the cell membrane. These two conditions have been tested with Photofrin and DNA. This technology may have applications in cell and molecular biology, cancer therapy, gene therapy, and others.

  11. Thermal diffusion by Brownian-motion-induced fluid stress

    NASA Astrophysics Data System (ADS)

    Kreft, Jennifer; Chen, Yeng-Long

    2007-08-01

    The Ludwig-Soret effect, the migration of a species due to a temperature gradient, has been extensively studied without a complete picture of its cause emerging. Here we investigate the dynamics of DNA and spherical particles subjected to a thermal gradient using a combination of Brownian dynamics and the lattice Boltzmann method. We observe that the DNA molecules will migrate to colder regions of the channel, an observation also made in experiments. In fact, the thermal diffusion coefficient found agrees quantitatively with the experimentally measured value. We also observe that the thermal diffusion coefficient decreases as the radius of the studied spherical particles increases. Furthermore, we observe that the thermal-fluctuation-fluid-momentum-flux coupling induces a gradient in the stress which leads to thermal migration in both systems.

  12. Thermal diffusion by Brownian-motion-induced fluid stress.

    PubMed

    Kreft, Jennifer; Chen, Yeng-Long

    2007-08-01

    The Ludwig-Soret effect, the migration of a species due to a temperature gradient, has been extensively studied without a complete picture of its cause emerging. Here we investigate the dynamics of DNA and spherical particles subjected to a thermal gradient using a combination of Brownian dynamics and the lattice Boltzmann method. We observe that the DNA molecules will migrate to colder regions of the channel, an observation also made in experiments. In fact, the thermal diffusion coefficient found agrees quantitatively with the experimentally measured value. We also observe that the thermal diffusion coefficient decreases as the radius of the studied spherical particles increases. Furthermore, we observe that the thermal-fluctuation-fluid-momentum-flux coupling induces a gradient in the stress which leads to thermal migration in both systems.

  13. RNA methyltransferase NSUN2 promotes stress-induced HUVEC senescence

    PubMed Central

    Tang, Hao; Hu, Han; Pang, Lijun; Xing, Junyue; Liu, Zhenyun; Luo, Yuhong; Jiang, Bin; Liu, Te; Gorospe, Myriam; Chen, Chuan; Wang, Wengong

    2016-01-01

    The tRNA methyltransferase NSUN2 delays replicative senescence by regulating the translation of CDK1 and CDKN1B mRNAs. However, whether NSUN2 influences premature cellular senescence remains untested. Here we show that NSUN2 methylates SHC mRNA in vitro and in cells, thereby enhancing the translation of the three SHC proteins, p66SHC, p52SHC, and p46SHC. Our results further show that the elevation of SHC expression by NSUN2-mediated mRNA methylation increased the levels of ROS, activated p38MAPK, thereby accelerating oxidative stress- and high-glucose-induced senescence of human vascular endothelial cells (HUVEC). Our findings highlight the critical impact of NSUN2-mediated mRNA methylation in promoting premature senescence. PMID:26992231

  14. Intermediate-conductance calcium-activated potassium channel KCa3.1 and chloride channel modulate chemokine ligand (CCL19/CCL21)-induced migration of dendritic cells.

    PubMed

    Shao, Zhifei; Gaurav, Rohit; Agrawal, Devendra K

    2015-07-01

    The role of ion channels is largely unknown in chemokine-induced migration in nonexcitable cells such as dendritic cells (DCs). Here, we examined the role of intermediate-conductance calcium-activated potassium channel (KCa3.1) and chloride channel (CLC3) in lymphatic chemokine-induced migration of DCs. The amplitude and kinetics of chemokine ligand (CCL19/CCL21)-induced Ca(2+) influx were associated with chemokine receptor 7 expression levels, extracellular-free Ca(2+) and Cl(-), and independent of extracellular K(+). Chemokines (CCL19 and CCL21) and KCa3.1 activator (1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) induced plasma membrane hyperpolarization and K(+) efflux, which was blocked by 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole, suggesting that KCa3.1 carried larger conductance than the inward calcium release-activated calcium channel. Blockade of KCa3.1, low Cl(-) in the medium, and low dose of 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS) impaired CCL19/CCL21-induced Ca(2+) influx, cell volume change, and DC migration. High doses of DIDS completely blocked DC migration possibly by significantly disrupting mitochondrial membrane potential. In conclusion, KCa3.1 and CLC3 are critical in human DC migration by synergistically regulating membrane potential, chemokine-induced Ca(2+) influx, and cell volume.

  15. The NFKB Inducing Kinase Modulates Hematopoiesis During Stress.

    PubMed

    González-Murillo, África; Fernández, Lucía; Baena, Sara; Melen, Gustavo J; Sánchez, Rebeca; Sánchez-Valdepeñas, Carmen; Segovia, José C; Liou, Hsiou-Chi; Schmid, Roland; Madero, Luís; Fresno, Manuel; Ramírez, Manuel

    2015-09-01

    The genetic programs that maintain hematopoiesis during steady state in physiologic conditions are different from those activated during stress. Here, we show that hematopoietic stem cells (HSCs) with deficiencies in components of the alternative NFκB pathway (the NFκB inducing kinase, NIK, and the downstream molecule NFκB2) had a defect in response to stressors such as supraphysiological doses of cytokines, chemotherapy, and hematopoietic transplantation. NIK-deficient mice had peripheral blood and bone marrow leukocyte numbers within normal ranges (except for the already reported defects in B-cell maturation); however, HSCs showed significantly slower expansion capacity in in vitro cultures compared to wild-type HSCs. This was due to a delayed cell cycle and increased apoptosis. In vivo experiments showed that NIK-deficient HSCs did not recover at the same pace as controls when challenged with myeloablative chemotherapy. Finally, NIK-deficient HSCs showed a significantly decreased competitive repopulation capacity in vivo. Using HSCs from mice deficient in one of two downstream targets of NIK, that is, either NFκB2 or c-Rel, only NFκB2 deficiency recapitulated the defects detected with NIK-deficient HSCs. Our results underscore the role of NIK and the alternative NFκB pathway for the recovery of normal levels of hematopoiesis after stress.

