Elevation of Serum Acid Sphingomyelinase Activity in Children with Acute Respiratory Syncytial Virus Bronchiolitis.

PubMed

Yoshida, Shuichiro; Noguchi, Atsuko; Kikuchi, Wataru; Fukaya, Hiroshi; Igarashi, Kiyoshi; Takahashi, Tsutomu

2017-12-01

Acid sphingomyelinase (ASM) is a lysosomal enzyme that hydrolyzes sphingomyelin into ceramide, a bioactive lipid to regulate cellular physiological functions. Thus, ASM activation has been reported as a key event in pathophysiological reactions including inflammation, cytokine release, oxidative stress, and endothelial damage in human diseases. Since ASM activation is associated with extracellular ASM secretion through unknown mechanisms, it can be detected by recognizing the elevation of secretory ASM (S-ASM) activity. Serum S-ASM activity has been reported to increase in chronic diseases, acute cardiac diseases, and systemic inflammatory diseases. However, the serum S-ASM has not been investigated in common acute illness. This study was designed to evaluate serum S-ASM activity in children with common acute illness. Fifty children with common acute illness and five healthy children were included in this study. The patients were categorized into five groups based on clinical diagnoses: acute respiratory syncytial virus (RSV) bronchiolitis, adenovirus infection, streptococcal infection, asthma, and other infections due to unknown origin. The serum S-ASM activity was significantly elevated at 6.9 ± 1.6 nmol/0.1 mL/6 h in the group of acute RSV bronchiolitis patients compared with healthy children who had a mean level of 1.8 ± 0.8 nmol/0.1 mL/6 h (p < 0.05). In the other illness groups, the serum S-ASM activity was not significantly elevated. The results suggest an association of ASM activation with RSV infection, a cause for common acute illness. This is the first report to describe the elevation of serum S-ASM activity in respiratory tract infection.

Prophylaxis with Bacopa monnieri attenuates acrylamide induced neurotoxicity and oxidative damage via elevated antioxidant function.

PubMed

Shinomol, George Kunnel; Raghunath, Narayanareddy; Bharath, Muchukunte Mukunda Srinivas; Muralidhara

2013-03-01

Acrylamide (ACR) is a water-soluble, vinyl monomer that has multiple chemical and industrial applications. Exposure to ACR causes neuropathy and associated neurological defects including gait abnormalities and skeletal muscle weakness, due to impaired neurotransmitter release and eventual neurodegeneration. Using in vivo and in vitro models, we examined whether oxidative events are involved in ACR-mediated neurotoxicity and whether these could be prevented by natural plant extracts. Administration (i.p.) of ACR in mice (40 mg/kg bw/ d for 5d) induced significant oxidative damage in the brain cortex and liver as evidenced by elevated lipid peroxidation, reactive oxygen species and protein carbonyls. This was associated with lowered antioxidant activities including antioxidant enzymes (catalase, glutathione-s-transferase) and reduced glutathione (GSH) compared to untreated controls. Similarly, exposure of N27 neuronal cells in culture to ACR (1-5 mM) caused dose-dependent neuronal death and lowered GSH. Interestingly, dietary supplementation with the leaf powder of Bacopa monnieri (BM) (which possesses neuroprotective properties and nootropic activity) in mice for 30 days offered significant protection against ACR toxicity and oxidative damage in vivo. Similarly, pretreatment with BM protected the N27 cells against ACR-induced cell death and associated oxidative damage. Co-treatment and pre-treatment of Drosophila melanogaster with BM extract protected against ACR-induced locomotor dysfunction and GSH depletion. We infer that BM displays prophylactic effects against ACR induced oxidative damage and neurotoxicity with potential therapeutic application in human pathology associated with neuropathy.

Curcumin targeting the thioredoxin system elevates oxidative stress in HeLa cells

DOE Office of Scientific and Technical Information (OSTI.GOV)

Cai, Wenqing; Zhang, Baoxin; Duan, Dongzhu

2012-08-01

The thioredoxin system, composed of thioredoxin reductase (TrxR), thioredoxin (Trx), and NADPH, is ubiquitous in all cells and involved in many redox-dependent signaling pathways. Curcumin, a naturally occurring pigment that gives a specific yellow color in curry food, is consumed in normal diet up to 100 mg per day. This molecule has also been used in traditional medicine for the treatment of a variety of diseases. Curcumin has numerous biological functions, and many of these functions are related to induction of oxidative stress. However, how curcumin elicits oxidative stress in cells is unclear. Our previous work has demonstrated the waymore » by which curcumin interacts with recombinant TrxR1 and alters the antioxidant enzyme into a reactive oxygen species (ROS) generator in vitro. Herein we reported that curcumin can target the cytosolic/nuclear thioredoxin system to eventually elevate oxidative stress in HeLa cells. Curcumin-modified TrxR1 dose-dependently and quantitatively transfers electrons from NADPH to oxygen with the production of ROS. Also, curcumin can drastically down-regulate Trx1 protein level as well as its enzyme activity in HeLa cells, which in turn remarkably decreases intracellular free thiols, shifting the intracellular redox balance to a more oxidative state, and subsequently induces DNA oxidative damage. Furthermore, curcumin-pretreated HeLa cells are more sensitive to oxidative stress. Knockdown of TrxR1 sensitizes HeLa cells to curcumin cytotoxicity, highlighting the physiological significance of targeting TrxR1 by curcumin. Taken together, our data disclose a previously unrecognized prooxidant mechanism of curcumin in cells, and provide a deep insight in understanding how curcumin works in vivo. -- Highlights: ► Curcumin induces oxidative stress by targeting the thioredoxin system. ► Curcumin-modified TrxR quantitatively oxidizes NADPH to generate ROS. ► Knockdown of TrxR1 augments curcumin's cytotoxicity in HeLa cells. �

Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury

PubMed Central

Mühl, Diana; Woth, Gábor; Drenkovics, Livia; Varga, Adrienn; Ghosh, Subhamay; Csontos, Csaba; Bogár, Lajos; Wéber, György; Lantos, János

2011-01-01

Background & objectives: We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis. Methods: In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed. Results: Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis. Interpretation & conclusions: Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns. PMID:21808137

A combination of He-Ne laser irradiation and exogenous NO application efficiently protect wheat seedling from oxidative stress caused by elevated UV-B stress.

PubMed

Li, Yongfeng; Gao, Limei; Han, Rong

2016-12-01

The elevated ultraviolet-B (UV-B) stress induces the accumulation of a variety of intracellular reactive oxygen species (ROS), which seems to cause oxidative stress for plants. To date, very little work has been done to evaluate the biological effects of a combined treatment with He-Ne laser irradiation and exogenous nitric oxide (NO) application on oxidative stress resulting from UV-B radiation. Thus, our study investigated the effects of a combination with He-Ne laser irradiation and exogenous NO treatment on oxidative damages in wheat seedlings under elevated UV-B stress. Our data showed that the reductions in ROS levels, membrane damage parameters, while the increments in antioxidant contents and antioxidant enzyme activity caused by a combination with He-Ne laser and exogenous NO treatment were greater than those of each individual treatment. Furthermore, these treatments had a similar effect on transcriptional activities of plant antioxidant enzymes. This implied that the protective effects of a combination with He-Ne laser irradiation and exogenous NO treatment on oxidative stress resulting from UV-B radiation was more efficient than each individual treatment with He-Ne laser or NO molecule. Our findings might provide beneficial theoretical references for identifying some effective new pathways for plant UV-B protection.

Elevation of oleate-activated phospholipase D activity during thymic atrophy

PubMed Central

Lee, Youngkyun; Song, Soo-Mee; Park, Heung Soon; Kim, Sungyeol; Koh, Eun-Hee; Choi, Myung Sun; Choi, Myung-Un

2002-01-01

Various phospholipases are thought to be associated with the in vitro apoptosis of thymocytes. In the present study, the in vivo phospholipase D (PLD) activity of rat thymus was studied after whole-body X-irradiation or injection of dexamethasone (DEX). Using exogenous [14C]dipalmitoyl phosphatidylcholine (PC) as the substrate, an elevation of oleate-activated PLD activity was observed during thymic atrophy. The activity increases were sevenfold at 48 hr after 5-Gy irradiation and fourfold at 72 hr after injection of 5 mg/kg DEX. The elevation of PLD activity appeared to parallel extensive thymus shrinkage. An increased level of thymic phosphatidic acid (PA), the presumed physiological product of PLD action on PC, was also detected. By comparing the acyl chains of PA with those of other phospholipids, PA appeared to originate from PC. To assess the role of PLD during thymic atrophy, thymocytes and stromal cells were isolated. Although thymocytes themselves exhibited significant PLD activation, the major elevation in PLD activity (greater than fourfold) was found in isolated stromal cells. PLD was also activated during in vitro phagocytosis of apoptotic thymocytes by the macrophage-like cell line P388D1. This in vitro phagocytosis was significantly inhibited by PLD action blockers, such as 2,3-diphosphoglycerate and 1-butanol. These observations strongly suggest that the alteration of oleate-activated PLD activity is part of an in vivo event in the progression of thymic atrophy, including phagocytic clearance of apoptotic thymocytes. PMID:12460188

Modeling Strength Degradation of Fiber-Reinforced Ceramic-Matrix Composites Subjected to Cyclic Loading at Elevated Temperatures in Oxidative Environments

NASA Astrophysics Data System (ADS)

Longbiao, Li

2018-02-01

In this paper, the strength degradation of non-oxide and oxide/oxide fiber-reinforced ceramic-matrix composites (CMCs) subjected to cyclic loading at elevated temperatures in oxidative environments has been investigated. Considering damage mechanisms of matrix cracking, interface debonding, interface wear, interface oxidation and fibers fracture, the composite residual strength model has been established by combining the micro stress field of the damaged composites, the damage models, and the fracture criterion. The relationships between the composite residual strength, fatigue peak stress, interface debonding, fibers failure and cycle number have been established. The effects of peak stress level, initial and steady-state interface shear stress, fiber Weibull modulus and fiber strength, and testing temperature on the degradation of composite strength and fibers failure have been investigated. The evolution of residual strength versus cycle number curves of non-oxide and oxide/oxide CMCs under cyclic loading at elevated temperatures in oxidative environments have been predicted.

Fluoxetine elevates allopregnanolone in female rat brain but inhibits a steroid microsomal dehydrogenase rather than activating an aldo-keto reductase

PubMed Central

Fry, J P; Li, K Y; Devall, A J; Cockcroft, S; Honour, J W; Lovick, T A

2014-01-01

Background and Purpose Fluoxetine, a selective serotonin reuptake inhibitor, elevates brain concentrations of the neuroactive progesterone metabolite allopregnanolone, an effect suggested to underlie its use in the treatment of premenstrual dysphoria. One report showed fluoxetine to activate the aldo-keto reductase (AKR) component of 3α-hydroxysteroid dehydrogenase (3α-HSD), which catalyses production of allopregnanolone from 5α-dihydroprogesterone. However, this action was not observed by others. The present study sought to clarify the site of action for fluoxetine in elevating brain allopregnanolone. Experimental Approach Adult male rats and female rats in dioestrus were treated with fluoxetine and their brains assayed for allopregnanolone and its precursors, progesterone and 5α-dihydroprogesterone. Subcellular fractions of rat brain were also used to investigate the actions of fluoxetine on 3α-HSD activity in both the reductive direction, producing allopregnanolone from 5α-dihydroprogesterone, and the reverse oxidative direction. Fluoxetine was also tested on these recombinant enzyme activities expressed in HEK cells. Key Results Short-term treatment with fluoxetine increased brain allopregnanolone concentrations in female, but not male, rats. Enzyme assays on native rat brain fractions and on activities expressed in HEK cells showed fluoxetine did not affect the AKR producing allopregnanolone from 5α-dihydroprogesterone but did inhibit the microsomal dehydrogenase oxidizing allopregnanolone to 5α-dihydroprogesterone. Conclusions and Implications Fluoxetine elevated allopregnanolone in female rat brain by inhibiting its oxidation to 5α-dihydroprogesterone by a microsomal dehydrogenase. This is a novel site of action for fluoxetine, with implications for the development of new agents and/or dosing regimens to raise brain allopregnanolone. PMID:25161074

Elevational diversity and distribution of ammonia-oxidizing archaea community in meadow soils on the Tibetan Plateau.

PubMed

Zhao, Kang; Kong, Weidong; Khan, Ajmal; Liu, Jinbo; Guo, Guangxia; Muhanmmad, Said; Zhang, Xianzhou; Dong, Xiaobin

2017-09-01

Unraveling elevational diversity patterns of plants and animals has long been attracting scientific interests. However, whether soil microorganisms exhibit similar elevational patterns remains largely less explored, especially for functional microbial communities, such as ammonia oxidizers. Here, we investigated the diversity and distribution pattern of ammonia-oxidizing archaea (AOA) in meadow soils along an elevation gradient from 4400 m to the grassline at 5100 m on the Tibetan Plateau using terminal restriction fragment length polymorphism (T-RFLP) and sequencing methods by targeting amoA gene. Increasing elevations led to lower soil temperature and pH, but higher nutrients and water content. The results showed that AOA diversity and evenness monotonically increased with elevation, while richness was relatively stable. The increase of diversity and evenness was attributed to the growth inhibition of warm-adapted AOA phylotypes by lower temperature and the growth facilitation of cold-adapted AOA phylotypes by richer nutrients at higher elevations. Low temperature thus played an important role in the AOA growth and niche separation. The AOA community variation was explained by the combined effect of all soil properties (32.6%), and 8.1% of the total variation was individually explained by soil pH. The total AOA abundance decreased, whereas soil potential nitrification rate (PNR) increased with increasing elevations. Soil PNR positively correlated with the abundance of cold-adapted AOA phylotypes. Our findings suggest that low temperature plays an important role in AOA elevational diversity pattern and niche separation, rising the negative effects of warming on AOA diversity and soil nitrification process in the Tibetan region.

Proprioceptive input patterns elevator activity in the locust flight system.

PubMed

Wolf, H; Pearson, K G

1988-06-01

1. In the locust, Locusta migratoria, the roles of two groups of wing sense organs, hind wing tegulae and wing-hinge stretch receptors, in the generation of the flight motor pattern were investigated. A preparation was employed that allowed the intracellular recording of neural activity in almost intact tethered flying locusts or after selective manipulations of sensory input. The functions of the two sets of receptors were assessed 1) by studying the phases of their discharges in the wingbeat cycle (Fig. 3), 2) by the selective ablation of input from the receptors (Figs. 4-7), and 3) by the selective stimulation of the receptor afferents (Figs. 8-12). 2. Input from the tegulae was found to be responsible for the initiation of elevator activity (Figs. 9 and 10) and for the generation of a distinct initial rapid depolarization (Figs. 4, 5, and 8) characteristic of elevator motor neuron activity in intact locusts (Figs. 1 and 16). 3. Input from the wing-hinge stretch receptors was found to control the duration of elevator depolarizations by the graded suppression of a second late component of the elevator depolarizations as wingbeat frequency increased (Figs. 6, 7, 11, and 12). The characteristics of this late component of elevator activity suggested that it is generated by the same (central nervous) mechanism that produces the elevator depolarizations recorded in deafferented animals (Fig. 2). Apparently this late component contributes to the intact pattern of elevator depolarizations only at lower wingbeat frequencies and is abolished by the action of stretch-receptor input at frequencies above approximately 15 Hz (Figs. 1, 2, and 4). At these high wingbeat frequencies elevator activity is dominated by the rapid depolarizations generated as a result of tegula input. 4. The present study demonstrates 1) that the timing of elevator motor neuron activity is determined by phasic afferent input from tegulae and stretch receptors and 2) that input from the stretch

Oxidation of high-temperature alloys (superalloys) at elevated temperatures in air: I

DOE Office of Scientific and Technical Information (OSTI.GOV)

Hussain, N.; Shahid, K.A.; Rahman, S.

1994-04-01

Four commercial alloys - Hastelloy C-4, alloy 1.4306S (SS 304L), Incoloy 800H, and Incoloy 825 - were studied for their oxidation behavior at elevated temperatures. Specimens were exposed to air from 600 to 1200[degree]C for 1 to 400 hr. Reaction kinetics of oxidation were determined, and the morphology of the surface-oxide scales was investigated. Hastelloy C-4 showed better resistance to oxidation for exposure temperatures up to 1000[degree]C in comparison with the other three alloys. In this temperature range, it follows a cubic rate law of oxidation due to formation of uniform, protective, and adherent oxide scales. The latter three alloysmore » obeyed the parabolic rate law at 1000[degree]C and 1200[degree]C, but for lower temperatures a mixed behavior was shown. The oxide layer developed on the alloy 1.4306S was always in the form of stratified nodules/warts. For longer exposures the nodules joined each other to form continuous but discrete layers. Incoloy 800H and Incoloy 825 behaved in an almost identical manner, their reaction kinetics being governed by the parabolic rate law throughout the temperature range. Oxide spalling was observed at all temperatures. In contrast to Incoloy 800H the Incoloy 825 was totally oxidized for longer exposures at 1200[degree]C. 16 refs., 12 figs., 1 tab.« less

Effect of Prior Exposure at Elevated Temperatures on Tensile Properties and Stress-Strain Behavior of Three Oxide/Oxide Ceramic Matrix Composites

DTIC Science & Technology

2015-03-26

OF THREE OXIDE/OXIDE CERAMIC MATRIX COMPOSITES THESIS Christopher J. Hull, Captain, USAF AFIT- ENY -MS-15-M-228 DEPARTMENT OF THE AIR FORCE...Government and is not subject to copyright protection in the United States. AFIT- ENY -MS-15-M-228 EFFECT OF PRIOR EXPOSURE AT ELEVATED TEMPERATURES ON...BS Captain, USAF March 2015 DISTRIBUTION STATEMENT A: APPROVED FOR PUBLIC RELEASE; DISTRIBUTION UNLIMITED AFIT- ENY - MS-15-M-228 EFFECT OF

Comparing trapezius muscle activity in the different planes of shoulder elevation

PubMed Central

Ishigaki, Tomonobu; Ishida, Tomoya; Samukawa, Mina; Saito, Hiroshi; Hirokawa, Motoki; Ezawa, Yuya; Sugawara, Makoto; Tohyama, Harukazu; Yamanaka, Masanori

2015-01-01

[Purpose] The purpose of this study was to compare the upper, middle, and lower trapezius muscles’ activity in the different planes of shoulder elevation. [Subjects] Twenty male subjects volunteered for this study. [Methods] Surface electromyographic (EMG) activity for each of the three regions of the trapezius muscles in the three different planes of elevation were collected while the participants maintained 30, 60, and 90 degrees of elevation in each plane. The EMG data were normalized with maximum voluntary isometric contraction (%MVIC), and compared among the planes at each angle of elevation. [Results] There were significantly different muscle activities among the elevation planes at each angle. [Conclusion] This study found that the three regions of the trapezius muscles changed their activity depending on the planes of shoulder elevation. These changes in the trapezius muscles could induce appropriate scapular motion to face the glenoid cavity in the correct directions in different planes of shoulder elevation. PMID:26157248

Comparing trapezius muscle activity in the different planes of shoulder elevation.

PubMed

Ishigaki, Tomonobu; Ishida, Tomoya; Samukawa, Mina; Saito, Hiroshi; Hirokawa, Motoki; Ezawa, Yuya; Sugawara, Makoto; Tohyama, Harukazu; Yamanaka, Masanori

2015-05-01

[Purpose] The purpose of this study was to compare the upper, middle, and lower trapezius muscles' activity in the different planes of shoulder elevation. [Subjects] Twenty male subjects volunteered for this study. [Methods] Surface electromyographic (EMG) activity for each of the three regions of the trapezius muscles in the three different planes of elevation were collected while the participants maintained 30, 60, and 90 degrees of elevation in each plane. The EMG data were normalized with maximum voluntary isometric contraction (%MVIC), and compared among the planes at each angle of elevation. [Results] There were significantly different muscle activities among the elevation planes at each angle. [Conclusion] This study found that the three regions of the trapezius muscles changed their activity depending on the planes of shoulder elevation. These changes in the trapezius muscles could induce appropriate scapular motion to face the glenoid cavity in the correct directions in different planes of shoulder elevation.

Non-activated high surface area expanded graphite oxide for supercapacitors

NASA Astrophysics Data System (ADS)

Vermisoglou, E. C.; Giannakopoulou, T.; Romanos, G. E.; Boukos, N.; Giannouri, M.; Lei, C.; Lekakou, C.; Trapalis, C.

2015-12-01

Microwave irradiation of graphite oxide constitutes a facile route toward production of reduced graphene oxide, since during this treatment both exfoliation and reduction of graphite oxide occurs. In this work, the effect of pristine graphite (type, size of flakes), pretreatment and oxidation cycles on the finally produced expanded material was examined. All the types of graphite that were tested afforded materials with high BET surface areas ranging from 940 m2/g to 2490 m2/g, without intervening an activation stage at elevated temperature. SEM and TEM images displayed exfoliated structures, where the flakes were significantly detached and curved. The quality of the reduced graphene oxide sheets was evidenced both by X-ray photoelectron spectroscopy and Raman spectroscopy. The electrode material capacitance was determined via electrochemical impedance spectroscopy and cyclic voltammetry. The materials with PEDOT binder had better performance (∼97 F/g) at low operation rates while those with PVDF binder performed better (∼20 F/g) at higher rates, opening up perspectives for their application in supercapacitors.

The Association Between Physical Activity and Sex-Specific Oxidative Stress in Older Adults

PubMed Central

Takahashi, Masaki; Miyashita, Masashi; Park, Jong-Hwan; Kim, Hyun-Shik; Nakamura, Yoshio; Sakamoto, Shizuo; Suzuki, Katsuhiko

2013-01-01

Oxidative stress increases with advancing age and is a mediator of several diseases including cancer, cardiovascular disease, and diabetes. Moreover, postmenopausal women have a lower estrogen concentration, which is associated with elevated oxidative stress. However, there is no definitive evidence regarding the relationship between daily physical activity and oxidative stress status in older adults, including postmenopausal women. Twenty-nine adults (age, 70.1 ± 1.0 years, mean ± SE; 12 women and 17 men) were examined in this cross-sectional study. Prior to blood collection, the participants were asked to wear a uniaxial accelerometer for 4 consecutive weeks to determine their level of physical activity. After a 48-h period of physical activity avoidance and a 10-h overnight fast, venous blood samples were obtained from each participant. Fasting plasma derivatives of reactive oxygen metabolites (d-ROMs) and malondialdehyde (MDA) concentrations of oxidative stress markers were negatively correlated with the amount of physical activity in women (d-ROMs; r = -0.708, p = 0.002) (MDA; r = -0.549, p = 0. 028), but not in men. Fasting plasma biological antioxidant potential of antioxidant capacity marker was positively correlated with the amount of physical activity in women (BAP; r = 0.657, p = 0.006) (GSH; r = 0.549, p = 0.028), but not in men. Moreover, superoxide dismutase activity of antioxidant capacity marker was positively correlated with the amount of physical activity in men (r = 0.627, p = 0.039), but not in women. There were no associations between physical activity and other oxidative stress markers (reduced and oxidized glutathione, glutathione peroxidise, thioredoxin). These findings suggest that regular physical activity may have a protective effect against oxidative stress by increasing total antioxidant capacity, especially in postmenopausal women. Key Points It is important to consider daily physical activity status when evaluating antioxidant

The association between physical activity and sex-specific oxidative stress in older adults.

PubMed

Takahashi, Masaki; Miyashita, Masashi; Park, Jong-Hwan; Kim, Hyun-Shik; Nakamura, Yoshio; Sakamoto, Shizuo; Suzuki, Katsuhiko

2013-01-01

Oxidative stress increases with advancing age and is a mediator of several diseases including cancer, cardiovascular disease, and diabetes. Moreover, postmenopausal women have a lower estrogen concentration, which is associated with elevated oxidative stress. However, there is no definitive evidence regarding the relationship between daily physical activity and oxidative stress status in older adults, including postmenopausal women. Twenty-nine adults (age, 70.1 ± 1.0 years, mean ± SE; 12 women and 17 men) were examined in this cross-sectional study. Prior to blood collection, the participants were asked to wear a uniaxial accelerometer for 4 consecutive weeks to determine their level of physical activity. After a 48-h period of physical activity avoidance and a 10-h overnight fast, venous blood samples were obtained from each participant. Fasting plasma derivatives of reactive oxygen metabolites (d-ROMs) and malondialdehyde (MDA) concentrations of oxidative stress markers were negatively correlated with the amount of physical activity in women (d-ROMs; r = -0.708, p = 0.002) (MDA; r = -0.549, p = 0. 028), but not in men. Fasting plasma biological antioxidant potential of antioxidant capacity marker was positively correlated with the amount of physical activity in women (BAP; r = 0.657, p = 0.006) (GSH; r = 0.549, p = 0.028), but not in men. Moreover, superoxide dismutase activity of antioxidant capacity marker was positively correlated with the amount of physical activity in men (r = 0.627, p = 0.039), but not in women. There were no associations between physical activity and other oxidative stress markers (reduced and oxidized glutathione, glutathione peroxidise, thioredoxin). These findings suggest that regular physical activity may have a protective effect against oxidative stress by increasing total antioxidant capacity, especially in postmenopausal women. Key PointsIt is important to consider daily physical activity status when evaluating antioxidant

Elevated nitric oxide in recurrent vulvovaginal candidiasis - association with clinical findings.

PubMed

Alvendal, Cathrin; Ehrström, Sophia; Brauner, Annelie; Lundberg, Jon O; Bohm-Starke, Nina

2017-03-01

Recurrent vulvovaginal candidiasis is defined as having three to four episodes per year and causes substantial suffering. Little is known about the mechanisms leading to relapses in otherwise healthy women. Nitric oxide is part of the nonspecific host defense and is increased during inflammation. Nitric oxide levels were measured and the expression of inducible nitric oxide synthase was analyzed in the vagina during an acute episode of recurrent vulvovaginal candidiasis and after treatment with fluconazole. Twenty-eight women with symptoms of recurrent vulvovaginal candidiasis were enrolled together with 31 healthy controls. Nitric oxide was measured with an air-filled 25-mL silicon catheter balloon incubated in the vagina for five minutes and then analyzed by chemiluminescence technique. Vaginal biopsies were analyzed for the expression of inducible nitric oxide synthase. Symptoms and clinical findings were surveyed using a scoring system. The measurements and biopsies were repeated in patients after six weeks of fluconazole treatment. Nitric oxide levels were increased during acute infection (median 352 ppb) compared with controls (median 6 ppb), p < 0.0001. The levels decreased after treatment (median 18 ppb) but were still higher than in controls. Increased expression of inducible nitric oxide synthase was observed in the epithelial basal layer in patients before and after treatment compared with controls. Before treatment, there were positive correlations between nitric oxide and symptom (r s  = 0.644) and examination scores (r s  = 0.677), p < 0.001. Nitric oxide is significantly elevated in patients with recurrent vulvovaginal candidiasis during acute episodes of infection and decreases after antifungal treatment. The results illustrate the pronounced inflammatory response in recurrent vulvovaginal candidiasis correlating to symptoms of pain and discomfort. © 2017 Nordic Federation of Societies of Obstetrics and Gynecology.

Metal chelator combined with permeability enhancer ameliorates oxidative stress-associated neurodegeneration in rat eyes with elevated intraocular pressure

PubMed Central

Liu, P.; Zhang, M.; Shoeb, M.; Hogan, D.; Tang, Luosheng; Syed, M. F.; Wang, C. Z.; Campbell, G.A.; Ansari, N.H.

2014-01-01

Since as many as half of glaucoma patients on intraocular pressure (IOP)-lowering therapy continue to experience optic nerve toxicity, it is imperative to find other effective therapies. Iron and calcium ions play key roles in oxidative stress, a hallmark of glaucoma. Therefore, we tested metal chelation by means of ethylenediaminetetraacetic acid (EDTA) combined with the permeability enhancer methyl sulfonyl methane (MSM) applied topically on the eye to determine if this non-invasive treatment is neuroprotective in rat optic nerve and retinal ganglion cells exposed to oxidative stress induced by elevated IOP. Hyaluronic acid (HA) was injected in the anterior chamber of the rat eye to elevate the IOP. EDTA-MSM was applied topically to the eye for 3 months. Eyeballs and optic nerves were processed for histological assessment of cytoarchitecture. Protein-lipid aldehyde adducts, and cyclooxygnease-2 (COX-2) were detected immunohistochemically. HA administration increased IOP and associated oxidative stress and inflammation. Elevated IOP was not affected by EDTA-MSM treatment. However oxidative damage and inflammation were ameliorated as reflected by decrease in formation of protein-lipid aldehyde adducts and COX-2 expression, respectively. Furthermore, EDTA-MSM treatment increased retinal ganglion cell survival and decreased demyelinization of optic nerve compared with untreated eyes. Chelation treatment with EDTA-MSM ameliorates sequelae of IOP-induced toxicity without affecting IOP. Since most current therapies aim at reducing IOP and damage occurs even in the absence of elevated IOP, EDTA-MSM has the potential to work in conjunction with pressure-reducing therapies to alleviate damage to the optic nerve and retinal ganglion cells. PMID:24509160

AMPK activation protects cells from oxidative stress-induced senescence via autophagic flux restoration and intracellular NAD(+) elevation.

PubMed

Han, Xiaojuan; Tai, Haoran; Wang, Xiaobo; Wang, Zhe; Zhou, Jiao; Wei, Xiawei; Ding, Yi; Gong, Hui; Mo, Chunfen; Zhang, Jie; Qin, Jianqiong; Ma, Yuanji; Huang, Ning; Xiang, Rong; Xiao, Hengyi

2016-06-01

AMPK activation is beneficial for cellular homeostasis and senescence prevention. However, the molecular events involved in AMPK activation are not well defined. In this study, we addressed the mechanism underlying the protective effect of AMPK on oxidative stress-induced senescence. The results showed that AMPK was inactivated in senescent cells. However, pharmacological activation of AMPK by metformin and berberine significantly prevented the development of senescence and, accordingly, inhibition of AMPK by Compound C was accelerated. Importantly, AMPK activation prevented hydrogen peroxide-induced impairment of the autophagic flux in senescent cells, evidenced by the decreased p62 degradation, GFP-RFP-LC3 cancellation, and activity of lysosomal hydrolases. We also found that AMPK activation restored the NAD(+) levels in the senescent cells via a mechanism involving mostly the salvage pathway for NAD(+) synthesis. In addition, the mechanistic relationship of autophagic flux and NAD(+) synthesis and the involvement of mTOR and Sirt1 activities were assessed. In summary, our results suggest that AMPK prevents oxidative stress-induced senescence by improving autophagic flux and NAD(+) homeostasis. This study provides a new insight for exploring the mechanisms of aging, autophagy and NAD(+) homeostasis, and it is also valuable in the development of innovative strategies to combat aging. © 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Active Oxidation of SiC

NASA Technical Reports Server (NTRS)

Jacobson, Nathan S.; Myers,Dwight L.; Harder, Bryan J.

2011-01-01

The high temperature oxidation of silicon carbide occurs in either a passive or active mode, depending on temperature and oxygen potential. Passive oxidation forms a protective oxide film which limits attack of the SiC:SiC(s) + 3/2 O2(g) = SiO2(s) + CO(g.) Active oxidation forms a volatile oxide and leads to extensive attack of the SiC: SiC(s) + O2(g) = SiO(g) + CO(g). The transition points and rates of active oxidation are a major issue. Previous studies are reviewed and the leading theories of passive/active transitions summarized. Comparisons are made to the active/passive transitions in pure Si, which are relatively well-understood. Critical questions remain about the difference between the active-to-passive transition and passive-to-active transition. For Si, Wagner [2] points out that the active-to-passive transition is governed by the criterion for a stable Si/SiO2 equilibria and the passive-to-active transition is governed by the decomposition of the SiO2 film. This suggests a significant oxygen potential difference between these two transitions and our experiments confirm this. For Si, the initial stages of active oxidation are characterized by the formation of SiO(g) and further oxidation to SiO2(s) as micron-sized rods, with a distinctive morphology. SiC shows significant differences. The active-to-passive and the passive-to-active transitions are close. The SiO2 rods only appear as the passive film breaks down. These differences are explained in terms of the reactions at the SiC/SiO2 interface. In order to understand the breakdown of the passive film, pre-oxidation experiments are conducted. These involve forming dense protective scales of 0.5, 1, and 2 microns and then subjecting the samples with these scales to a known active oxidation environment. Microstructural studies show that SiC/SiO2 interfacial reactions lead to a breakdown of the scale with a distinct morphology.