  16. Oxidative Stress Mediates Radiation Lung Injury by Inducing Apoptosis

    SciTech Connect

    Zhang Yu; Zhang Xiuwu; Rabbani, Zahid N.; Jackson, Isabel L.; Vujaskovic, Zeljko

    2012-06-01

    Purpose: Apoptosis in irradiated normal lung tissue has been observed several weeks after radiation. However, the signaling pathway propagating cell death after radiation remains unknown. Methods and Materials: C57BL/6J mice were irradiated with 15 Gy to the whole thorax. Pro-apoptotic signaling was evaluated 6 weeks after radiation with or without administration of AEOL10150, a potent catalytic scavenger of reactive oxygen and nitrogen species. Results: Apoptosis was observed primarily in type I and type II pneumocytes and endothelium. Apoptosis correlated with increased PTEN expression, inhibition of downstream PI3K/AKT signaling, and increased p53 and Bax protein levels. Transforming growth factor-{beta}1, Nox4, and oxidative stress were also increased 6 weeks after radiation. Therapeutic administration of AEOL10150 suppressed pro-apoptotic signaling and dramatically reduced the number of apoptotic cells. Conclusion: Increased PTEN signaling after radiation results in apoptosis of lung parenchymal cells. We hypothesize that upregulation of PTEN is influenced by Nox4-derived oxidative stress. To our knowledge, this is the first study to highlight the role of PTEN in radiation-induced pulmonary toxicity.

  17. Biotic and abiotic stress can induce cystatin expression in chestnut.

    PubMed

    Pernas, M; Sánchez-Monge, R; Salcedo, G

    2000-02-11

    A cysteine proteinase inhibitor (cystatin) from chestnut (Castanea sativa) seeds, designated CsC, has been previously characterized. Its antifungal, acaricide and inhibitory activities have allowed to involve CsC in defence mechanisms. The CsC transcription levels decreased during seed maturation and increased throughout germination, an opposite behavior to that shown by most phytocystatins. No inhibition of endogenous proteinase activity by purified CsC was found during the seed maturation or germination processes. CsC message accumulation was induced in chestnut leaves after fungal infection, as well as by wounding and jasmonic acid treatment. Induction in roots was also observed by the last two treatments. Furthermore, CsC transcript levels strongly raised, both in roots and leaves, when chestnut plantlets were subjected to cold- and saline-shocks, and also in roots by heat stress. All together, these data suggest that chestnut cystatin is not only involved in defence responses to pests and pathogen invasion, but also in those related to abiotic stress.

  18. Dopamine alleviates salt-induced stress in Malus hupehensis.

    PubMed

    Li, Chao; Sun, Xiangkai; Chang, Cong; Jia, Dongfeng; Wei, Zhiwei; Li, Cuiying; Ma, Fengwang

    2015-04-01

    Dopamine mediates many physiological processes in plants. We investigated its role in regulating growth, ion homeostasis and the response to salinity in Malus hupehensis Rehd. Both hydroponics and field-pot experiments were conducted under saline conditions. Salt-stressed plants had reduced growth and a marked decline in their net photosynthetic rates, values for Fv /Fm and chlorophyll contents. However, pretreatment with 100 or 200 μM dopamine significantly alleviated this inhibition and enabled plants to maintain their photosynthetic capacity. In addition to changing stomatal behavior, supplementation with dopamine positively influenced the uptake of K, N, P, S, Cu and Mn ions but had an inhibitory effect on Na and Cl uptake, the balance of which is responsible for managing the response to salinity by Malus plants. Dopamine pretreatment also controlled the burst of hydrogen peroxide, possibly through direct scavenging and by enhancing the activities of antioxidative enzymes and the capacity of the ascorbate-glutathione cycle. We also investigated whether dopamine might regulate salt overly sensitive pathway genes under salinity. Here, MdHKT1, MdNHX1 and MdSOS1 were greatly upregulated in roots and leaves, which possibly contributed to the maintenance of ion homeostasis and, thus, improved salinity resistance in plants exposed earlier to exogenous dopamine. These results support our conclusion that dopamine alleviates salt-induced stress not only at the level of antioxidant defense but also by regulating other mechanisms of ion homeostasis.

  19. Prenatal stress enhances stress- and corticotropin-releasing factor-induced stimulation of hippocampal acetylcholine release in adult rats.

    PubMed

    Day, J C; Koehl, M; Deroche, V; Le Moal, M; Maccari, S

    1998-03-01

    There is growing evidence that stressors occurring during pregnancy can impair biological and behavioral responses to stress in the adult offspring. For instance, prenatal stress enhances emotional reactivity, anxiety, and depressive-like behaviors associated with a prolonged stress-induced corticosterone secretion and a reduction in hippocampal corticosteroid receptors. Among the neurotransmitters involved in these hormonal and behavioral responses, acetylcholine may play a critical role. However, it is unknown whether prenatal stressful events also may influence the development of cholinergic systems. In the present study, hippocampal acetylcholine was measured, by in vivo microdialysis, in both male and female adult prenatally stressed rats, under basal conditions, after a mild stress (saline injection) or after intracerebroventricular administration of corticotropin-releasing factor (CRF; 0.1 nM). No difference in basal release of acetylcholine was observed between control and prenatally stressed rats of both genders. Mild stress was found to increase hippocampal acetylcholine release to a greater extent in prenatally stressed rats than in controls. In males, the CRF-induced increase in hippocampal acetylcholine release was larger in prenatally stressed rats, as compared with controls, during the first hour after the injection and in females during the third hour after the injection. These data indicate that prenatal stress has long-term effects on the development of forebrain cholinergic systems. The augmented increase in hippocampal acetylcholine release after the mild stress and CRF injection in prenatally stressed rats may be involved in some of the hormonal and behavioral abnormalities found in prenatally stressed rats. PMID:9465013

  20. No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder.

    PubMed

    Hernaus, D; Collip, D; Kasanova, Z; Winz, O; Heinzel, A; van Amelsvoort, T; Shali, S M; Booij, J; Rong, Y; Piel, M; Pruessner, J; Mottaghy, F M; Myin-Germeys, I

    2015-01-01

    Stress is an important risk factor in the etiology of psychotic disorder. Preclinical work has shown that stress primarily increases dopamine (DA) transmission in the frontal cortex. Given that DA-mediated hypofrontality is hypothesized to be a cardinal feature of psychotic disorder, stress-related extrastriatal DA release may be altered in psychotic disorder. Here we quantified for the first time stress-induced extrastriatal DA release and the spatial extent of extrastriatal DA release in individuals with non-affective psychotic disorder (NAPD). Twelve healthy volunteers (HV) and 12 matched drug-free NAPD patients underwent a single infusion [(18)F]fallypride positron emission tomography scan during which they completed the control and stress condition of the Montreal Imaging Stress Task. HV and NAPD did not differ in stress-induced [(18)F]fallypride displacement and the spatial extent of stress-induced [(18)F]fallypride displacement in medial prefrontal cortex (mPFC) and temporal cortex (TC). In the whole sample, the spatial extent of stress-induced radioligand displacement in right ventro-mPFC, but not dorso-mPFC or TC, was positively associated with task-induced subjective stress. Psychotic symptoms during the scan or negative, positive and general subscales of the Positive and Negative Syndrome Scale were not associated with stress-induced [(18)F]fallypride displacement nor the spatial extent of stress-induced [(18)F]fallypride displacement in NAPD. Our results do not offer evidence for altered stress-induced extrastriatal DA signaling in NAPD, nor altered functional relevance. The implications of these findings for the role of the DA system in NAPD and stress processing are discussed.

  1. Stress-induced nuclear export of 5-lipoxygenase

    SciTech Connect

    Hanaka, Hiromi; Shimizu, Takao; Izumi, Takashi . E-mail: takizumi@med.gunma-u.ac.jp

    2005-12-09

    A key enzyme for leukotriene biosynthesis is 5-lipoxygenase (5-LO), which we found is exported from the nucleus when p38 MAPK is activated. CHO-K1 cells stably express green fluorescent protein-5-lipoxygenase fusion protein (GFP-5LO), which is located predominantly in the nucleus, and is exported by anisomycin, hydrogen peroxide, and sorbitol, with activation of p38 MAPK. SB203580, an inhibitor of p38 MAPK, and Leptomycin B, an inhibitor of the nuclear export, blocked the anisomycin-induced export of GFP-5LO. When HEK293 cells were transformed with plasmids for wild-type GFP-5LO, GFP-5LO-S271A or GFP-5LO-S271E mutants, most wild-type GFP-5LO and GFP-5LO-S271A localized in the nucleus, but GFP-5LO-S271E localized in the cytosol. Thus, phosphorylation at Ser-271 of 5-LO is important for its export. Endogenous 5-LO in RBL cells stimulated with anisomycin was also exported from the nucleus. These results suggest that the nuclear export of 5-LO depends on the stress-induced activation of the p38 MAPK pathway.

  2. Electrical stress-induced instability of amorphous indium-gallium-zinc oxide thin-film transistors under bipolar ac stress

    SciTech Connect

    Lee, Sangwon; Jeon, Kichan; Park, Jun-Hyun; Kim, Sungchul; Kong, Dongsik; Kim, Dong Myong; Kim, Dae Hwan; Kim, Sangwook; Kim, Sunil; Hur, Jihyun; Park, Jae Chul; Song, Ihun; Kim, Chang Jung; Park, Youngsoo; Jung, U-In

    2009-09-28

    Bipolar ac stress-induced instability of amorphous indium-gallium-zinc oxide (a-IGZO) thin-film transistors is comparatively investigated with that under a positive dc gate bias stress. While the positive dc gate bias stress-induced threshold voltage shift ({delta}V{sub T}) is caused by the charge trapping into the interface/gate dielectric as reported in previous works, the dominant mechanism of the ac stress-induced {delta}V{sub T} is observed to be due to the increase in the acceptorlike deep states of the density of states (DOS) in the a-IGZO active layer. Furthermore, it is found that the variation of deep states in the DOS makes a parallel shift in the I{sub DS}-V{sub GS} curve with an insignificant change in the subthreshold slope, as well as the deformation of the C{sub G}-V{sub G} curves.

  3. Heat-stress and light-stress induce different cellular pathologies in the symbiotic dinoflagellate during coral bleaching.

    PubMed

    Downs, C A; McDougall, Kathleen E; Woodley, Cheryl M; Fauth, John E; Richmond, Robert H; Kushmaro, Ariel; Gibb, Stuart W; Loya, Yossi; Ostrander, Gary K; Kramarsky-Winter, Esti

    2013-01-01

    Coral bleaching is a significant contributor to the worldwide degradation of coral reefs and is indicative of the termination of symbiosis between the coral host and its symbiotic algae (dinoflagellate; Symbiodinium sp. complex), usually by expulsion or xenophagy (symbiophagy) of its dinoflagellates. Herein, we provide evidence that during the earliest stages of environmentally induced bleaching, heat stress and light stress generate distinctly different pathomorphological changes in the chloroplasts, while a combined heat- and light-stress exposure induces both pathomorphologies; suggesting that these stressors act on the dinoflagellate by different mechanisms. Within the first 48 hours of a heat stress (32°C) under low-light conditions, heat stress induced decomposition of thylakoid structures before observation of extensive oxidative damage; thus it is the disorganization of the thylakoids that creates the conditions allowing photo-oxidative-stress. Conversely, during the first 48 hours of a light stress (2007 µmoles m(-2) s(-1) PAR) at 25°C, condensation or fusion of multiple thylakoid lamellae occurred coincidently with levels of oxidative damage products, implying that photo-oxidative stress causes the structural membrane damage within the chloroplasts. Exposure to combined heat- and light-stresses induced both pathomorphologies, confirming that these stressors acted on the dinoflagellate via different mechanisms. Within 72 hours of exposure to heat and/or light stresses, homeostatic processes (e.g., heat-shock protein and anti-oxidant enzyme response) were evident in the remaining intact dinoflagellates, regardless of the initiating stressor. Understanding the sequence of events during bleaching when triggered by different environmental stressors is important for predicting both severity and consequences of coral bleaching.