Activation of surface lattice oxygen in single-atom Pt/CeO 2 for low-temperature CO oxidation

DOE Office of Scientific and Technical Information (OSTI.GOV)

Nie, Lei; Mei, Donghai; Xiong, Haifeng

While single-atom catalysts can provide high catalytic activity and selectivity, application in industrial catalysts demands long term performance and the ability to regenerate the catalysts. We have investigated the factors that lead to improved catalytic activity of a Pt/CeO2 catalyst for low temperature CO oxidation. Single-atom Pt/CeO2 becomes active for CO oxidation under lean condition only at elevated temperatures, because CO is strongly bound to ionic Pt sites. Reducing the catalyst, even under mild conditions, leads to onset of CO oxidation activity even at room temperature. This high activity state involves the transformation of mononuclear Pt species to sub-nanometer sizedmore » Pt particles. Under oxidizing conditions, the Pt can be restored to its stable, single-atom state. The key to facile regeneration is the ability to create mobile Pt species and suitable trapping sites on the support, making this a prototypical catalyst system for industrial application of single-atom catalysis.« less

Interaction of vitamin E and exercise training on oxidative stress and antioxidant enzyme activities in rat skeletal muscles.

PubMed

Chang, Chen-Kang; Huang, Hui-Yu; Tseng, Hung-Fu; Hsuuw, Yan-Der; Tso, Tim K

2007-01-01

It has been shown that free radicals are increased during intensive exercise. We hypothesized that vitamin E (vit E) deficiency, which will increase oxidative stress, would augment the training-induced adaptation of antioxidant enzymes. This study investigated the interaction effect of vit E and exercise training on oxidative stress markers and activities of antioxidant enzymes in red quadriceps and white gastrocnemius of rats in a 2x2 design. Thirty-two male rats were divided into trained vit E-adequate, trained vit E-deficient, untrained vit E-adequate, and untrained vit E-deficient groups. The two trained groups swam 6 h/day, 6 days/week for 8 weeks. The two vit E-deficient groups consumed vit E-free diet for 8 weeks. Vitamin E-training interaction effect was significant on thiobarbituric acid reactive substances (TBARSs), glutathione peroxidase (GPX), and superoxide dismutase (SOD) in both muscles. The trained vit E-deficient group showed the highest TBARS and GPX activity and the lowest SOD activity in both muscles. A significant vit E effect on glutathione reductase and catalase was present in both muscles. Glutathione reductase and catalase activities were significantly lower in the two vit E-adequate groups combined than in the two vit E-deficient groups combined in both muscles. This study shows that vit E status and exercise training have interactive effect on oxidative stress and GPX and SOD activities in rat skeletal muscles. Vitamin E deprivation augmented the exercise-induced elevation in GPX activity while inhibiting exercise-induced SOD activity, possibly through elevated oxidative stress.

Creep performance of oxide ceramic fiber materials at elevated temperature in air and in steam

NASA Astrophysics Data System (ADS)

Armani, Clinton J.

Structural aerospace components that operate in severe conditions, such as extreme temperatures and detrimental environments, require structural materials that have superior long-term mechanical properties and that are thermochemically stable over a broad range of service temperatures and environments. Ceramic matrix composites (CMCs) capable of excellent mechanical performance in harsh environments are prime candidates for such applications. Oxide ceramic materials have been used as constituents in CMCs. However, recent studies have shown that high-temperature mechanical performance of oxide-oxide CMCs deteriorate in a steam-rich environment. The degradation of strength at elevated temperature in steam has been attributed to the environmentally assisted subcritical crack growth in the oxide fibers. Furthermore, oxide-oxide CMCs have shown significant increases in steady-state creep rates in steam. The present research investigated the effects of steam on the high-temperature creep and monotonic tension performance of several oxide ceramic materials. Experimental facilities were designed and configured, and experimental methods were developed to explore the influence of steam on the mechanical behaviors of ceramic fiber tows and of ceramic bulk materials under temperatures in the 1100--1300°C range. The effects of steam on creep behavior of Nextel(TM)610 and Nextel(TM)720 fiber tows were examined. Creep rates at elevated temperatures in air and in steam were obtained for both types of fibers. Relationships between creep rates and applied stresses were modeled and underlying creep mechanisms were identified. For both types of fiber tows, a creep life prediction analysis was performed using linear elastic fracture mechanics and a power-law crack velocity model. These results have not been previously reported and have critical design implications for CMC components operating in steam or near the recommended design limits. Predictions were assessed and validated via

Demonstration of nitric oxide synthase activity in crustacean hemocytes and anti-microbial activity of hemocyte-derived nitric oxide.

PubMed

Yeh, Feng-Ching; Wu, Su-Hua; Lai, Chi-Yung; Lee, Chi-Ying

2006-05-01

We determined the biochemical characteristics of nitric oxide synthase (NOS) in hemocytes of the crayfish Procambarus clarkii and investigated the roles of hemocyte-derived NO in host defense. Biochemical analysis indicated the presence of a Ca2+ -independent NOS activity, which was elevated by lipopolysaccharide (LPS) treatment. When bacteria (Staphylococcus aureus) and hemocytes were co-incubated, adhesion of bacteria to hemocytes was observed. NO donor sodium nitroprusside (SNP) significantly increased the numbers of hemocytes to which bacteria adhered. Similarly, LPS elicited bacterial adhesion and the LPS-induced adhesion was prevented by NOS inhibitor NG-monomethyl-L-arginine (L-NMMA). Finally, plate count assay demonstrated that addition of LPS to the hemocytes/bacteria co-incubation resulted in a significant decrease in bacterial colony forming unit (CFU), and that L-NMMA reversed the decreasing effect of LPS on CFU. The combined results demonstrate the presence of a Ca2+ -independent LPS-inducible NOS activity in crayfish hemocytes and suggest that hemocyte-derived NO is involved in promoting bacterial adhesion to hemocytes and enhancing bactericidal activity of hemocytes.

Overexpression of PGC-1α increases peroxisomal activity and mitochondrial fatty acid oxidation in human primary myotubes.

PubMed

Huang, Tai-Yu; Zheng, Donghai; Houmard, Joseph A; Brault, Jeffrey J; Hickner, Robert C; Cortright, Ronald N

2017-04-01

Peroxisomes are indispensable organelles for lipid metabolism in humans, and their biogenesis has been assumed to be under regulation by peroxisome proliferator-activated receptors (PPARs). However, recent studies in hepatocytes suggest that the mitochondrial proliferator PGC-1α (peroxisome proliferator-activated receptor gamma coactivator-1α) also acts as an upstream transcriptional regulator for enhancing peroxisomal abundance and associated activity. It is unknown whether the regulatory mechanism(s) for enhancing peroxisomal function is through the same node as mitochondrial biogenesis in human skeletal muscle (HSkM) and whether fatty acid oxidation (FAO) is affected. Primary myotubes from vastus lateralis biopsies from lean donors (BMI = 24.0 ± 0.6 kg/m 2 ; n = 6) were exposed to adenovirus encoding human PGC-1α or GFP control. Peroxisomal biogenesis proteins (peroxins) and genes ( PEXs ) responsible for proliferation and functions were assessed by Western blotting and real-time qRT-PCR, respectively. [1- 14 C]palmitic acid and [1- 14 C]lignoceric acid (exclusive peroxisomal-specific substrate) were used to assess mitochondrial oxidation of peroxisomal-derived metabolites. After overexpression of PGC-1α, 1 ) peroxisomal membrane protein 70 kDa (PMP70), PEX19, and mitochondrial citrate synthetase protein content were significantly elevated ( P < 0.05), 2 ) PGC-1α , PMP70 , key PEXs , and peroxisomal β-oxidation mRNA expression levels were significantly upregulated ( P < 0.05), and 3 ) a concomitant increase in lignoceric acid oxidation by both peroxisomal and mitochondrial activity was observed ( P < 0.05). These novel findings demonstrate that, in addition to the proliferative effect on mitochondria, PGC-1α can induce peroxisomal activity and accompanying elevations in long-chain and very-long-chain fatty acid oxidation by a peroxisomal-mitochondrial functional cooperation, as observed in HSkM cells. Copyright © 2017 the American Physiological Society.

Elevated fetal steroidogenic activity in autism.

PubMed

Baron-Cohen, S; Auyeung, B; Nørgaard-Pedersen, B; Hougaard, D M; Abdallah, M W; Melgaard, L; Cohen, A S; Chakrabarti, B; Ruta, L; Lombardo, M V

2015-03-01

Autism affects males more than females, giving rise to the idea that the influence of steroid hormones on early fetal brain development may be one important early biological risk factor. Utilizing the Danish Historic Birth Cohort and Danish Psychiatric Central Register, we identified all amniotic fluid samples of males born between 1993 and 1999 who later received ICD-10 (International Classification of Diseases, 10th Revision) diagnoses of autism, Asperger syndrome or PDD-NOS (pervasive developmental disorder not otherwise specified) (n=128) compared with matched typically developing controls. Concentration levels of Δ4 sex steroids (progesterone, 17α-hydroxy-progesterone, androstenedione and testosterone) and cortisol were measured with liquid chromatography tandem mass spectrometry. All hormones were positively associated with each other and principal component analysis confirmed that one generalized latent steroidogenic factor was driving much of the variation in the data. The autism group showed elevations across all hormones on this latent generalized steroidogenic factor (Cohen's d=0.37, P=0.0009) and this elevation was uniform across ICD-10 diagnostic label. These results provide the first direct evidence of elevated fetal steroidogenic activity in autism. Such elevations may be important as epigenetic fetal programming mechanisms and may interact with other important pathophysiological factors in autism.

Resveratrol protects vascular endothelial cells from high glucose-induced apoptosis through inhibition of NADPH oxidase activation-driven oxidative stress.

PubMed

Chen, Feng; Qian, Li-Hua; Deng, Bo; Liu, Zhi-Min; Zhao, Ying; Le, Ying-Ying

2013-09-01

Hyperglycemia-induced oxidative stress has been implicated in diabetic vascular complications in which NADPH oxidase is a major source of reactive oxygen species (ROS) generation. Resveratrol is a naturally occurring polyphenol, which has vasoprotective effects in diabetic animal models and inhibits high glucose (HG)-induced oxidative stress in endothelial cells. We aimed to examine whether HG-induced NADPH oxidase activation and ROS production contribute to glucotoxicity to endothelial cells and the effect of resveratrol on glucotoxicity. Using a murine brain microvascular endothelial cell line bEnd3, we found that NADPH oxidase inhibitor (apocynin) and resveratrol both inhibited HG-induced endothelial cell apoptosis. HG-induced elevation of NADPH oxidase activity and production of ROS were inhibited by apocynin, suggesting that HG induces endothelial cell apoptosis through NADPH oxidase-mediated ROS production. Mechanistic studies revealed that HG upregulated NADPH oxidase subunit Nox1 but not Nox2, Nox4, and p22(phox) expression through NF-κB activation, which resulted in elevation of NADPH oxidase activity and consequent ROS production. Resveratrol prevented HG-induced endothelial cell apoptosis through inhibiting HG-induced NF-κB activation, NADPH oxidase activity elevation, and ROS production. HG induces endothelial cell apoptosis through NF-κB/NADPH oxidase/ROS pathway, which was inhibited by resveratrol. Our findings provide new potential therapeutic targets against brain vascular complications of diabetes. © 2013 John Wiley & Sons Ltd.

Plasma homocysteine is associated with increased oxidative stress and antioxidant enzyme activity in welders.

PubMed

Liu, Hung-Hsin; Shih, Tung-Sheng; Huang, Hsin-Ru; Huang, Shih-Chien; Lee, Lien-Hsiung; Huang, Yi-Chia

2013-01-01

The purpose of this study was to examine the association of vitamin B6 status and plasma homocysteine with oxidative stress and antioxidant capacities in welders. Workers were divided into either the welding exposure group (n = 57) or the nonexposure controls (n = 42) based on whether they were employed as welders. There were no significant differences in vitamin B₆ status and plasma homocysteine concentration between the welding exposure group and the nonexposure controls. The welding exposure group had significantly higher levels of oxidized low-density lipoprotein cholesterol and lower erythrocyte glutathione concentration and superoxide dismutase (SOD) activities when compared to nonexposure controls. Plasma pyridoxal 5'-phosphate concentration did not correlate with oxidative stress indicators or antioxidant capacities in either group. However, plasma homocysteine significantly correlated with total antioxidant capacity (TAC) (partial r(s) = -0.34, P < 0.05) and erythrocyte SOD activities (partial r(s) = 0.29, P < 0.05) after adjusting for potential confounders in the welding exposure group. In the welding exposure group, adequate vitamin B₆ status was not associated with oxidative stress or antioxidant capacities. However, elevated plasma homocysteine seemed to be a major contributing factor to antioxidant capacities (TAC and erythrocyte SOD activities) in welders.

Endoplasmic Reticulum Stress Links Oxidative Stress to Impaired Pancreatic Beta-Cell Function Caused by Human Oxidized LDL.

PubMed

Plaisance, Valérie; Brajkovic, Saška; Tenenbaum, Mathie; Favre, Dimitri; Ezanno, Hélène; Bonnefond, Amélie; Bonner, Caroline; Gmyr, Valéry; Kerr-Conte, Julie; Gauthier, Benoit R; Widmann, Christian; Waeber, Gérard; Pattou, François; Froguel, Philippe; Abderrahmani, Amar

2016-01-01

Elevated plasma concentration of the pro-atherogenic oxidized low density lipoprotein cholesterol (LDL) triggers adverse effects in pancreatic beta-cells and is associated with type 2 diabetes. Here, we investigated whether the endoplasmic reticulum (ER) stress is a key player coupling oxidative stress to beta-cell dysfunction and death elicited by human oxidized LDL. We found that human oxidized LDL activates ER stress as evidenced by the activation of the inositol requiring 1α, and the elevated expression of both DDIT3 (also called CHOP) and DNAJC3 (also called P58IPK) ER stress markers in isolated human islets and the mouse insulin secreting MIN6 cells. Silencing of Chop and inhibition of ER stress markers by the chemical chaperone phenyl butyric acid (PBA) prevented cell death caused by oxidized LDL. Finally, we found that oxidative stress accounts for activation of ER stress markers induced by oxidized LDL. Induction of Chop/CHOP and p58IPK/P58IPK by oxidized LDL was mimicked by hydrogen peroxide and was blocked by co-treatment with the N-acetylcystein antioxidant. As a conclusion, the harmful effects of oxidized LDL in beta-cells requires ER stress activation in a manner that involves oxidative stress. This mechanism may account for impaired beta-cell function in diabetes and can be reversed by antioxidant treatment.

Elevated fetal steroidogenic activity in autism

PubMed Central

Baron-Cohen, S; Auyeung, B; Nørgaard-Pedersen, B; Hougaard, D M; Abdallah, M W; Melgaard, L; Cohen, A S; Chakrabarti, B; Ruta, L; Lombardo, M V

2015-01-01

Autism affects males more than females, giving rise to the idea that the influence of steroid hormones on early fetal brain development may be one important early biological risk factor. Utilizing the Danish Historic Birth Cohort and Danish Psychiatric Central Register, we identified all amniotic fluid samples of males born between 1993 and 1999 who later received ICD-10 (International Classification of Diseases, 10th Revision) diagnoses of autism, Asperger syndrome or PDD-NOS (pervasive developmental disorder not otherwise specified) (n=128) compared with matched typically developing controls. Concentration levels of Δ4 sex steroids (progesterone, 17α-hydroxy-progesterone, androstenedione and testosterone) and cortisol were measured with liquid chromatography tandem mass spectrometry. All hormones were positively associated with each other and principal component analysis confirmed that one generalized latent steroidogenic factor was driving much of the variation in the data. The autism group showed elevations across all hormones on this latent generalized steroidogenic factor (Cohen's d=0.37, P=0.0009) and this elevation was uniform across ICD-10 diagnostic label. These results provide the first direct evidence of elevated fetal steroidogenic activity in autism. Such elevations may be important as epigenetic fetal programming mechanisms and may interact with other important pathophysiological factors in autism. PMID:24888361

Anchorage of iron hydro(oxide) nanoparticles onto activated carbon to remove As(V) from water.