  4. Heat-Stress and Light-Stress Induce Different Cellular Pathologies in the Symbiotic Dinoflagellate during Coral Bleaching

    PubMed Central

    Downs, C. A.; McDougall, Kathleen E.; Woodley, Cheryl M.; Fauth, John E.; Richmond, Robert H.; Kushmaro, Ariel; Gibb, Stuart W.; Loya, Yossi; Ostrander, Gary K.; Kramarsky-Winter, Esti

    2013-01-01

    Coral bleaching is a significant contributor to the worldwide degradation of coral reefs and is indicative of the termination of symbiosis between the coral host and its symbiotic algae (dinoflagellate; Symbiodinium sp. complex), usually by expulsion or xenophagy (symbiophagy) of its dinoflagellates. Herein, we provide evidence that during the earliest stages of environmentally induced bleaching, heat stress and light stress generate distinctly different pathomorphological changes in the chloroplasts, while a combined heat- and light-stress exposure induces both pathomorphologies; suggesting that these stressors act on the dinoflagellate by different mechanisms. Within the first 48 hours of a heat stress (32°C) under low-light conditions, heat stress induced decomposition of thylakoid structures before observation of extensive oxidative damage; thus it is the disorganization of the thylakoids that creates the conditions allowing photo-oxidative-stress. Conversely, during the first 48 hours of a light stress (2007 µmoles m−2 s−1 PAR) at 25°C, condensation or fusion of multiple thylakoid lamellae occurred coincidently with levels of oxidative damage products, implying that photo-oxidative stress causes the structural membrane damage within the chloroplasts. Exposure to combined heat- and light-stresses induced both pathomorphologies, confirming that these stressors acted on the dinoflagellate via different mechanisms. Within 72 hours of exposure to heat and/or light stresses, homeostatic processes (e.g., heat-shock protein and anti-oxidant enzyme response) were evident in the remaining intact dinoflagellates, regardless of the initiating stressor. Understanding the sequence of events during bleaching when triggered by different environmental stressors is important for predicting both severity and consequences of coral bleaching. PMID:24324575

  5. Prazosin Effects on Stress- and Cue-Induced Craving and Stress Response in Alcohol Dependent Individuals: Preliminary Findings

    PubMed Central

    Anderson, George M; Tuit, Keri; Hansen, Julie; Kimmerling, Anne; Siedlarz, Kristen M; Morgan, Peter T; Sinha, Rajita

    2011-01-01

    Background Stress, alcohol cues and dysregulated stress responses increase alcohol craving and relapse susceptibility, but few pharmacologic agents are known to decrease stress and cue-induced alcohol craving and associated stress dysregulation in humans. Here we report findings from a preliminary efficacy study of the alpha1 receptor antagonist, prazosin, in modulating these relapse-relevant factors in alcohol dependent (AD) individuals. Methods Seventeen early abstinent, treatment-seeking alcohol dependent individuals (12 Males /5 Females) were randomly assigned to receive either placebo or 16 mg daily prazosin in a double-blind, placebo controlled manner over four weeks. During week 4, all patients participated in a 3-day laboratory experiment involving 5-min guided imagery exposure to stress, alcohol cue and neutral-relaxing/control conditions, one exposure per day, on consecutive days in a random, counterbalanced order. Alcohol craving, anxiety and negative emotion, cardiovascular measures, plasma hypothalamic-pituitary-adrenal (HPA; cortisol, ACTH) were assessed repeatedly in each session. Results The prazosin group (n=9) versus the placebo group (n=8) showed significantly lower alcohol craving, anxiety and negative emotion following stress exposure. The placebo group also showed significantly increased stress and cue-induced alcohol craving, anxiety, negative emotion and blood pressure as well as a blunted HPA response relative to the neutral condition, while the prazosin group showed no such increases in craving, anxiety, negative emotion and blood pressure, and no blunted HPA response to stress and alcohol cue exposure. Conclusions Prazosin appears efficacious in decreasing stress- and cue-induced alcohol craving and may normalize the stress dysregulation associated with early recovery from alcoholism. Further research to assess the efficacy of prazosin in reducing alcohol craving and stress-related relapse risk is warranted. PMID:21919922

  6. Regulation of OSU-03012 toxicity by ER stress proteins and ER stress-inducing drugs.

    PubMed

    Booth, Laurence; Roberts, Jane L; Cruickshanks, Nichola; Grant, Steven; Poklepovic, Andrew; Dent, Paul

    2014-10-01

    The present studies examined the toxic interaction between the non-coxib celecoxib derivative OSU-03012 and phosphodiesterase 5 (PDE5) inhibitors, and also determined the roles of endoplasmic reticulum stress response regulators in cell survival. PDE5 inhibitors interacted in a greater than additive fashion with OSU-03012 to kill parental glioma and stem-like glioma cells. Knockdown of the endoplasmic reticulum stress response proteins IRE1 or XBP1 enhanced the lethality of OSU-03012, and of [OSU-03012 + PDE5 inhibitor] treatment. Pan-caspase and caspase-9 inhibition did not alter OSU-03012 lethality but did abolish enhanced killing in the absence of IRE1 or XBP1. Expression of the mitochondrial protective protein BCL-XL or the caspase-8 inhibitor c-FLIP-s, or knockdown of death receptor CD95 or the death receptor caspase-8 linker protein FADD, suppressed killing by [OSU-03012 + PDE5 inhibitor] treatment. CD95 activation was blocked by the nitric oxide synthase inhibitor L-NAME. Knockdown of the autophagy regulatory proteins Beclin1 or ATG5 protected the cells from OSU-03012 and from [OSU-03012 + PDE5 inhibitor] toxicity. Knockdown of IRE1 enhanced OSU-03012/[OSU-03012 + PDE5 inhibitor]-induced JNK activation, and inhibition of JNK suppressed the elevated killing caused by IRE1 knockdown. Knockdown of CD95 blunted JNK activation. Collectively, our data demonstrate that PDE5 inhibitors recruit death receptor signaling to enhance OSU-03012 toxicity in glioblastoma multiforme (GBM) cells. PMID:25103559

  7. Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells.