PubMed

Nieto-Delgado, Cesar; Rangel-Mendez, Jose Rene

2012-06-01

The adsorption of arsenic (V) by granular iron hydro(oxides) has been proven to be a reliable technique. However, due to the low mechanical properties of this material, it is difficult to apply it in full scale water treatment. Hence, the aim of this research is to develop a methodology to anchor iron hydro(oxide) nanoparticles onto activated carbon, in which the iron hydro(oxide) nanoparticles will give the activated carbon an elevated active surface area for arsenic adsorption and also help avoid the blockage of the activated carbon pores. Three activated carbons were modified by employing the thermal hydrolysis of iron as the anchorage procedure. The effects of hydrolysis temperature (60-120 °C), hydrolysis time (4-16 h), and FeCl(3) concentration (0.4-3 mol Fe/L) were studied by the surface response methodology. The iron content of the modified samples ranged from 0.73 to 5.27%, with the higher end of the range pertaining to the carbons with high oxygen content. The materials containing smaller iron hydro(oxide) particles exhibited an enhanced arsenic adsorption capacity. The best adsorbent material reported an arsenic adsorption capacity of 4.56 mg As/g at 1.5 ppm As at equilibrium and pH 7. Copyright © 2012 Elsevier Ltd. All rights reserved.

Elevation of Serum Acid Sphingomyelinase Activity in Acute Kawasaki Disease.

PubMed

Konno, Yuuki; Takahashi, Ikuko; Narita, Ayuko; Takeda, Osamu; Koizumi, Hiromi; Tamura, Masamichi; Kikuchi, Wataru; Komatsu, Akira; Tamura, Hiroaki; Tsuchida, Satoko; Noguchi, Atsuko; Takahashi, Tsutomu

2015-10-01

Kawasaki disease (KD) is an acute systemic vasculitis that affects both small and medium-sized vessels including the coronary arteries in infants and children. Acid sphingomyelinase (ASM) is a lysosomal glycoprotein that hydrolyzes sphingomyelin to ceramide, a lipid, that functions as a second messenger in the regulation of cell functions. ASM activation has been implicated in numerous cellular stress responses and is associated with cellular ASM secretion, either through alternative trafficking of the ASM precursor protein or by means of an unidentified mechanism. Elevation of serum ASM activity has been described in several human diseases, suggesting that patients with diseases involving vascular endothelial cells may exhibit a preferential elevation of serum ASM activity. As acute KD is characterized by systemic vasculitis that could affect vascular endothelial cells, the elevation of serum ASM activity should be considered in these patients. In the present study, serum ASM activity in the sera of 15 patients with acute KD was determined both before and after treatment with infusion of high-dose intravenous immunoglobulin (IVIG), a first-line treatment for acute KD. Serum ASM activity before IVIG was significantly elevated in KD patients when compared to the control group (3.85 ± 1.46 nmol/0.1 ml/6 h vs. 1.15 ± 0.10 nmol/0.1 ml/6 h, p < 0.001), suggesting that ASM activation may be involved in the pathophysiology of this condition. Serum ASM activity before IVIG was significantly correlated with levels of C-reactive protein (p < 0.05). These results suggest the involvement of sphingolipid metabolism in the pathophysiology of KD.

Stabilizing Nanocrystalline Oxide Nanofibers at Elevated Temperatures by Coating Nanoscale Surface Amorphous Films.

PubMed

Yao, Lei; Pan, Wei; Luo, Jian; Zhao, Xiaohui; Cheng, Jing; Nishijima, Hiroki

2018-01-10

Nanocrystalline materials often exhibit extraordinary mechanical and physical properties but their applications at elevated temperatures are impaired by the rapid grain growth. Moreover, the grain growth in nanocrystalline oxide nanofibers at high temperatures can occur at hundreds of degrees lower than that would occur in corresponding bulk nanocrystalline materials, which would eventually break the fibers. Herein, by characterizing a model system of scandia-stabilized zirconia using hot-stage in situ scanning transmission electron microscopy, we discover that the enhanced grain growth in nanofibers is initiated at the surface. Subsequently, we demonstrate that coating the fibers with nanometer-thick amorphous alumina layer can enhance their temperature stability by nearly 400 °C via suppressing the surface-initiated grain growth. Such a strategy can be effectively applied to other oxide nanofibers, such as samarium-doped ceria, yttrium-stabilized zirconia, and lanthanum molybdate. The nanocoatings also increase the flexibility of the oxide nanofibers and stabilize the high-temperature phases that have 10 times higher ionic conductivity. This study provides new insights into the surface-initiated grain growth in nanocrystalline oxide nanofibers and develops a facile yet innovative strategy to improve the high-temperature stability of nanofibers for a broad range of applications.

Separating the roles of nitrogen and oxygen in high pressure-induced blood-borne microparticle elevations, neutrophil activation, and vascular injury in mice.

PubMed

Yang, Ming; Bhopale, Veena M; Thom, Stephen R

2015-08-01

An elevation in levels of circulating microparticles (MPs) due to high air pressure exposure and the associated inflammatory changes and vascular injury that occur with it may be due to oxidative stress. We hypothesized that these responses arise due to elevated partial pressures of N2 and not because of high-pressure O2. A comparison was made among high-pressure air, normoxic high-pressure N2, and high-pressure O2 in causing an elevation in circulating annexin V-positive MPs, neutrophil activation, and vascular injury by assessing the leakage of high-molecular-weight dextran in a murine model. After mice were exposed for 2 h to 790 kPa air, there were over 3-fold elevations in total circulating MPs as well as subgroups bearing Ly6G, CD41, Ter119, CD31, and CD142 surface proteins-evidence of neutrophil activation; platelet-neutrophil interaction; and vascular injury to brain, omentum, psoas, and skeletal muscles. Similar changes were found in mice exposed to high-pressure N2 using a gas mixture so that O2 partial pressure was the same as that of ambient air, whereas none of these changes occurred after exposures to 166 kPa O2, the same partial pressure that occurs during high-pressure air exposures. We conclude that N2 plays a central role in intra- and perivascular changes associated with exposure to high air pressure and that these responses appear to be a novel form of oxidative stress. Copyright © 2015 the American Physiological Society.

Elevated Levels of Urinary Markers of Oxidative DNA and RNA Damage in Type 2 Diabetes with Complications.

PubMed

Liu, Xinle; Gan, Wei; Zou, Yuangao; Yang, Bin; Su, Zhenzhen; Deng, Jin; Wang, Lanlan; Cai, Jianping

2016-01-01

The mechanisms underlying progression of type 2 diabetes are complex and varied. Recent studies indicated that oxidative stress provided a new sight. To further assess the relationship between nucleic acid oxidation and complications in patients with type 2 diabetes and explore its possible molecular mechanisms, we studied 1316 subjects, including 633 type 2 diabetes patients and 683 age- and sex-matched healthy controls. Urinary levels of DNA oxidation marker 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) and RNA oxidation marker 8-oxo-7,8-dihydroguanosine (8-oxoGuo) were measured by ultraperformance liquid chromatography and mass spectrometry (UPLC-MS/MS). Serum glucose, HbA1c, total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides (TG) were also determined. The results showed significantly elevated levels of both the urinary 8-oxodGuo and 8-oxoGuo in diabetes patients with/without complications compared with age-matched healthy control subjects (p = 0.02 and p < 0.001, resp.). Patients with complications, especially macrovascular complications, exhibited higher levels of 8-oxoGuo than those without complications, while there was no difference in the concentrations of serum glucose and lipids. The finding indicates the role for oxidative damage to DNA and RNA, as a molecular mechanism contributing to the progression of type 2 diabetes. Elevated levels of 8-oxoGuo may be a risk factor for type 2 diabetes complications, especially in diabetic macrovascular complications.

Serum nitric oxide metabolites and disease activity in patients with systemic sclerosis.

PubMed

Mok, Mo Yin; Fung, Peter Chin Wah; Ooi, Clara; Tse, Hung Fat; Wong, Yik; Lam, Yui Ming; Wong, Woon Sing; Lau, Chak Sing

2008-03-01

There is no surrogate marker in serum for defining disease activity in scleroderma (SSc). Nitric oxide (NO), which regulates vasodilation and possesses pro-inflammatory actions, has been implicated in the pathogenesis of SSc. We compared serum NO(x) (total nitrate and nitrite) level in SSc patients to healthy controls and evaluated its correlation with detailed symptomatology and scoring systems for various organ involvement. Symptoms and physical findings that suggested disease activity in regard to various organs were documented. Lung function test, high-resolution computed tomographic (HRCT) scan of thorax and echocardiography were performed. Serum NO(x) was measured by chemiluminescence. Serum NO(x) levels in SSc (n = 43) were significantly higher (72.4 +/- 47.8 microM) than age- and sex-matched controls (n = 41; 37.1 +/- 13.5 microM; p < 0.001). Serum NO(x) were not found to be associated with lung fibrosis defined by lung function parameters or inflammation and fibrosis scores on HRCT. Twenty-two patients were found to have elevated serum NO(x) level defined as mean +/- 2 SD of normal controls. Logistic regression analysis revealed that age (OR 1.12, p = 0.02) and elevated pulmonary arterial pressure (PAP) (n = 9; OR 145.3, p = 0.01) were predictive factors for elevated serum NO(x). Prednisolone use was associated with lower serum NO(x) level (OR 0.06, p = 0.04). Elevated PAP of increasing severity was found to be associated with higher level of serum NO(x) (p = 0.004 by trend). Serum NO(x) in SSc patients were elevated compared to healthy controls. Serum NO(x) level was determined by multiple factors including age, prednisolone use, and elevated PAP.

Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving.

PubMed

Yang, Ming; Barak, Otto F; Dujic, Zeljko; Madden, Dennis; Bhopale, Veena M; Bhullar, Jasjeet; Thom, Stephen R

2015-08-15

Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role that oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 wk later ascorbic acid (2 g) daily for 6 days prior to performing either a 47-min dive to 18 m of sea water while breathing air (∼222 kPa N2/59 kPa O2) or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 min (∼40 kPa N2/59 kPa O2). Within 30 min after the 18-m dive in the placebo group, neutrophil activation, and platelet-neutrophil interactions occurred, and the total number of microparticles, as well as subgroups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine, increased approximately twofold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by transthoracic echocardiography. We conclude that high-pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation. Copyright © 2015 the American Physiological Society.

Plasma Homocysteine Is Associated with Increased Oxidative Stress and Antioxidant Enzyme Activity in Welders

PubMed Central

Liu, Hung-Hsin; Shih, Tung-Sheng; Huang, Hsin-Ru; Huang, Shih-Chien; Lee, Lien-Hsiung; Huang, Yi-Chia

2013-01-01

The purpose of this study was to examine the association of vitamin B6 status and plasma homocysteine with oxidative stress and antioxidant capacities in welders. Workers were divided into either the welding exposure group (n = 57) or the nonexposure controls (n = 42) based on whether they were employed as welders. There were no significant differences in vitamin B6 status and plasma homocysteine concentration between the welding exposure group and the nonexposure controls. The welding exposure group had significantly higher levels of oxidized low-density lipoprotein cholesterol and lower erythrocyte glutathione concentration and superoxide dismutase (SOD) activities when compared to nonexposure controls. Plasma pyridoxal 5′-phosphate concentration did not correlate with oxidative stress indicators or antioxidant capacities in either group. However, plasma homocysteine significantly correlated with total antioxidant capacity (TAC) (partial r s = −0.34, P < 0.05) and erythrocyte SOD activities (partial r s = 0.29, P < 0.05) after adjusting for potential confounders in the welding exposure group. In the welding exposure group, adequate vitamin B6 status was not associated with oxidative stress or antioxidant capacities. However, elevated plasma homocysteine seemed to be a major contributing factor to antioxidant capacities (TAC and erythrocyte SOD activities) in welders. PMID:24106453

Elevational characteristics of the archaeal community in full-scale activated sludge wastewater treatment plants at a 3,660-meter elevational scale.

PubMed

Niu, Lihua; Zhang, Xue; Li, Yi; Wang, Peifang; Zhang, Wenlong; Wang, Chao; Wang, Qing

2017-07-01

Due to the important roles of archaea in wastewater treatment processes, archaeal communities have been studied extensively in various anaerobic reactors, but the knowledge of archaeal communities in full-scale activated sludge wastewater treatment plants (WWTPs) remains quite poor. In this study, 454-pyrosequencing was for the first time employed to investigate archaeal communities from 20 full-scale activated sludge WWTPs distributed at a 3,660-meter elevational scale in China. Results showed that archaeal communities from WWTPs were dominated by Methanosarcinales (84.6%). A core archaeal population (94.5%) composed of Methanosaeta, Methanosarcina, Methanogenium and Methanobrevibacter was shared among WWTPs. The elevational pattern of archaeal communities was observed in WWTPs, with an elevational threshold associated with archaeal community richness and structures at approximately 1,500 meters above sea level (masl). A declining trend in community richness with increasing elevation was observed at higher elevations, whereas no trend was presented at lower elevations. Spearman correlation analysis indicated that the archaeal community richness at higher elevations was associated with more environmental variables than that at lower elevations. Redundancy analysis indicated that wastewater variables were the dominant contributors to the variation of community structures at higher elevations, followed by operational variables and elevation.

Microstructure and elevated-temperature erosion-oxidation behaviour of aluminized 9Cr-1Mo Steel

NASA Astrophysics Data System (ADS)

Huttunen-Saarivirta, E.; Honkanen, M.; Tsipas, S. A.; Omar, H.; Tsipas, D.

2012-10-01

Degradation of materials by a combination of erosive wear and atmospheric oxidation at elevated temperatures constitutes a problem in some power generation processes, such as fluidized-bed combustion. In this work, 9Cr-1Mo steel, a common tube material in combustion chambers, is coated by a pack cementation method from an Al-containing pack in order to improve the resistance to erosion-oxidation at elevated temperatures. The resulting coating is studied in terms of microstructure and microhardness and tested for its resistance against impacts by sand particles in air at temperatures of 550-700 °C under several conditions, with thickness changes and appearance of the exposed surfaces being studied. The coating was found to contain several phases and layers, the outermost of which was essentially Al-rich and contained e.g., small AlN precipitates. The microhardness values for such coating ranged from 950 to 1100 HV20g. The coating provided the substrate with increased protection particularly against normal particle impacts, as manifested by smaller thickness losses for coated specimens as compared to uncoated counterparts. However, much of the coating was lost under all test conditions, despite the fact that particle debris formed a homogeneous layer on the surface. These results are described and discussed in this paper.

Cystic Fibrosis Transmembrane Conductance Regulator Controls Lung Proteasomal Degradation and Nuclear Factor-κB Activity in Conditions of Oxidative Stress

PubMed Central

Boncoeur, Emilie; Roque, Telma; Bonvin, Elise; Saint-Criq, Vinciane; Bonora, Monique; Clement, Annick; Tabary, Olivier; Henrion-Caude, Alexandra; Jacquot, Jacky

2008-01-01

Cystic fibrosis is a lethal inherited disorder caused by mutations in a single gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein, resulting in progressive oxidative lung damage. In this study, we evaluated the role of CFTR in the control of ubiquitin-proteasome activity and nuclear factor (NF)-κB/IκB-α signaling after lung oxidative stress. After a 64-hour exposure to hyperoxia-mediated oxidative stress, CFTR-deficient (cftr−/−) mice exhibited significantly elevated lung proteasomal activity compared with wild-type (cftr+/+) animals. This was accompanied by reduced lung caspase-3 activity and defective degradation of NF-κB inhibitor IκB-α. In vitro, human CFTR-deficient lung cells exposed to oxidative stress exhibited increased proteasomal activity and decreased NF-κB-dependent transcriptional activity compared with CFTR-sufficient lung cells. Inhibition of the CFTR Cl− channel by CFTRinh-172 in the normal bronchial immortalized cell line 16HBE14o− increased proteasomal degradation after exposure to oxidative stress. Caspase-3 inhibition by Z-DQMD in CFTR-sufficient lung cells mimicked the response profile of increased proteasomal degradation and reduced NF-κB activity observed in CFTR-deficient lung cells exposed to oxidative stress. Taken together, these results suggest that functional CFTR Cl− channel activity is crucial for regulation of lung proteasomal degradation and NF-κB activity in conditions of oxidative stress. PMID:18372427

Elevated Glucose Oxidation, Reduced Insulin Secretion, and a Fatty Heart May Be Protective Adaptions in Ischemic CAD.