    PubMed

    Ahn, Bong-Hyun; Park, Mi Hee; Lee, Young Han; Kwon, Taeg Kyu; Min, Do Sik

    2007-12-01

    Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers. In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl(2))-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells. CoCl(2) stimulated PLD activity and synthesis of COX-2 protein in a dose and time-dependent manner. Moreover, elevated expression of PLD1 and PLD2 increased hypoxia-induced COX-2 expression and prostaglandin E2 (PGE(2)) production. Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed CoCl(2)-induced COX-2 expression and PGE(2) formation. In addition, evidence that PLD activity was involved in the stimulation of COX-2 expression was provided by the observations that overexpression of wild type PLD isozymes, but not catalytically inactive PLD isozymes, stimulated CoCl(2)-induced COX-2 expression and PGE(2) production. PLD1 enhanced COX-2 expression by CoCl(2) via reactive oxygen species (ROS), p38 MAPK kinase, PKC-delta, and PKA, but not ERK, whereas PLD2 enhanced CoCl(2)-induced COX-2 expression via ROS and p38 MAPK, but not ERK, PKC-delta, and PKA. Differential regulation of COX-2 expression mediated through PLD isozymes was comparable with that of CoCl(2)-induced PLD activity in these two PLD isozymes. Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl(2)-induced COX-2 expression through differential signaling pathways in astroglioma cells.

  8. NMDA receptor blockade alters stress-induced dendritic remodeling in medial prefrontal cortex.

    PubMed

    Martin, Kathryn P; Wellman, Cara L

    2011-10-01

    The development and relapse of many psychopathologies can be linked to both stress and prefrontal cortex dysfunction. Glucocorticoid stress hormones target medial prefrontal cortex (mPFC) and either chronic stress or chronic administration of glucocorticoids produces dendritic remodeling in prefrontal pyramidal neurons. Exposure to stress also causes an increase in the release of the excitatory amino acid glutamate, which binds to N-methyl-D-aspartate (NMDA) receptors, which are plentiful in mPFC. NMDA receptor activation is crucial for producing hippocampal dendritic remodeling due to stress and for dendritic reorganization in frontal cortex after cholinergic deafferentation. Thus, NMDA receptors could mediate stress-induced dendritic retraction in mPFC. To test this hypothesis, dendritic morphology of pyramidal cells in mPFC was assessed after blocking NMDA receptors with the competitive NMDA antagonist ±3-(2-carboxypiperazin-4yl)propyl-1-phosphonic acid (CPP) during restraint stress. Administration of CPP prevented stress-induced dendritic atrophy. Instead, CPP-injected stressed rats showed hypertrophy of apical dendrites compared with controls. These results suggest that NMDA activation is crucial for stress-induced dendritic atrophy in mPFC. Furthermore, NMDA receptor blockade uncovers a new pattern of stress-induced dendritic changes, suggesting that other neurohormonal changes in concert with NMDA receptor activation underlie the net dendritic retraction seen after chronic stress.

  9. Microflow-induced shear stress on biomaterial wall by ultrasound-induced encapsulated microbubble oscillation

    NASA Astrophysics Data System (ADS)

    Hu, Ji-Wen; Qian, Sheng-You; Sun, Jia-Na; Lü, Yun-Bin; Hu, Ping

    2015-09-01

    A model of an ultrasound-driven encapsulated microbubble (EMB) oscillation near biomaterial wall is presented and used for describing the microflow-induced shear stress on the wall by means of a numerical method. The characteristic of the model lies in the explicit treatment of different types of wall for the EMB responses. The simulation results show that the radius-time change trends obtained by our model are consistent with the existing models and experimental results. In addition, the effect of the elastic wall on the acoustic EMB response is stronger than that of the rigid wall, and the shear stress on the elastic wall is larger than that of the rigid wall. The closer the EMB to the wall, the greater the shear stress on the wall. The substantial shear stress on the wall surface occurs inside a circular zone with a radius about two-thirds of the bubble radius. This paper may be of interest in the study of potential damage mechanisms to the microvessel for drug and gene delivery due to sonoporation. Projects supported by the National Natural Science Foundation of China (Grant Nos. 11174077 and 11474090), the Natural Science Foundation of Hunan Province, China (Grant No. 13JJ3076), the Science Research Program of Education Department of Hunan Province, China (Grant No. 14A127), and the Doctoral Fund of University of South China (Grant No. 2011XQD46).

  10. Stability of sublethal acid stress adaptaion and induced cross protection against lauric arginate in Listeria monocytogenes

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The stability of acid stress adaptation in Listeria monocytogenes and its induced cross protection effect against GRAS (generally recognized as safe) antimicrobial compounds has never been investigated before. In the present study, the acid stress adaptation in L. monocytogenes was initially induced...

  11. Stress induced premature senescence : a new culprit in ovarian tumorigenesis?

    PubMed Central

    Raghuram, Gorantla Venkata; Mishra, Pradyumna Kumar

    2014-01-01

    Stress induced premature senescence (SIPS) is a relative extension to the concept of exogenous cellular insult. Besides persistent double strand (ds) DNA breaks and increased β-galactosidase activity, biological significance of telomeric attrition in conjunction with senescence associated secretory phenotype (SASP) has been highlighted in SIPS. To gain insight on the potential role of this unique phenomenon invoked upon environmental stress, we sequentially validated the molecular repercussions of this event in ovarian epithelial cells after exposure to methyl isocyanate, an elegant regulator of cellular biotransformation. Persistent accumulation of DNA damage response factors phospho-ATM/γ-H2AX, morphological changes with increased cell size and early yet incremental β-gal staining, imply the inception of premature senescence. Advent of SASP is attributed by prolonged secretion of pro-inflammatory cytokines along with untimely but significant G1/S cell cycle arrest. Telomeric dysfunction associated with premature senescence is indicative of early loss of TRF2 (telomeric repeat binding factor 2) protein and resultant multiple translocations. Induction of senescence-associated heterochromatic foci formation showcases the chromatin alterations in form of trimethylated H3K9me3 in conjunction with H4 hypoacetylation and altered miRNA expression. Anchorage-independent neoplastic growth observed in treated cells reaffirms the oncogenic transformation following the exposure. Collectively, we infer the possible role of SIPS, as a central phenomenon, to perturbed genomic integrity in ovarian surface epithelium, orchestrated through SASP and chromatin level alterations, a hitherto unknown molecular paradigm. Although translational utility of SIPS as a biomarker for estimating ovarian cancer risk seems evident, further investigations will be imperative to provide a tangible way for its precise validation in clinical settings. PMID:25673532

  12. Adaptive lenticular microlens array based on voltage-induced waves at the surface of polyvinyl chloride/dibutyl phthalate gels.