PubMed

Hannukainen, J C; Lautamäki, R; Mari, A; Pärkkä, J P; Bucci, M; Guzzardi, M A; Kajander, S; Tuokkola, T; Knuuti, J; Iozzo, P

2016-07-01

Insulin resistance, β-cell dysfunction, and ectopic fat deposition have been implicated in the pathogenesis of coronary artery disease (CAD) and type 2 diabetes, which is common in CAD patients. We investigated whether CAD is an independent predictor of these metabolic abnormalities and whether this interaction is influenced by superimposed myocardial ischemia. We studied CAD patients with (n = 8) and without (n = 14) myocardial ischemia and eight non-CAD controls. Insulin sensitivity and secretion and substrate oxidation were measured during fasting and oral glucose tolerance testing. We used magnetic resonance imaging/spectroscopy, positron emission and computerized tomography to characterize CAD, cardiac function, pericardial and abdominal adipose tissue, and myocardial, liver, and pancreatic triglyceride contents. Ischemic CAD was characterized by elevated oxidative glucose metabolism and a proportional decline in β-cell insulin secretion and reduction in lipid oxidation. Cardiac function was preserved in CAD groups, whereas cardiac fat depots were elevated in ischemic CAD compared to non-CAD subjects. Liver and pancreatic fat contents were similar in all groups and related with surrounding adipose masses or systemic insulin sensitivity. In ischemic CAD patients, glucose oxidation is enhanced and correlates inversely with insulin secretion. This can be seen as a mechanism to prevent glucose lowering because glucose is required in oxygen-deprived tissues. On the other hand, the accumulation of cardiac triglycerides may be a physiological adaptation to the limited fatty acid oxidative capacity. Our results underscore the urgent need of clinical trials that define the optimal/safest glycemic range in situations of myocardial ischemia.

Elevated Glucose Oxidation, Reduced Insulin Secretion, and a Fatty Heart May Be Protective Adaptions in Ischemic CAD

PubMed Central

Hannukainen, J. C.; Lautamäki, R.; Mari, A.; Pärkkä, J. P.; Bucci, M.; Guzzardi, M. A.; Kajander, S.; Tuokkola, T.; Knuuti, J.

2016-01-01

Background: Insulin resistance, β-cell dysfunction, and ectopic fat deposition have been implicated in the pathogenesis of coronary artery disease (CAD) and type 2 diabetes, which is common in CAD patients. We investigated whether CAD is an independent predictor of these metabolic abnormalities and whether this interaction is influenced by superimposed myocardial ischemia. Methods and Results: We studied CAD patients with (n = 8) and without (n = 14) myocardial ischemia and eight non-CAD controls. Insulin sensitivity and secretion and substrate oxidation were measured during fasting and oral glucose tolerance testing. We used magnetic resonance imaging/spectroscopy, positron emission and computerized tomography to characterize CAD, cardiac function, pericardial and abdominal adipose tissue, and myocardial, liver, and pancreatic triglyceride contents. Ischemic CAD was characterized by elevated oxidative glucose metabolism and a proportional decline in β-cell insulin secretion and reduction in lipid oxidation. Cardiac function was preserved in CAD groups, whereas cardiac fat depots were elevated in ischemic CAD compared to non-CAD subjects. Liver and pancreatic fat contents were similar in all groups and related with surrounding adipose masses or systemic insulin sensitivity. Conclusions: In ischemic CAD patients, glucose oxidation is enhanced and correlates inversely with insulin secretion. This can be seen as a mechanism to prevent glucose lowering because glucose is required in oxygen-deprived tissues. On the other hand, the accumulation of cardiac triglycerides may be a physiological adaptation to the limited fatty acid oxidative capacity. Our results underscore the urgent need of clinical trials that define the optimal/safest glycemic range in situations of myocardial ischemia. PMID:27045985

Modelling the descent of nitric oxide during the elevated stratopause event of January 2013

NASA Astrophysics Data System (ADS)

Orsolini, Yvan J.; Limpasuvan, Varavut; Pérot, Kristell; Espy, Patrick; Hibbins, Robert; Lossow, Stefan; Raaholt Larsson, Katarina; Murtagh, Donal

2017-03-01

Using simulations with a whole-atmosphere chemistry-climate model nudged by meteorological analyses, global satellite observations of nitrogen oxide (NO) and water vapour by the Sub-Millimetre Radiometer instrument (SMR), of temperature by the Microwave Limb Sounder (MLS), as well as local radar observations, this study examines the recent major stratospheric sudden warming accompanied by an elevated stratopause event (ESE) that occurred in January 2013. We examine dynamical processes during the ESE, including the role of planetary wave, gravity wave and tidal forcing on the initiation of the descent in the mesosphere-lower thermosphere (MLT) and its continuation throughout the mesosphere and stratosphere, as well as the impact of model eddy diffusion. We analyse the transport of NO and find the model underestimates the large descent of NO compared to SMR observations. We demonstrate that the discrepancy arises abruptly in the MLT region at a time when the resolved wave forcing and the planetary wave activity increase, just before the elevated stratopause reforms. The discrepancy persists despite doubling the model eddy diffusion. While the simulations reproduce an enhancement of the semi-diurnal tide following the onset of the 2013 SSW, corroborating new meteor radar observations at high northern latitudes over Trondheim (63.4°N), the modelled tidal contribution to the forcing of the mean meridional circulation and to the descent is a small portion of the resolved wave forcing, and lags it by about ten days.

Progranulin causes adipose insulin resistance via increased autophagy resulting from activated oxidative stress and endoplasmic reticulum stress.

PubMed

Guo, Qinyue; Xu, Lin; Li, Huixia; Sun, Hongzhi; Liu, Jiali; Wu, Shufang; Zhou, Bo

2017-01-31

Progranulin (PGRN) has recently emerged as an important regulator for insulin resistance. However, the direct effect of progranulin in adipose insulin resistance associated with the autophagy mechanism is not fully understood. In the present study, progranulin was administered to 3T3-L1 adipocytes and C57BL/6 J mice with/without specific inhibitors of oxidative stress and endoplasmic reticulum stress, and metabolic parameters, oxidative stress, endoplasmic reticulum stress and autophagy markers were assessed. Progranulin treatment increased iNOS expression, NO synthesis and ROS generation, and elevated protein expressions of CHOP, GRP78 and the phosphorylation of PERK, and caused a significant increase in Atg7 and LC3-II protein expression and a decreased p62 expression, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and glucose uptake, demonstrating that progranulin activated oxidative stress and ER stress, elevated autophagy and induced insulin insensitivity in adipocytes and adipose tissue of mice. Interestingly, inhibition of iNOS and ER stress both reversed progranulin-induced stress response and increased autophagy, protecting against insulin resistance in adipocytes. Furthermore, the administration of the ER stress inhibitor 4-phenyl butyric acid reversed the negative effect of progranulin in vivo. Our findings showed the clinical potential of the novel adipokine progranulin in the regulation of insulin resistance, suggesting that progranulin might mediate adipose insulin resistance, at least in part, by inducing autophagy via activated oxidative stress and ER stress.

Inhibition of autophagy promotes CYP2E1-dependent toxicity in HepG2 cells via elevated oxidative stress, mitochondria dysfunction and activation of p38 and JNK MAPK☆

PubMed Central

Wu, Defeng; Cederbaum, Arthur I.

2013-01-01

Autophagy has been shown to be protective against drug and alcohol-induced liver injury. CYP2E1 plays a role in the toxicity of ethanol, carcinogens and certain drugs. Inhibition of autophagy increased ethanol-toxicity and accumulation of fat in wild type and CYP2E1 knockin mice but not in CYP2E1 knockout mice as well as in HepG2 cells expressing CYP2E1 (E47 cells) but not HepG2 cells lacking CYP2E1 (C34 cells). The goal of the current study was to evaluate whether modulation of autophagy can affect CYP2E1-dependent cytotoxicity in the E47 cells. The agents used to promote CYP2E1 –dependent toxicity were a polyunsaturated fatty acid, arachidonic acid (AA), buthionine sulfoximine (BSO), which depletes GSH, and CCl4, which is metabolized to the CCl3 radical. These three agents produced a decrease in E47 cell viability which was enhanced upon inhibition of autophagy by 3-methyladenine (3-MA) or Atg 7 siRNA. Toxicity was lowered by rapamycin which increased autophagy and was much lower to the C34 cells which do not express CYP2E1. Toxicity was mainly necrotic and was associated with an increase in reactive oxygen production and oxidative stress; 3-MA increased while rapamycin blunted the oxidative stress. The enhanced toxicity and ROS formation produced when autophagy was inhibited was prevented by the antioxidant N-Acetyl cysteine. AA, BSO and CCl4 produced mitochondrial dysfunction, lowered cellular ATP levels and elevated mitochondrial production of ROS. This mitochondrial dysfunction was enhanced by inhibition of autophagy with 3-MA but decreased when autophagy was increased by rapamycin. The mitogen activated protein kinases p38 MAPK and JNK were activated by AA especially when autophagy was inhibited and chemical inhibitors of p38 MAPK and JNK lowered the elevated toxicity of AA produced by 3-MA. These results show that autophagy was protective against the toxicity produced by several agents known to be activated by CYP2E1. Since CYP2E1 plays an important role

A comparison of bat activity at low and high elevations in the Black Hills of western Washington

USGS Publications Warehouse

Erickson, J.; Adams, Michael J.

2003-01-01

We examined the differences in activity patterns and community structure of bats between low (<150 m) and high ( ! 575 m) elevation sites in two habitats of the Capitol State Forest, Washington. Total bat activity averaged four times higher at low elevation sites than at high elevation sites. Feeding activity was almost 20 times higher at low elevation sites. However, the non-myotis group had similar activity levels at high and low elevation, whereas myotis group activity decreased at higher elevations. Different levels of activity between elevations could be the result of differences in insect availability, climatic conditions, and morphology of the bat species.

Activation of NMDA receptor by elevated homocysteine in chronic liver disease contributes to encephalopathy.

PubMed

Choudhury, Sabanum; Borah, Anupom

2015-07-01

Liver diseases lead to a complex syndrome characterized by neurological, neuro-psychiatric and motor complications, called hepatic encephalopathy, which is prevalent in patients and animal models of acute, sub-chronic and chronic liver failure. Although alterations in GABAergic, glutamatergic, cholinergic and serotonergic neuronal functions have been implicated in HE, the molecular mechanisms that lead to HE in chronic liver disease (CLD) is least illustrated. Due to hepatocellular failure, levels of ammonia and homocysteine (Hcy), in addition to others, are found to increase in the brain as well as plasma. Hcy, a non-protein forming amino acid and an excitotoxin, activates ionotropic glutamate (n-methyl-d-aspartate; NMDA) receptors, and thereby leads to influx of Ca(2+) into neurons, which in turn activates several pathways that trigger oxidative stress, inflammation and apoptosis, collectively called excitotoxicity. Elevated levels of Hcy in the plasma and brain, a condition called Hyperhomocysteinemia (HHcy), and the resultant NMDA receptor-mediated excitotoxicity has been implicated in several diseases, including Parkinson's disease and Alzheimer's disease. Although, hyperammonemia has been shown to cause excitotoxicity, the role of HHcy in the development of behavioral and neurochemical alterations that occur in HE has not been illustrated yet. It is hypothesized that CLD-induced HHcy plays a major role in the development of HE through activation of NMDA receptors. It is further hypothesized that HHcy synergizes with hyperammonemia to activate NMDA receptor in the brain, and thereby cause oxidative stress, inflammation and apoptosis, and neuronal loss that leads to HE. Copyright © 2015 Elsevier Ltd. All rights reserved.

Elevated serum angiotensin-converting enzyme (SACE) activity in acute pulmonary histoplasmosis.

PubMed

Davies, S F; Rohrbach, M S; Thelen, V; Kuritsky, J; Gruninger, R; Simpson, M L; DeRemee, R A

1984-03-01

Serum angiotensin-converting enzyme (SACE) levels were measured in 44 subjects six weeks after acute pulmonary histoplasmosis. All patients were infected in a common-source outbreak of histoplasmosis which occurred on one day. All patients had both strictly defined clinical and serologic evidence of infection. The SACE activity was elevated at six weeks compared to normal controls, and seven of the 44 had levels more than 2 SD above the normal mean. SACE levels were also measured at three and 24 weeks after acute infection in a smaller number of the same subjects. Serial observations demonstrated that all subjects (including those with normal and elevated SACE at six weeks) had a rise and fall in SACE activity following symptomatic acute pulmonary histoplasmosis. Our findings suggest that elevated SACE does not reliably separate sarcoidosis from histoplasmosis, although elevations in histoplasmosis are much less common and may occur only briefly following acute pulmonary histoplasmosis. More important, it seems that SACE activity rises acutely in all patients with symptomatic acute histoplasmosis and then falls gradually toward baseline over several months, coinciding temporally with the granulomatous response.

Chronic treatment with fibrates elevates superoxide dismutase in adult mouse brain microvessels

PubMed Central

Wang, Guangming; Liu, Xiaowei; Guo, Qingmin; Namura, Shobu

2010-01-01

Fibrates are activators of peroxisome proliferator-activated receptor (PPAR) α. Pretreatment with fibrates has been shown to protect brain against ischemia in mice. We hypothesized that fibrates elevate superoxide dismutase (SOD) levels in the brain microvessels (BMV). BMV were isolated from male C57BL/6 and PPARα null mice that had been treated with fenofibrate or gemfibrozil for 7 days. To examine the effect of discontinuation of fenofibrate, another animal group treated with fenofibrate was examined on post-discontinuation day 3 (D-3). To examine whether SOD elevations attenuate oxidative stress in the ischemic brain, separate animals treated with fenofibrate for 7 days were subjected to 60 minutes focal ischemia on post-discontinuation day 0 (D-0) or D-3. Fenofibrate (30 mg/kg) increased mRNA levels of all three isoforms of SOD and activity level in BMV on D-0 but these effects were not detected on D-3. The elevations were not detected in PPARα null mice. SOD levels were also elevated by gemfibrozil (30 mg/kg). Fenofibrate significantly reduced superoxide production and protein oxidation in the ischemic brain at 30 minutes after reperfusion. Fenofibrate reduced infarct size measured at 24 hours after reperfusion on D-0; however, the infarct reduction was not seen when ischemia was induced on D-3. These findings suggest that fibrates elevate SOD in BMV through PPARα, which contributes to the infarct reduction, at least in part. Further studies are needed to establish the link between the SOD elevations and the brain protection by fibrates against ischemia. PMID:20813100

Evidence that elevated CO2 levels can indirectly increase rhizosphere denitrifier activity

NASA Technical Reports Server (NTRS)

Smart, D. R.; Ritchie, K.; Stark, J. M.; Bugbee, B.

1997-01-01

We examined the influence of elevated CO2 concentration on denitrifier enzyme activity in wheat rhizoplanes by using controlled environments and solution culture techniques. Potential denitrification activity was from 3 to 24 times higher on roots that were grown under an elevated CO2 concentration of 1,000 micromoles of CO2 mol-1 than on roots grown under ambient levels of CO2. Nitrogen loss, as determined by a nitrogen mass balance, increased with elevated CO2 levels in the shoot environment and with a high NO3- concentration in the rooting zone. These results indicated that aerial CO2 concentration can play a role in rhizosphere denitrifier activity.

SIRT1 activation by curcumin pretreatment attenuates mitochondrial oxidative damage induced by myocardial ischemia reperfusion injury.

PubMed

Yang, Yang; Duan, Weixun; Lin, Yan; Yi, Wei; Liang, Zhenxing; Yan, Juanjuan; Wang, Ning; Deng, Chao; Zhang, Song; Li, Yue; Chen, Wensheng; Yu, Shiqiang; Yi, Dinghua; Jin, Zhenxiao

2013-12-01

Ischemia reperfusion (IR) injury (IRI) is harmful to the cardiovascular system and causes mitochondrial oxidative stress. Silent information regulator 1 (SIRT1), a type of histone deacetylase, contributes to IRI. Curcumin (Cur) is a strong natural antioxidant and is the active component in Curcuma longa; Cur has protective effects against IRI and may regulate the activity of SIRT1. This study was designed to investigate the protective effect of Cur pretreatment on myocardial IRI and to elucidate this potential mechanism. Isolated and in vivo rat hearts and cultured neonatal rat cardiomyocytes were subjected to IR. Prior to this procedure, the hearts or cardiomyocytes were exposed to Cur in the absence or presence of the SIRT1 inhibitor sirtinol or SIRT1 siRNA. Cur conferred a cardioprotective effect, as shown by improved postischemic cardiac function, decreased myocardial infarct size, decreased myocardial apoptotic index, and several biochemical parameters, including the up-regulation of the antiapoptotic protein Bcl2 and the down-regulation of the proapoptotic protein Bax. Sirtinol and SIRT1 siRNA each blocked the Cur-mediated cardioprotection by inhibiting SIRT1 signaling. Cur also resulted in a well-preserved mitochondrial redox potential, significantly elevated mitochondrial superoxide dismutase activity, and decreased formation of mitochondrial hydrogen peroxide and malondialdehyde. These observations indicated that the IR-induced mitochondrial oxidative damage was remarkably attenuated. However, this Cur-elevated mitochondrial function was reversed by sirtinol or SIRT1 siRNA treatment. In summary, our results demonstrate that Cur pretreatment attenuates IRI by reducing IR-induced mitochondrial oxidative damage through the activation of SIRT1 signaling. © 2013 Elsevier Inc. All rights reserved.

A benzoxazine derivative induces vascular endothelial cell apoptosis in the presence of fibroblast growth factor-2 by elevating NADPH oxidase activity and reactive oxygen species levels.

PubMed

Zhao, Jing; He, Qiuxia; Cheng, Yizhe; Zhao, Baoxiang; Zhang, Yun; Zhang, Shangli; Miao, Junying

2009-09-01

Previously, we found that 6,8-dichloro-2,3-dihydro-3-hydroxymethyl-1,4-benzoxazine (DBO) promoted apoptosis of human umbilical vascular endothelial cells (HUVECs) deprived of growth factors. In this study, we aimed to investigate the effect of DBO and its mechanism of action on angiogenesis and apoptosis of HUVECs in the presence of fibroblast growth factor-2 (FGF-2), which promotes angiogenesis and inhibits apoptosis in vivo and in vitro. DBO significantly inhibited capillary-like tube formation by promoting apoptosis of HUVECs in the presence of FGF-2 in vitro. Furthermore, DBO elevated the levels of reactive oxygen species (ROS) and nitric oxide (NO) and increased the activity of NADPH oxidase and inducible nitric oxide synthase (iNOS) in promoting apoptosis under this condition. Moreover, when NADPH oxidase was inhibited by its specific inhibitor, dibenziodolium chloride (DPI), DBO could not elevate ROS and NO levels in HUVECs. The data suggest that DBO is a new modulator of apoptosis in vitro, and it might function by increasing the activity of NADPH oxidase and iNOS, subsequently elevating the levels of ROS and NO in HUVECs. The findings of this study provide a new small molecule for investigating the FGF-2/NADPH oxidase/iNOS signaling pathway in apoptosis.

Elevated nitrogen metabolism and nitric oxide production are involved in Arabidopsis resistance to acid rain.

PubMed

Qiao, Fang; Zhang, Xi-Min; Liu, Xiang; Chen, Juan; Hu, Wen-Jun; Liu, Ting-Wu; Liu, Ji-Yun; Zhu, Chun-Quan; Ghoto, Kabir; Zhu, Xue-Yi; Zheng, Hai-Lei

2018-06-01

Acid rain (AR) can induce great damages to plants and could be classified into different types according to the different SO 4 2- /NO 3 - ratio. However, the mechanism of plants' responding to different types of AR has not been elucidated clearly. Here, we found that nitric-rich simulated AR (N-SiAR) induced less leaves injury as lower necrosis percentage, better physiological parameters and reduced oxidative damage in the leaves of N-SiAR treated Arabidopsis thaliana compared with sulfate and nitrate mixed (SN-SiAR) or sulfuric-rich (S-SiAR) simulated AR treated ones. Of these three types of SiAR, N-SiAR treated Arabidopsis maintained the highest of nitrogen (N) content, nitrate reductase (NR) and nitrite reductase (NiR) activity as well as N metabolism related genes expression level. Nitric oxide (NO) content showed that N-SiAR treated seedlings had a higher NO level compared to SN-SiAR or S-SiAR treated ones. A series of NO production and elimination related reagents and three NO production-related mutants were used to further confirm the role of NO in regulating acid rain resistance in N-SiAR treated Arabidopsis seedlings. Taken together, we concluded that an elevated N metabolism and enhanced NO production are involved in the tolerance to different types of AR in Arabidopsis. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Active Oxidation of a UHTC-Based CMC

NASA Technical Reports Server (NTRS)

Glass, David E.; Splinter, Scott C.

2012-01-01

The active oxidation of ceramic matrix composites (CMC) is a severe problem that must be avoided for multi-use hypersonic vehicles. Much work has been performed studying the active oxidation of silicon-based CMCs such as C/SiC and SiC-coated carbon/carbon (C/C). Ultra high temperature ceramics (UTHC) have been proposed as a possible material solution for high-temperature applications on hypersonic vehicles. However, little work has been performed studying the active oxidation of UHTCs. The intent of this paper is to present test data indicating an active oxidation process for a UHTC-based CMC similar to the active oxidation observed with Si-based CMCs. A UHTC-based CMC was tested in the HyMETS arc-jet facility (or plasma wind tunnel, PWT) at NASA Langley Research Center, Hampton, VA. The coupon was tested at a nominal surface temperature of 3000 F (1650 C), with a stagnation pressure of 0.026 atm. A sudden and large increase in surface temperature was noticed with negligible increase in the heat flux, indicative of the onset of active oxidation. It is shown that the surface conditions, both temperature and pressure, fall within the region for a passive to active transition (PAT) of the oxidation.

Amino acid modified Ni catalyst exhibits reversible H2 oxidation/production over a broad pH range at elevated temperatures

DOE PAGES

Dutta, Arnab; DuBois, Daniel L.; Roberts, John A.; ...

2014-11-18

Hydrogenases interconvert H2 and protons at high rates and with high energy efficiencies, providing inspiration for the development of molecular catalysts. Studies designed to determine how the protein scaffold can influence a catalytically active site has led to the synthesis of amino acid derivatives, [Ni(PCy2NAmino acid2)2]2+ (CyAA), of [Ni(PR2NR'2)2]2+ complexes. It is shown that these CyAA derivatives can catalyze fully reversible H2 production/oxidation, a feature reminiscent of enzymes. The reversibility is achieved in acidic aqueous solutions, 0.25% H2/Ar, and elevated temperatures (tested up to 348 K) for the glycine (CyGly), arginine (CyArg), and arginine methyl ester (CyArgOMe) derivatives. As expectedmore » for a reversible process, the activity is dependent upon H2 and proton concentration. CyArg is significantly faster in both directions than the other two derivatives (~300 s-1 H2 production and 20 s-1 H2 oxidation; pH=1, 348 K). The significantly slower rates for CyArgOMe (35 s-1 production and 7 s-1 oxidation) compared to CyArg suggests an important role for the COOH group during catalysis. That CyArg is faster than CyGly (3 s-1 production and 4 s-1 oxidation under the same conditions) suggests that the additional structural features imparted by the guanidinium groups facilitate fast and reversible H2 addition/release. These observations demonstrate that appended, outer coordination sphere amino acids work in synergy with the active site and can play an equally important role for synthetic molecular electrocatalysts as the protein scaffold does for redox active enzymes. This work was funded by the Office of Science Early Career Research Program through the US DOE, BES (AD, WJS), and the Center for Molecular Electrocatalysis, an Energy Frontier Research Center funded by the US DOE, BES (DLD, JASR). PNNL is operated by Battelle for the US DOE.« less

Magnetic graphene oxide-polystyrene and magnetic activated carbon-polystyrene nanocomposites as sorbents for bisphenol A.

NASA Astrophysics Data System (ADS)

Rekos, Kyriazis; Kampouraki, Zoi Christina; Samanidou, Victoria; Deliyanni, Eleni

2016-04-01

Magnetic graphene oxide-polystyrene and magnetic activated carbon-polystyrene nanocomposites as sorbents for bisphenol A. Kyriazis Rekos1, Zoi Christina Kampouraki1, Victoria Samanidou2, Eleni Deliyanni1 1 Laboratory of General and Inorganic Chemical Technology, Department of Chemistry, Aristotle University of Thessaloniki, GR-541 24 Thessaloniki, Greece 2 Laboratory of Analytical Chemistry, Department of Chemistry, Aristotle University of Thessaloniki, GR-541 24 Thessaloniki, Greece The aim of this work was to prepare and characterize novel composites of magnetic activated carbon or magnetic graphene oxide with polystyrene (GO/PSm), through one step simple and effective route. Μagnetite nanoparticles, prepared in the laboratory, were dispersed in the presence of activated carbon (C) or graphene oxide (GO) in a polystyrene (PS) solution in dimethylformamide, at elevated temperature, for the fabrication of the magnetite-Carbon-PS (C-PSm) and magnetite- Graphene Oxide-PS (GO-PSm) hybrid-nanoparticles. For comparison, C-PS and GO-PS composites were also prepared in the same route. The nanocomposites were tested for their sorption ability for an endocrine disruptor, bisphenol A. The effect of solution pH, initial concentration, contact time and temperature were examined. The magnetic graphite oxide-polystyrene presented higher adsorption capacity (100 mg/g) than the non magnetic composites (70 mg/g), as well as than initial graphite oxide (20 mg/g). FTIR, XRD, BET, TGA, VSM and SEM were performed in order to investigate the role of the PS on the better adsorption performance of the mGO-PS nanocomposites. The characterization with these techniques revealed the possible interactions of the surface functional groups of activated carbon and/or graphite oxide with polystyrene that resulted in the better performance of the magnetic nanocomposites for bisphenol A adsorption.

Oxidative stress induces transient O-GlcNAc elevation and tau dephosphorylation in SH-SY5Y cells.

PubMed

Kátai, Emese; Pál, József; Poór, Viktor Soma; Purewal, Rupeena; Miseta, Attila; Nagy, Tamás

2016-12-01

O-linked β-N-acetlyglucosamine or O-GlcNAc modification is a dynamic post-translational modification occurring on the Ser/Thr residues of many intracellular proteins. The chronic imbalance between phosphorylation and O-GlcNAc on tau protein is considered as one of the main hallmarks of Alzheimer's disease. In recent years, many studies also showed that O-GlcNAc levels can elevate upon acute stress and suggested that this might facilitate cell survival. However, many consider chronic stress, including oxidative damage as a major risk factor in the development of the disease. In this study, using the neuronal cell line SH-SY5Y we investigated the dynamic nature of O-GlcNAc after treatment with 0.5 mM H 2 O 2 for 30 min. to induce oxidative stress. We found that overall O-GlcNAc quickly increased and reached peak level at around 2 hrs post-stress, then returned to baseline levels after about 24 hrs. Interestingly, we also found that tau protein phosphorylation at site S262 showed parallel, whereas at S199 and PHF1 sites showed inverse dynamic to O-Glycosylation. In conclusion, our results show that temporary elevation in O-GlcNAc modification after H 2 O 2 -induced oxidative stress is detectable in cells of neuronal origin. Furthermore, oxidative stress changes the dynamic balance between O-GlcNAc and phosphorylation on tau proteins. © 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

Secretory sphingomyelinase (S-SMase) activity is elevated in patients with rheumatoid arthritis.

PubMed

Hanaoka, Beatriz Y; Ormseth, Michelle J; Michael Stein, C; Banerjee, Daipayan; Nikolova-Karakashian, Mariana; Crofford, Leslie J

2018-05-01

The goals of this study were to determine if secretory sphingomyelinase (S-SMase) activity is elevated in patients with rheumatoid arthritis (RA) compared to control subjects and to examine the relationships of S-SMase activity with functional status, quality of life, and RA disease activity measurements. We collected data on 33 patients who were diagnosed with RA and 17 non-RA controls who were comparable in terms of age, sex, and race. Demographic, clinical data and self-reported measures of fatigue, pain, and physical function were obtained directly from patients and controls. RA patients also completed quantitative joint assessment using a 28-joint count and functional status and quality of life assessment using the Modified Health Assessment Questionnaire (MHAQ). Archived serum samples were used to analyze retrospectively serum S-SMase activity in patients and controls. The mean serum S-SMase activity was 1.4-fold higher in patients with RA (RA 2.8 ± 1.0 nmol/ml/h vs. controls 2.0 ± 0.8 nmol/ml/h; p = 0.014). Spearman's rho correlations between S-SMase activity and oxidant activity, markers of inflammation and endothelial activation with the exception of P-selectin (rho = 0.40, p = 0.034), measures of disease activity, functional status, and quality of life were not statistically significant in patients with RA. We confirmed that S-SMase activity is higher among RA patients compared to controls, as in other acute and chronic inflammatory diseases. Future studies can build on the present findings to understand more fully the biologic role(s) of S-SMase activity in RA.

Urinary Angiotensinogen Excretion Level Is Associated With Elevated Blood Pressure in the Normotensive General Population.

PubMed

Sato, Emiko; Wang, An Yi; Satoh, Michihiro; Nishikiori, Yoko; Oba-Yabana, Ikuko; Yoshida, Mai; Sato, Hiroshi; Ito, Sadayoshi; Hida, Wataru; Mori, Takefumi

2018-05-07

Inflammation, intrarenal renin-angiotensin system (RAS) activation, oxidative stress, and carbonyl stress have been postulated to play a fundamental role in controlling blood pressure. However, little is known about the association among renal RAS activation, carbonyl stress, and blood pressure elevation. We evaluated the relationship between blood pressure elevation and either renal RAS activity or carbonyl stress in the general population (N = 355) in Japan. To minimize the effect of antihypertensive drug therapy, we divided participants into 3 groups (normotensive, hypertensive-with-non-medication, and hypertensive-with-medication). Intrarenal RAS activity and carbonyl stress were indicated by the urinary angiotensinogen (AGT) and carbonyl compound excretion levels, respectively. The urinary AGT and carbonyl compound excretion levels were significantly associated with blood pressure. Using a stepwise multiple regression analysis, we found that the urinary AGT excretion levels were strongly associated with blood pressure elevation, compared with inflammation, oxidative stress, and carbonyl stress markers, in all groups. Urinary carbonyl compound excretion was significantly associated with blood pressure in only the hypertensive-without-medication group. Furthermore, blood pressure was significantly increased in these participants, and both the urinary AGT and carbonyl compound levels were high. The urinary AGT excretion levels were strongly associated with elevated blood pressure in normotensive people, and inappropriate renal RAS activity and carbonyl stress independently contributed to the development of hypertension. These findings suggest that RAS activation, particularly renal RAS activation exert a fundamental role in the pathogenesis of hypertension in the general population.

Doxycycline blocks gastric ulcer by regulating matrix metalloproteinase-2 activity and oxidative stress

PubMed Central

Singh, Laishram Pradeepkumar; Mishra, Amartya; Saha, Debjit; Swarnakar, Snehasikta

2011-01-01

AIM: To examine the effect of doxycycline on the activity of matrix metalloproteinases (MMPs) and oxidative stress in gastric tissues of rats following gastric injury. METHODS: Gastric ulcers were generated in rats by administration of 70% ethanol, and activity of doxycycline was tested by administration 30 min prior to ethanol. Similarly, the effect of doxycycline was tested in an indomethacin-induced gastric ulcer model. The activities and expression of MMPs were examined by zymography and Western blot analysis. RESULTS: Gastric injury in rats as judged by elevated ulcer indices following exposure to ulcerogen, either indomethacin or ethanol, was reversed significantly by doxycycline. Indomethacin-induced ulcerated gastric tissues exhibited about 12-fold higher proMMP-9 activity and about 5-fold higher proMMP-3 activity as compared to control tissues. Similarly, ethanol induced about 22-fold and about 6-fold higher proMMP-9 and proMMP-3 activities, respectively, in rat gastric tissues. Both proMMP-9 and MMP-3 activities were markedly decreased by doxycycline in ulcerogen treated rat gastric tissues. In contrast, the reduced MMP-2 activity in ulcerated tissues was increased by doxycycline during ulcer prevention. On the other hand, doxycycline inhibited significantly proMMP-9, -2 and -3 activities in vitro. In addition, doxycycline reduced oxidative load in gastric tissues and scavenged H2O2 in vitro. Our results suggest a novel regulatory role of doxycycline on MMP-2 activity in addition to inhibitory action on MMP-9 and MMP-3 during prevention of gastric ulcers. CONCLUSION: This is the first demonstration of dual action of doxycycline, that is, regulation of MMP activity and reduction of oxidative stress in arresting gastric injury. PMID:21876619

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

PubMed Central

Satapati, Santhosh; Kucejova, Blanka; Duarte, Joao A.G.; Fletcher, Justin A.; Reynolds, Lacy; Sunny, Nishanth E.; He, Tianteng; Nair, L. Arya; Livingston, Kenneth; Fu, Xiaorong; Merritt, Matthew E.; Sherry, A. Dean; Malloy, Craig R.; Shelton, John M.; Lambert, Jennifer; Parks, Elizabeth J.; Corbin, Ian; Magnuson, Mark A.; Browning, Jeffrey D.; Burgess, Shawn C.