    PubMed

    Xu, Miao; Jin, Boya; He, Rui; Ren, Hongwen

    2016-04-18

    We report a new approach to preparing a lenticular microlens array (LMA) using polyvinyl chloride (PVC)/dibutyl phthalate (DBP) gels. The PVD/DBP gels coated on a glass substrate form a membrane. With the aid of electrostatic repulsive force, the surface of the membrane can be reconfigured with sinusoidal waves by a DC voltage. The membrane with wavy surface functions as a LMA. By switching over the anode and cathode, the convex shape of each lenticular microlens in the array can be converted to the concave shape. Therefore, the LMA can present a large dynamic range. The response time is relatively fast and the driving voltage is low. With the advantages of compact structure, optical isotropy, and good mechanical stability, our LMA has potential applications in imaging, information processing, biometrics, and displays. PMID:27137253

  13. Stress-induced hyperlocomotion as a confounding factor in anxiety and depression models in mice.

    PubMed

    Strekalova, T; Spanagel, R; Dolgov, O; Bartsch, D

    2005-05-01

    Chronic stress is broadly used to model anxiety and depression. However, in chronic stress models, anxiety- and depression-like behaviors might be masked by unspecific effects of stress. We tested whether chronic stress in mice can induce unspecific changes in locomotion, and whether these changes interfere with the measurement of anxiety and forced-swimming behaviors. Also, we studied these latter behaviors in relation to the duration of stress, the lighting conditions during testing, and after the injection of diazepam. We employed a 4-week chronic stress paradigm, adopted from a model of stress-induced anhedonia and a 1-week subchronic stress, both consisting of rat exposure, restraint stress and tail suspension. Chronically stressed mice, tested under bright and moderate illumination, exhibited 'anxiolytic-like' behavior along with prolonged swimming and hyperactivity. These behaviors were not detectable under weak illumination or after the injection of diazepam (0.25 mg/kg). Instead, normal locomotion, increased anxiety and inhibited swimming were revealed under these conditions. Thus, chronic stress can induce hyperlocomotion in mice, which is triggered by acute stressors such as light, and interferes with the evaluation of anxiety and forced swimming. One week of stress did not change locomotion and forced swimming, and increased anxiety irrespective of illumination applied during testing. Our data can possibly explain previously reported contradictions in the behavioral testing of mice with chronic stress models of anxiety and depression.

  14. Prenatal Hypoxia-Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone.

    PubMed

    Jantzie, Lauren L; Getsy, Paulina M; Denson, Jesse L; Firl, Daniel J; Maxwell, Jessie R; Rogers, Danny A; Wilson, Christopher G; Robinson, Shenandoah

    2015-01-01

    Infants who suffer perinatal brain injury, including those with encephalopathy of prematurity, are prone to chronic neurological deficits, including epilepsy, cognitive impairment, and behavioral problems, such as anxiety, inattention, and poor social interaction. These deficits, especially in combination, pose the greatest hindrance to these children becoming independent adults. Cerebral function depends on adequate development of essential inhibitory neural circuits and the appropriate amount of excitation and inhibition at specific stages of maturation. Early neuronal synaptic responses to γ-amino butyric acid (GABA) are initially excitatory. During the early postnatal period, GABAAR responses switch to inhibitory with the upregulation of potassium-chloride co-transporter KCC2. With extrusion of chloride by KCC2, the Cl(-) reversal potential shifts and GABA and glycine responses become inhibitory. We hypothesized that prenatal hypoxic-ischemic brain injury chronically impairs the developmental upregulation of KCC2 that is essential for cerebral circuit formation. Following late gestation hypoxia-ischemia (HI), diffusion tensor imaging in juvenile rats shows poor microstructural integrity in the hippocampal CA3 subfield, with reduced fractional anisotropy and elevated radial diffusivity. The loss of microstructure correlates with early reduced KCC2 expression on NeuN-positive pyramidal neurons, and decreased monomeric and oligomeric KCC2 protein expression in the CA3 subfield. Together with decreased inhibitory post-synaptic currents during a critical window of development, we document for the first time that prenatal transient systemic HI in rats impairs hippocampal CA3 inhibitory tone. Failure of timely development of inhibitory tone likely contributes to a lower seizure threshold and impaired cognitive function in children who suffer perinatal brain injury. PMID:26388734

  15. Prenatal Hypoxia–Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone

    PubMed Central

    Jantzie, Lauren L.; Getsy, Paulina M.; Denson, Jesse L.; Firl, Daniel J.; Maxwell, Jessie R.; Rogers, Danny A.; Wilson, Christopher G.; Robinson, Shenandoah

    2015-01-01

    Infants who suffer perinatal brain injury, including those with encephalopathy of prematurity, are prone to chronic neurological deficits, including epilepsy, cognitive impairment, and behavioral problems, such as anxiety, inattention, and poor social interaction. These deficits, especially in combination, pose the greatest hindrance to these children becoming independent adults. Cerebral function depends on adequate development of essential inhibitory neural circuits and the appropriate amount of excitation and inhibition at specific stages of maturation. Early neuronal synaptic responses to γ-amino butyric acid (GABA) are initially excitatory. During the early postnatal period, GABAAR responses switch to inhibitory with the upregulation of potassium-chloride co-transporter KCC2. With extrusion of chloride by KCC2, the Cl− reversal potential shifts and GABA and glycine responses become inhibitory. We hypothesized that prenatal hypoxic–ischemic brain injury chronically impairs the developmental upregulation of KCC2 that is essential for cerebral circuit formation. Following late gestation hypoxia–ischemia (HI), diffusion tensor imaging in juvenile rats shows poor microstructural integrity in the hippocampal CA3 subfield, with reduced fractional anisotropy and elevated radial diffusivity. The loss of microstructure correlates with early reduced KCC2 expression on NeuN-positive pyramidal neurons, and decreased monomeric and oligomeric KCC2 protein expression in the CA3 subfield. Together with decreased inhibitory post-synaptic currents during a critical window of development, we document for the first time that prenatal transient systemic HI in rats impairs hippocampal CA3 inhibitory tone. Failure of timely development of inhibitory tone likely contributes to a lower seizure threshold and impaired cognitive function in children who suffer perinatal brain injury. PMID:26388734

  16. Delayed germination of Arabidopsis seeds under chilling stress by overexpressing an abiotic stress inducible GhTPS11.

    PubMed

    Wang, Cai-Li; Zhang, Shi-Cai; Qi, Sheng-Dong; Zheng, Cheng-Chao; Wu, Chang-Ai

    2016-01-10

    Trehalose-6-phosphate synthase (TPS) plays an important role in metabolic regulation and stress responses in a variety of organisms. However information about cotton TPS is poor. Here a cotton TPS gene GhTPS11 was isolated and characterized. Expression analysis revealed that GhTPS11 was induced in 20-day old cotton seedlings by heat drought and high salt stresses as well as GA and ABA. Moreover GhTPS11 was induced by chilling stress and mannitol while was depressed by sucrose. Tissue expression analysis indicated that GhTPS11 expressed higher in leaves than in stems and roots of 20-day old cotton seedlings. The GhTPS11 overexpressing Arabidopsis seeds germinated slower than the wild-type (WT) under chilling stress. Trehalose-6-phosphate (T6P) and trehalose contents were evidently higher in GhTPS11 overexpressing lines 3, 5, and 22 than in WT under normal germination condition as well as chilling stress. Further analysis demonstrated that the expression of ICE1 CBF3 and RCI2A was induced lower whereas that of CBF1 and CBF2 was induced higher under chilling stress in the GhTPS11 overexpressing seeds than WT respectively. These results suggested that GhTPS11 encoded a stress-responsive TPS protein and functioned in chilling stress during seed germination. Perhaps the chilling stress sensitivity of transgenic Arabidopsis seeds was caused by the expression changes of at least some chilling-related genes such as ICE1 CBFs and RCI2A other than HOS1. So this article provided the useful information for GhTPS11 usage for crop molecular breeding.

  17. Delayed germination of Arabidopsis seeds under chilling stress by overexpressing an abiotic stress inducible GhTPS11.

    PubMed

    Wang, Cai-Li; Zhang, Shi-Cai; Qi, Sheng-Dong; Zheng, Cheng-Chao; Wu, Chang-Ai

    2016-01-10

    Trehalose-6-phosphate synthase (TPS) plays an important role in metabolic regulation and stress responses in a variety of organisms. However information about cotton TPS is poor. Here a cotton TPS gene GhTPS11 was isolated and characterized. Expression analysis revealed that GhTPS11 was induced in 20-day old cotton seedlings by heat drought and high salt stresses as well as GA and ABA. Moreover GhTPS11 was induced by chilling stress and mannitol while was depressed by sucrose. Tissue expression analysis indicated that GhTPS11 expressed higher in leaves than in stems and roots of 20-day old cotton seedlings. The GhTPS11 overexpressing Arabidopsis seeds germinated slower than the wild-type (WT) under chilling stress. Trehalose-6-phosphate (T6P) and trehalose contents were evidently higher in GhTPS11 overexpressing lines 3, 5, and 22 than in WT under normal germination condition as well as chilling stress. Further analysis demonstrated that the expression of ICE1 CBF3 and RCI2A was induced lower whereas that of CBF1 and CBF2 was induced higher under chilling stress in the GhTPS11 overexpressing seeds than WT respectively. These results suggested that GhTPS11 encoded a stress-responsive TPS protein and functioned in chilling stress during seed germination. Perhaps the chilling stress sensitivity of transgenic Arabidopsis seeds was caused by the expression changes of at least some chilling-related genes such as ICE1 CBFs and RCI2A other than HOS1. So this article provided the useful information for GhTPS11 usage for crop molecular breeding. PMID:26325072

  18. Accumulation of brachycerine, an antioxidant glucosidic indole alkaloid, is induced by abscisic acid, heavy metal, and osmotic stress in leaves of Psychotria brachyceras.

    PubMed

    do Nascimento, Naíla Cannes; Menguer, Paloma Koprovski; Henriques, Amélia Teresinha; Fett-Neto, Arthur Germano

    2013-12-01

    Psychotria brachyceras Muell. Arg. produces the antioxidant monoterpene indole alkaloid (MIA) brachycerine, which, besides retaining a glucose residue, has its terpenoid moiety derived not from secologanin, but probably from epiloganin, representing a new subclass of MIAs. In this work we showed that osmotic stress agents, such as sodium chloride, sorbitol and polyethylene glycol (PEG), induced brachycerine accumulation in leaf disks of P. brachyceras. Other oxidative stress inducers, such as exposure to aluminum and silver, also increased brachycerine content. Abscisic acid (ABA) treatment was shown to increase brachycerine yield, suggesting its involvement in brachycerine induction during osmotic stress. Ascorbate peroxidase activity was induced in PEG-treated leaf disks, whereas superoxide dismutase (SOD) activity remained unaltered. Assays with specific inhibitors of the cytosolic mevalonate (MVA) and plastidic 2-C-methyl-D-erythritol 4-phosphate (MEP) pathways showed that the terpenoid moiety of brachycerine derived predominantly from the MEP pathway. These results suggest a potential involvement of brachycerine in plant defense against osmotic/oxidative stress damage, possibly contributing to detoxification of hydroxyl radical and superoxide anion as a SOD-like molecule.

  19. Central anandamide deficiency predicts stress-induced anxiety: behavioral reversal through endocannabinoid augmentation.