2015-01-01

Mitochondria are critical for respiration in all tissues; however, in liver, these organelles also accommodate high-capacity anaplerotic/cataplerotic pathways that are essential to gluconeogenesis and other biosynthetic activities. During nonalcoholic fatty liver disease (NAFLD), mitochondria also produce ROS that damage hepatocytes, trigger inflammation, and contribute to insulin resistance. Here, we provide several lines of evidence indicating that induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backed by elevated oxidative metabolism and hence contributes to oxidative stress and inflammation during NAFLD. First, in murine livers, elevation of fatty acid delivery not only induced oxidative metabolism, but also amplified anaplerosis/cataplerosis and caused a proportional rise in oxidative stress and inflammation. Second, loss of anaplerosis/cataplerosis via genetic knockdown of phosphoenolpyruvate carboxykinase 1 (Pck1) prevented fatty acid–induced rise in oxidative flux, oxidative stress, and inflammation. Flux appeared to be regulated by redox state, energy charge, and metabolite concentration, which may also amplify antioxidant pathways. Third, preventing elevated oxidative metabolism with metformin also normalized hepatic anaplerosis/cataplerosis and reduced markers of inflammation. Finally, independent histological grades in human NAFLD biopsies were proportional to oxidative flux. Thus, hepatic oxidative stress and inflammation are associated with elevated oxidative metabolism during an obesogenic diet, and this link may be provoked by increased work through anabolic pathways. PMID:26571396

5-hydroxytryptamine actions in adipocytes: involvement of monoamine oxidase-dependent oxidation and subsequent PPARγ activation.

PubMed

Grès, Sandra; Gomez-Zorita, Saioa; Gomez-Ruiz, Ana; Carpéné, Christian

2013-06-01

Serotonin (5-HT) is a brain neurotransmitter instrumental for the antidepressant action of selective inhibitors of serotonin reuptake (SSRIs) while it also plays important roles in peripheral organs. Recently, the 5-HT oxidation products, 5-hydroxyindoleacetate and 5-methoxy-indoleacetate, have been shown to bind to peroxisome proliferator-activated receptor γ (PPARγ) and to enhance lipid accumulation in preadipocytes. Since we already reported that adipocytes exhibit elevated monoamine oxidase (MAO) and primary amine oxidase activities, we verified how adipocytes readily oxidize 5-HT, with the objective to determine whether such oxidation promotes PPARγ activation and lipid storage. To this aim, serotonin was tested on cultured 3T3 F442A preadipocytes and on human adipocytes. Results showed that 5-HT was oxidized by MAO in both models. Daily treatment of 3T3 F442A preadipocytes for 8 days with 100-500 μM 5-HT promoted triglyceride accumulation and emergence of adipogenesis markers. At 250 μM, 5-HT alone reproduced half of 50 nM insulin-induced adipogenesis, and exhibited an additive differentiating effect when combined with insulin. Moreover, the 5-HT-induced expression of PPARγ-responsive genes (PEPCK, aP2/FABP4) was blocked by GW 9662, a PPARγ-inhibitor, or by pargyline, a MAO-inhibitor. In human fat cells, 6-h exposure to 100 μM 5-HT increased PEPCK expression as did the PPARγ-agonist rosiglitazone. Since hydrogen peroxide, another amine oxidation product, did not reproduce such enhancement, we propose that serotonin can promote PPARγ activation in fat cells, via the indoleacetate produced during MAO-dependent oxidation. Such pathway could be involved in the adverse effects of several antidepressant SSRIs on body weight gain.

Selectivity of protein oxidative damage during aging in Drosophila melanogaster.

PubMed Central

Das, N; Levine, R L; Orr, W C; Sohal, R S

2001-01-01

The purpose of the present study was to determine whether oxidation of various proteins during the aging process occurs selectively or randomly, and whether the same proteins are damaged in different species. Protein oxidative damage to the proteins, present in the matrix of mitochondria in the flight muscles of Drosophila melanogaster and manifested as carbonyl modifications, was detected immunochemically with anti-dinitrophenyl-group antibodies. Aconitase was found to be the only protein in the mitochondrial matrix that exhibited an age-associated increase in carbonylation. The accrual of oxidative damage was accompanied by an approx. 50% loss in aconitase activity. An increase in ambient temperature, which elevates the rate of metabolism and shortens the life span of flies, caused an elevation in the amount of aconitase carbonylation and an accelerated loss in its activity. Exposure to 100% ambient oxygen showed that aconitase was highly susceptible to undergo oxidative damage and loss of activity under oxidative stress. Administration of fluoroacetate, a competitive inhibitor of aconitase activity, resulted in a dose-dependent decrease in the life span of the flies. Results of the present study demonstrate that protein oxidative damage during aging is a selective phenomenon, and might constitute a mechanism by which oxidative stress causes age-associated losses in specific biochemical functions. PMID:11696009

CNTF-ACM promotes mitochondrial respiration and oxidative stress in cortical neurons through upregulating L-type calcium channel activity.

PubMed

Sun, Meiqun; Liu, Hongli; Xu, Huanbai; Wang, Hongtao; Wang, Xiaojing

2016-09-01

A specialized culture medium termed ciliary neurotrophic factor-treated astrocyte-conditioned medium (CNTF-ACM) allows investigators to assess the peripheral effects of CNTF-induced activated astrocytes upon cultured neurons. CNTF-ACM has been shown to upregulate neuronal L-type calcium channel current activity, which has been previously linked to changes in mitochondrial respiration and oxidative stress. Therefore, the aim of this study was to evaluate CNTF-ACM's effects upon mitochondrial respiration and oxidative stress in rat cortical neurons. Cortical neurons, CNTF-ACM, and untreated control astrocyte-conditioned medium (UC-ACM) were prepared from neonatal Sprague-Dawley rat cortical tissue. Neurons were cultured in either CNTF-ACM or UC-ACM for a 48-h period. Changes in the following parameters before and after treatment with the L-type calcium channel blocker isradipine were assessed: (i) intracellular calcium levels, (ii) mitochondrial membrane potential (ΔΨm), (iii) oxygen consumption rate (OCR) and adenosine triphosphate (ATP) formation, (iv) intracellular nitric oxide (NO) levels, (v) mitochondrial reactive oxygen species (ROS) production, and (vi) susceptibility to the mitochondrial complex I toxin rotenone. CNTF-ACM neurons displayed the following significant changes relative to UC-ACM neurons: (i) increased intracellular calcium levels (p < 0.05), (ii) elevation in ΔΨm (p < 0.05), (iii) increased OCR and ATP formation (p < 0.05), (iv) increased intracellular NO levels (p < 0.05), (v) increased mitochondrial ROS production (p < 0.05), and (vi) increased susceptibility to rotenone (p < 0.05). Treatment with isradipine was able to partially rescue these negative effects of CNTF-ACM (p < 0.05). CNTF-ACM promotes mitochondrial respiration and oxidative stress in cortical neurons through elevating L-type calcium channel activity.

N-acetyl-cysteine exhibits potent anti-mycobacterial activity in addition to its known anti-oxidative functions.

PubMed

Amaral, Eduardo P; Conceição, Elisabete L; Costa, Diego L; Rocha, Michael S; Marinho, Jamocyr M; Cordeiro-Santos, Marcelo; D'Império-Lima, Maria Regina; Barbosa, Theolis; Sher, Alan; Andrade, Bruno B

2016-10-28

Mycobacterium tuberculosis infection is thought to induce oxidative stress. N-acetyl-cysteine (NAC) is widely used in patients with chronic pulmonary diseases including tuberculosis due to its mucolytic and anti-oxidant activities. Here, we tested whether NAC exerts a direct antibiotic activity against mycobacteria. Oxidative stress status in plasma was compared between pulmonary TB (PTB) patients and those with latent M. tuberculosis infection (LTBI) or healthy uninfected individuals. Lipid peroxidation, DNA oxidation and cell death, as well as accumulation of reactive oxygen species (ROS) were measured in cultures of primary human monocyte-derived macrophages infected with M. tuberculosis and treated or not with NAC. M. tuberculosis, M. avium and M. bovis BCG cultures were also exposed to different doses of NAC with or without medium pH adjustment to control for acidity. The anti-mycobacterial effect of NAC was assessed in M. tuberculosis infected human THP-1 cells and bone marrow-derived macrophages from mice lacking a fully functional NADPH oxidase system. The capacity of NAC to control M. tuberculosis infection was further tested in vivo in a mouse (C57BL/6) model. PTB patients exhibited elevated levels of oxidation products and a reduction of anti-oxidants compared with LTBI cases or uninfected controls. NAC treatment in M. tuberculosis-infected human macrophages resulted in a decrease of oxidative stress and cell death evoked by mycobacteria. Importantly, we observed a dose-dependent reduction in metabolic activity and in vitro growth of NAC treated M. tuberculosis, M. avium and M. bovis BCG. Furthermore, anti-mycobacterial activity in infected macrophages was shown to be independent of the effects of NAC on the host NADPH oxidase system in vitro. Short-term NAC treatment of M. tuberculosis infected mice in vivo resulted in a significant reduction of mycobacterial loads in the lungs. NAC exhibits potent anti-mycobacterial effects and may limit M

Activities of Tricarboxylic Acid Cycle Enzymes, Glyoxylate Cycle Enzymes, and Fructose Diphosphatase in Bakers' Yeast During Adaptation to Acetate Oxidation

PubMed Central

Gosling, J. P.; Duggan, P. F.

1971-01-01

Bakers' yeast oxidizes acetate at a high rate only after an adaptation period during which the capacity of the glyoxylate cycle is found to increase. There was apparently no necessity for the activity of acetyl-coenzyme A synthetase, the capacity of the tricarboxylic acid cycle, or the concentrations of the cytochromes to increase for this adaptation to occur. Elevation of fructose 1,6 diphosphatase occurred only when acetate oxidation was nearly maximal. Cycloheximide almost completely inhibited adaptation as well as increases in the activities of isocitrate lyase and aconitate hydratase, the only enzymes assayed. p-Fluorophenylalanine was partially effective and chloramphenicol did not inhibit at all. The presence of ammonium, which considerably delayed adaptation of the yeast to acetate oxidation, inhibited the increases in the activities of the glyoxylate cycle enzymes to different degrees, demonstrating noncoordinate control of these enzymes. Under the various conditions, the only enzyme activity increase consistently related to the rising oxygen uptake rate was that of isocitrate lyase which apparently limited the activity of the cycle. PMID:5557595

Elevated Hepatic Iron Activates NF-E2–Related Factor 2–Regulated Pathway in a Dietary Iron Overload Mouse Model

PubMed Central

Isom, Harriet C.

2012-01-01

Hepatic iron overload has been associated classically with the genetic disorder hereditary hemochromatosis. More recently, it has become apparent that mild-to-moderate degrees of elevated hepatic iron stores observed in other liver diseases also have clinical relevance. The goal was to use a mouse model of dietary hepatic iron overload and isobaric tag for relative and absolute quantitation proteomics to identify, at a global level, differentially expressed proteins in livers from mice fed a control or 3,5,5-trimethyl-hexanoyl-ferrocene (TMHF) supplemented diet for 4 weeks. The expression of 74 proteins was altered by ≥ ±1.5-fold, showing that the effects of iron on the liver proteome were extensive. The top canonical pathway altered by TMHF treatment was the NF-E2–related factor 2 (NRF2–)–mediated oxidative stress response. Because of the long-standing association of elevated hepatic iron with oxidative stress, the remainder of the study was focused on NRF2. TMHF treatment upregulated 25 phase I/II and antioxidant proteins previously categorized as NRF2 target gene products. Immunoblot analyses showed that TMHF treatment increased the levels of glutathione S-transferase (GST) M1, GSTM4, glutamate-cysteine ligase (GCL) catalytic subunit, GCL modifier subunit, glutathione synthetase, glutathione reductase, heme oxygenase 1, epoxide hydrolase 1, and NAD(P)H dehydrogenase quinone 1. Immunofluorescence, carried out to determine the cellular localization of NRF2, showed that NRF2 was detected in the nucleus of hepatocytes from TMHF-treated mice and not from control mice. We conclude that elevated hepatic iron in a mouse model activates NRF2, a key regulator of the cellular response to oxidative stress. PMID:22649188

Iron-Induced Activation of Ordered Mesoporous Nickel Cobalt Oxide Electrocatalyst for the Oxygen Evolution Reaction.

PubMed

Deng, Xiaohui; Öztürk, Secil; Weidenthaler, Claudia; Tüysüz, Harun

2017-06-28

Herein, ordered mesoporous nickel cobalt oxides prepared by the nanocasting route are reported as highly active oxygen evolution reaction (OER) catalysts. By using the ordered mesoporous structure as a model system and afterward elevating the optimal catalysts composition, it is shown that, with a simple electrochemical activation step, the performance of nickel cobalt oxide can be significantly enhanced. The electrochemical impedance spectroscopy results indicated that charge transfer resistance increases for Co 3 O 4 spinel after an activation process, while this value drops for NiO and especially for CoNi mixed oxide significantly, which confirms the improvement of oxygen evolution kinetics. The catalyst with the optimal composition (Co/Ni 4/1) reaches a current density of 10 mA/cm 2 with an overpotential of a mere 336 mV and a Tafel slope of 36 mV/dec, outperforming benchmarked and other reported Ni/Co-based OER electrocatalysts. The catalyst also demonstrates outstanding durability for 14 h and maintained the ordered mesoporous structure. The cyclic voltammograms along with the electrochemical measurements in Fe-free KOH electrolyte suggest that the activity boost is attributed to the generation of surface Ni(OH) 2 species that incorporate Fe impurities from the electrolyte. The incorporation of Fe into the structure is also confirmed by inductively coupled plasma optical emission spectrometry.

Assessment of adenosine deaminase (ADA) activity and oxidative stress in patients with chronic tonsillitis.

PubMed

Garca, Mehmet Fatih; Demir, Halit; Turan, Mahfuz; Bozan, Nazım; Kozan, Ahmet; Belli, Şeyda Bayel; Arslan, Ayşe; Cankaya, Hakan

2014-06-01

To emphasize the effectiveness of adenosine deaminase (ADA) enzyme, which has important roles in the differentiation of lymphoid cells, and oxidative stress in patients with chronic tonsillitis. Serum and tissue samples were obtained from 25 patients who underwent tonsillectomy due to recurrent episodes of acute tonsillitis. In the control group, which also had 25 subjects, only serum samples were taken as obtaining tissue samples would not have been ethically appropriate. ADA enzyme activity, catalase (CAT), carbonic anhydrase (CA), nitric oxide (NO) and malondialdehyde (MDA) were measured in the serum and tissue samples of patients and control group subjects. The serum values of both groups were compared. In addition, the tissue and serum values of patients were compared. Serum ADA activity and the oxidant enzymes MDA and NO values of the patient group were significantly higher than those of the control group (p < 0.001), the antioxidant enzymes CA and CAT values of the patient group were significantly lower than those of the control group (p < 0.001). In addition, while CA, CAT and NO enzyme levels were found to be significantly higher in the tonsil tissue of the patient group when compared to serum levels (p < 0.05), there was no difference between tissue and serum MDA and ADA activity (p > 0.05). Elevated ADA activity may be effective in the pathogenesis of chronic tonsillitis both by impairing tissue structure and contributing to SOR formation.