    PubMed

    Bluett, R J; Gamble-George, J C; Hermanson, D J; Hartley, N D; Marnett, L J; Patel, S

    2014-07-08

    Stress is a major risk factor for the development of mood and anxiety disorders; elucidation of novel approaches to mitigate the deleterious effects of stress could have broad clinical applications. Pharmacological augmentation of central endogenous cannabinoid (eCB) signaling may be an effective therapeutic strategy to mitigate the adverse behavioral and physiological consequences of stress. Here we show that acute foot-shock stress induces a transient anxiety state measured 24 h later using the light-dark box assay and novelty-induced hypophagia test. Acute pharmacological inhibition of the anandamide-degrading enzyme, fatty acid amide hydrolase (FAAH), reverses the stress-induced anxiety state in a cannabinoid receptor-dependent manner. FAAH inhibition does not significantly affect anxiety-like behaviors in non-stressed mice. Moreover, whole brain anandamide levels are reduced 24 h after acute foot-shock stress and are negatively correlated with anxiety-like behavioral measures in the light-dark box test. These data indicate that central anandamide levels predict acute stress-induced anxiety, and that reversal of stress-induced anandamide deficiency is a key mechanism subserving the therapeutic effects of FAAH inhibition. These studies provide further support that eCB-augmentation is a viable pharmacological strategy for the treatment of stress-related neuropsychiatric disorders.

  20. Calorie-induced ER stress suppresses uroguanylin satiety signaling in diet-induced obesity

    PubMed Central

    Kim, G W; Lin, J E; Snook, A E; Aing, A S; Merlino, D J; Li, P; Waldman, S A

    2016-01-01

    Background/Objectives: The uroguanylin-GUCY2C gut–brain axis has emerged as one component regulating feeding, energy homeostasis, body mass and metabolism. Here, we explore a role for this axis in mechanisms underlying diet-induced obesity (DIO). Subjects/Methods: Intestinal uroguanylin expression and secretion, and hypothalamic GUCY2C expression and anorexigenic signaling, were quantified in mice on high-calorie diets for 14 weeks. The role of endoplasmic reticulum (ER) stress in suppressing uroguanylin in DIO was explored using tunicamycin, an inducer of ER stress, and tauroursodeoxycholic acid (TUDCA), a chemical chaperone that inhibits ER stress. The impact of consumed calories on uroguanylin expression was explored by dietary manipulation. The role of uroguanylin in mechanisms underlying obesity was examined using Camk2a-Cre-ERT2-Rosa-STOPloxP/loxP-Guca2b mice in which tamoxifen induces transgenic hormone expression in brain. Results: DIO suppressed intestinal uroguanylin expression and eliminated its postprandial secretion into the circulation. DIO suppressed uroguanylin through ER stress, an effect mimicked by tunicamycin and blocked by TUDCA. Hormone suppression by DIO reflected consumed calories, rather than the pathophysiological milieu of obesity, as a diet high in calories from carbohydrates suppressed uroguanylin in lean mice, whereas calorie restriction restored uroguanylin in obese mice. However, hypothalamic GUCY2C, enriched in the arcuate nucleus, produced anorexigenic signals mediating satiety upon exogenous agonist administration, and DIO did not impair these responses. Uroguanylin replacement by transgenic expression in brain repaired the hormone insufficiency and reconstituted satiety responses opposing DIO and its associated comorbidities, including visceral adiposity, glucose intolerance and hepatic steatosis. Conclusions: These studies reveal a novel pathophysiological mechanism contributing to obesity in which calorie-induced suppression

  1. Electrocatalytic Production of C3-C4 Compounds by Conversion of CO2 on a Chloride-Induced Bi-Phasic Cu2O-Cu Catalyst.

    PubMed

    Lee, Seunghwa; Kim, Dahee; Lee, Jaeyoung

    2015-12-01

    Electrocatalytic conversion of carbon dioxide (CO2) has recently received considerable attention as one of the most feasible CO2 utilization techniques. In particular, copper and copper-derived catalysts have exhibited the ability to produce a number of organic molecules from CO2. Herein, we report a chloride (Cl)-induced bi-phasic cuprous oxide (Cu2O) and metallic copper (Cu) electrode (Cu2OCl) as an efficient catalyst for the formation of high-carbon organic molecules by CO2 conversion, and identify the origin of electroselectivity toward the formation of high-carbon organic compounds. The Cu2OCl electrocatalyst results in the preferential formation of multi-carbon fuels, including n-propanol and n-butane C3-C4 compounds. We propose that the remarkable electrocatalytic conversion behavior is due to the favorable affinity between the reaction intermediates and the catalytic surface. PMID:26473324

  2. Electrocatalytic Production of C3-C4 Compounds by Conversion of CO2 on a Chloride-Induced Bi-Phasic Cu2O-Cu Catalyst.

    PubMed

    Lee, Seunghwa; Kim, Dahee; Lee, Jaeyoung

    2015-12-01

    Electrocatalytic conversion of carbon dioxide (CO2) has recently received considerable attention as one of the most feasible CO2 utilization techniques. In particular, copper and copper-derived catalysts have exhibited the ability to produce a number of organic molecules from CO2. Herein, we report a chloride (Cl)-induced bi-phasic cuprous oxide (Cu2O) and metallic copper (Cu) electrode (Cu2OCl) as an efficient catalyst for the formation of high-carbon organic molecules by CO2 conversion, and identify the origin of electroselectivity toward the formation of high-carbon organic compounds. The Cu2OCl electrocatalyst results in the preferential formation of multi-carbon fuels, including n-propanol and n-butane C3-C4 compounds. We propose that the remarkable electrocatalytic conversion behavior is due to the favorable affinity between the reaction intermediates and the catalytic surface.

  3. Development of chloride-induced corrosion in pre-cracked RC beams under sustained loading: Effect of load-induced cracks, concrete cover, and exposure conditions

    SciTech Connect

    Yu, Linwen; François, Raoul; Dang, Vu Hiep; L'Hostis, Valérie; Gagné, Richard

    2015-01-15

    This paper deals with corrosion initiation and propagation in pre-cracked reinforced concrete beams under sustained loading during exposure to a chloride environment. Specimen beams that were cast in 2010 were compared to specimens cast in 1984. The only differences betwe