Oxidative Stress and Inflammation Differentially Elevated in Objective Versus Habitual Subjective Reduced Sleep Duration in Obstructive Sleep Apnea

PubMed Central

DeMartino, Theresanne; Ghoul, Rawad El; Wang, Lu; Bena, James; Hazen, Stanley L.; Tracy, Russel; Patel, Sanjay R.; Auckley, Dennis; Mehra, Reena

2016-01-01

Study Objectives: Data have demonstrated adverse health effects of sleep deprivation. We postulate that oxidative stress and systemic inflammation biomarkers will be elevated in relation to short-term and long-term sleep duration reduction. Methods: We analyzed data from the baseline examination of a randomized controlled trial involving participants with moderate to severe obstructive sleep apnea (OSA). Baseline polysomnography provided the total sleep time (PSG-TST, primary predictor); self-reported habitual sleep duration (SR-HSD) data was collected. Morning measures of oxidative stress and systemic inflammation included: myeloperoxidase (MPO, pmol/L), oxidized low-density lipoprotein (ox-LDL, U/L), F2-isoprostane (ng/mg), paraoxonase 1 (PON1, nmol·min−1·mL−1), and aryl esterase (μmol·min−1·mL−1). Linear models adjusted for age, sex, race, body mass index (BMI), cardiovascular disease (CVD), smoking, statin/anti-inflammatory medications, and apnea-hypopnea index were utilized (beta estimates and 95% confidence intervals). Results: One hundred forty-seven participants comprised the final analytic sample; they were overall middle-aged (51.0 ± 11.7 y), obese (BMI = 37.3 ± 8.1 kg/m2), and 17% had CVD. Multivariable models demonstrated a significant inverse association of PSG-TST and MPO (β [95% CI] = −20.28 [−37.48, −3.08], P = 0.021), i.e., 20.3 pmol/L MPO reduction per hour increase PSG-TST. Alternatively, a significant inverse association with ox-LDL and SR-HSD was observed (β [95% CI] = 0.98 [0.96, 0.99], P = 0.027), i.e., 2% ox-LDL reduction per hour increase SR-HSD. Conclusions: Even after consideration of obesity and OSA severity, inverse significant findings were observed such that reduced PSG-TST was associated with elevated MPO levels and SR-HSD with ox-LDL, suggesting differential up-regulation of oxidative stress and pathways of inflammation in acute versus chronic sleep curtailment. Clinical Trial Registration: NIH clinical trials

Oxidative stress inhibition and oxidant activity by fibrous clays.

PubMed

Cervini-Silva, Javiera; Nieto-Camacho, Antonio; Gómez-Vidales, Virginia

2015-09-01

Fibrous clays (sepiolite, palygorskite) are produced at 1.2m tonnes per year and have a wide range of industrial applications needing to replace long-fibre length asbestos. However, information on the beneficial effects of fibrous clays on health remains scarce. This paper reports on the effect of sepiolite (Vallecas, Spain) and palygorskite (Torrejón El Rubio, Spain) on cell damage via oxidative stress (determined as the progress of lipid peroxidation, LP). The extent of LP was assessed using the Thiobarbituric Acid Reactive Substances assay. The oxidant activity by fibrous clays was quantified using Electron-Paramagnetic Resonance. Sepiolite and palygorskite inhibited LP, whereby corresponding IC50 values were 6557±1024 and 4250±289μgmL(-1). As evidenced by dose-response experiments LP inhibition by palygorskite was surface-controlled. Fibrous clay surfaces did not stabilize HO species, except for suspensions containing 5000μgmL(-1). A strong oxidant (or weak anti-oxidant) activity favours the inhibition of LP by fibrous clays. Copyright © 2015 Elsevier B.V. All rights reserved.

Elevated hydrostatic pressures induce apoptosis and oxidative stress through mitochondrial membrane depolarization in PC12 neuronal cells: A cell culture model of glaucoma.

PubMed

Tök, Levent; Nazıroğlu, Mustafa; Uğuz, Abdülhadi Cihangir; Tök, Ozlem

2014-10-01

Despite the importance of oxidative stress and apoptosis through mitochondrial depolarization in neurodegenerative diseases, their roles in etiology of glaucoma are poorly understood. We aimed to investigate whether oxidative stress and apoptosis formation are altered in rat pheochromocytoma-derived cell line-12 (PC12) neuronal cell cultures exposed to elevated different hydrostatic pressures as a cell culture model of glaucoma. Cultured PC12 cells were subjected to 0, 15 and 70 mmHg hydrostatic pressure for 1 and 24 h. Then, the following values were analyzed: (a) cell viability; (b) lipid peroxidation and intracellular reactive oxygen species production; (c) mitochondrial membrane depolarization; (d) cell apoptosis; (e) caspase-3 and caspase-9 activities; (f) reduced glutathione (GSH) and glutathione peroxidase (GSH-Px). The hydrostatic pressures (15 and 70 mmHg) increased oxidative cell damage through a decrease of GSH and GSH-Px values, and increasing mitochondrial membrane potential. Additionally, 70 mmHg hydrostatic pressure for 24 h indicated highest apoptotic effects, as demonstrated by plate reader analyses of apoptosis, caspase-3 and -9 values. The present data indicated oxidative stress, apoptosis and mitochondrial changes in PC12 cell line during different hydrostatic pressure as a cell culture model of glaucoma. This findings support the view that mitochondrial oxidative injury contributes early to glaucomatous optic neuropathy.

Disturbances in Pro-Oxidant-Antioxidant Balance after Passive Body Overheating and after Exercise in Elevated Ambient Temperatures in Athletes and Untrained Men

PubMed Central

Pilch, Wanda; Szygula, Zbigniew; Tyka, Anna K.; Palka, Tomasz; Tyka, Aleksander; Cison, Tomasz; Pilch, Pawel; Teleglow, Aneta

2014-01-01

The aim of the study was to investigate pro-oxidant-antioxidant balance in two series of examinations with two types of stressors (exogenous heat and the combined exogenous and endogenous heat) in trained and untrained men. The exogenous stressor was provided by Finnish sauna session, whereas the combined stressor was represented by the exercise in elevated ambient temperature. The men from the two groups performed the physical exercise on a cycle ergometer with the load of 53±2% maximal oxygen uptake at the temperature of 33±1°C and relative humidity of 70% until their rectal temperature rose by 1.2°C. After a month from completion of the exercise test the subjects participated in a sauna bathing session with the temperature of 96±2°C, and relative humidity of 16±5%. 15-minutes heating and 2-minute cool-down in a shower with the temperature of 20°C was repeated until rectal temperature rose by 1.2°C compared to the initial value. During both series of tests rectal temperature was measured at 5-minute intervals. Before both series of tests and after them body mass was measured and blood samples were taken for biochemical tests. Serum total protein, serum concentration of lipid peroxidation products and serum antioxidants were determined. The athletes were characterized by higher level of antioxidant status and lower concentration of lipid peroxidation products. Physical exercise at elevated ambient temperature caused lower changes in oxidative stress indices compared to sauna bathing. Sauna induced a shift in pro-oxidant-antioxidant balance towards oxidation, which was observed less intensively in the athletes compared to the untrained men. This leads to the conclusion that physical exercise increases tolerance to elevated ambient temperature and oxidative stress. PMID:24465535

Activation of caspase-3 is associated with oxidative stress in the hydropic guinea pig cochlea.

PubMed

Labbé, Daniel; Teranishi, Masa-Aki; Hess, Alexander; Bloch, Wilhelm; Michel, Olaf

2005-04-01

The aim of this study was to investigate the involvement of oxidative stress and apoptosis in an animal model of Meniere's disease. Endolymphatic hydrops (ELH) is generally accepted as the decisive histological characteristic of Meniere's disease. Closure of the endolymphatic duct (Kimura's method) was used to induce endolymphatic hydrops in guinea pigs. Sham-operated animals served as controls. After 4 weeks the animals operated showed a significant elevation of the hearing thresholds as measured by audiometric brainstem responses (ABR) pre- and postoperatively. Immediately after the second ABR measurement, the animals were sacrificed for further immunohistological examinations of the inner ear with specific antibodies to active caspase-3 (cas-3) as a marker for apoptosis and antibodies to 8-isoprostane (8-iso) and nitrotyrosine (NT) as indicators of oxidative stress. Compared with the sham-operated controls, hydropic cochleae showed strong immunostaining for both oxidative stress markers in spiral ganglion cells, in the blood-vessels and fibrocytes of the lateral wall, as well as in supporting cells of the organ of Corti. Activation of cas-3 in spiral ganglion cells and the lateral wall was found exclusively in hydropic cochleae. Our findings suggest that oxidative stress is involved in the development of endolymphatic hydrops and may lead to cellular damage which induces apoptosis by activation of cas-3. Apoptotic cell death might contribute to the sensorineural hearing loss found in later stages of Meniere's disease.

Sulforaphane Inhibits Mitochondrial Permeability Transition and Oxidative Stress

PubMed Central

Greco, Tiffany; Shafer, Jonathan; Fiskum, Gary

2012-01-01

Exposure of mitochondria to oxidative stress and elevated Ca2+ promotes opening of the mitochondrial permeability transition pore (PTP), resulting in membrane depolarization, uncoupling of oxidative phosphorylation, and potentially cell death. This study tested the hypothesis that treatment of rats with sulforaphane (SFP), an activator of the Nrf2 pathway of antioxidant gene expression, increases the resistance of liver mitochondria to redox-regulated PTP opening and elevates mitochondrial levels of antioxidants. Rats were injected with SFP or drug vehicle and liver mitochondria were isolated 40 hr later. Respiring mitochondria actively accumulated added Ca2+, which was then released through PTP opening induced by agents that either cause an oxidized shift in the mitochondrial redox state or that directly oxidize protein thiol groups. SFP treatment of rats inhibited the rate of pro-oxidant-induced mitochondrial Ca2+ release and increased expression of the glutathione peroxidase/reductase system, thioredoxin, and malic enzyme. These results are the first to demonstrate that SFP treatment of animals increases liver mitochondrial antioxidant defenses and inhibits redox-sensitive PTP opening. This novel form of preconditioning could protect against a variety of pathologies that include oxidative stress and mitochondrial dysfunction in their etiologies. PMID:21986339

Activation of PPAR-γ by pioglitazone attenuates oxidative stress in aging rat cerebral arteries through upregulating UCP2.

PubMed

Wang, Peijian; Li, Binghu; Cai, Guocai; Huang, Mingqing; Jiang, Licheng; Pu, Jing; Li, Lu; Wu, Qi; Zuo, Li; Wang, Qiulin; Zhou, Peng

2014-12-01

Increasing amounts of evidence implicate oxidative stress as having a pivotal role in age-related cerebrovascular dysfunction, which is an important risk factor for the development of cerebrovascular disease. Previous studies have shown that the activation of the expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) in vascular endothelial cells results in an improvement of vascular function. Pioglitazone, a well-known PPAR-γ agonist, protects against oxidative stress in the rostral ventrolateral medulla by the upregulation of mitochondrial uncoupling protein 2 (UCP2). In this study, we sought to explore the effects and the underlying mechanisms of pioglitazone on age-related oxidative stress elevation and cerebrovascular dysfunction in aging rat cerebral arteries. A natural aging model was constructed and used in these experiments. One-month oral administration of pioglitazone (20 mg·kg·d) ameliorated the production of reactive oxygen species, promoted endothelial nitric oxide synthase phosphorylation and increased the nitric oxide available, thus improving endothelium-dependent relaxation in aging rat cerebral arteries. One-month pioglitazone administration also restored PPAR-γ expression and increased the levels of UCP2 in aging rat cerebral arteries. Using in vitro studies, we demonstrated that pioglitazone attenuated reactive oxygen species levels in aging human umbilical vein endothelial cells through PPAR-γ activation. Furthermore, we found that this occurs in an UCP2-dependent manner. Our study demonstrated that the activation of PPAR-γ by pioglitazone protected against oxidative stress damage in aging cerebral arteries by upregulating UCP2. PPAR-γ may be a new target in treating age-related cerebrovascular dysfunction.

BDE-47 induces oxidative stress, activates MAPK signaling pathway, and elevates de novo lipogenesis in the copepod Paracyclopina nana.

PubMed

Lee, Min-Chul; Puthumana, Jayesh; Lee, Seung-Hwi; Kang, Hye-Min; Park, Jun Chul; Jeong, Chang-Bum; Han, Jeonghoon; Hwang, Dae-Sik; Seo, Jung Soo; Park, Heum Gi; Om, Ae-Son; Lee, Jae-Seong

2016-12-01

Brominated flame retardant, 2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47), has received grave concerns as a persistent organic pollutant, which is toxic to marine organisms, and a suspected link to endocrine abnormalities. Despite the wide distribution in the marine ecosystem, very little is known about the toxic impairments on marine organisms, particularly on invertebrates. Thus, we examined the adverse effects of BDE-47 on life history trait (development), oxidative markers, fatty acid composition, and lipid accumulation in response to BDE-47-induced stress in the marine copepod Paracyclopina nana. Also, activation level of mitogen-activated protein kinase (MAPK) signaling pathways along with the gene expression profile of de novo lipogenesis (DNL) pathways were addressed. As a result, BDE-47 induced oxidative stress (e.g. reactive oxygen species, ROS) mediated activation of extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) signaling cascades in MAPK pathways. Activated MAPK pathways, in turn, induced signal molecules that bind to the transcription factors (TFs) responsible for lipogenesis to EcR, SREBP, ChREBP promoters. Also, the stress stimulated the conversion of saturated fatty acids (SFAs) to polyunsaturated fatty acids (PUFAs), a preparedness of the organism to adapt the observed stress, which could be correlated with the elongase and desaturase gene (e.g. ELO3, Δ5-DES, Δ9-DES) expressions, and then extended to the delayed early post-embryonic development and increased accumulation of lipid droplets in P. nana. This study will provide a better understanding of how BDE-47 effects on marine invertebrates particularly on the copepods, an important link in the marine food chain. Copyright © 2016 Elsevier B.V. All rights reserved.

Oxidation of benzoic acid by heat-activated persulfate: Effect of temperature on transformation pathway and product distribution.

PubMed

Zrinyi, Nick; Pham, Anh Le-Tuan

2017-09-01

Heat activates persulfate (S 2 O 8 2- ) into sulfate radical (SO 4 - ), a powerful oxidant capable of transforming a wide variety of contaminants. Previous studies have shown that an increase in temperature accelerates the rates of persulfate activation and contaminant transformation. However, few studies have considered the effect of temperature on contaminant transformation pathway. The objective of this study was to determine how temperature (T = 22-70 °C) influences the activation of persulfate, the transformation of benzoic acid (i.e., a model compound), and the distribution of benzoic acid oxidation products. The time-concentration profiles of the products suggest that benzoic acid was transformed via decarboxylation and hydroxylation mechanisms, with the former becoming increasingly important at elevated temperatures. The pathway through which the products were further oxidized was also influenced by the temperature of persulfate activation. Our findings suggest that the role of temperature in the persulfate-based treatment systems is not limited only to controlling the rates of sulfate and hydroxyl radical generation. The ability of sulfate radical to initiate decarboxylation reactions and, more broadly, fragmentation reactions, as well as the effect of temperature on these transformation pathways could be important to the transformation of a number of organic contaminants. Copyright © 2017 Elsevier Ltd. All rights reserved.

Impact of trans-resveratrol-sulfates and -glucuronides on endothelial nitric oxide synthase activity, nitric oxide release and intracellular reactive oxygen species.

PubMed

Ladurner, Angela; Schachner, Daniel; Schueller, Katharina; Pignitter, Marc; Heiss, Elke H; Somoza, Veronika; Dirsch, Verena M

2014-10-17

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a polyphenolic natural product mainly present in grape skin, berries and peanuts. In the vasculature resveratrol is thought to boost endothelial function by increasing endothelial nitric oxide synthase (eNOS) expression, by enhancing eNOS activity, and by reduction of reactive oxygen species (ROS) levels. Recent studies show that dietary resveratrol is metabolized in the liver and intestine into resveratrol-sulfate and -glucuronide derivatives questioning the relevance of multiple reported mechanistic in vitro data on resveratrol. In this study, we compare side by side different physiologically relevant resveratrol metabolites (resveratrol sulfates- and -glucuronides) and their parent compound in their influence on eNOS enzyme activity, endothelial NO release, and intracellular ROS levels. In contrast to resveratrol, none of the tested resveratrol metabolites elevated eNOS enzyme activity and endothelial NO release or affected intracellular ROS levels, leaving the possibility that not tested metabolites are active and able to explain in vivo findings.

Impact of Trans-Resveratrol-Sulfates and -Glucuronides on Endothelial Nitric Oxide Synthase Activity, Nitric Oxide Release and Intracellular Reactive Oxygen Species

PubMed Central

Ladurner, Angela; Schachner, Daniel; Schueller, Katharina; Pignitter, Marc; Heiss, Elke H.; Somoza, Veronika; Dirsch, Verena M.

2015-01-01

Resveratrol (3,5,4′-trihydroxy-trans-stilbene) is a polyphenolic natural product mainly present in grape skin, berries and peanuts. In the vasculature resveratrol is thought to boost endothelial function by increasing endothelial nitric oxide synthase (eNOS) expression, by enhancing eNOS activity, and by reduction of reactive oxygen species (ROS) levels. Recent studies show that dietary resveratrol is metabolized in the liver and intestine into resveratrol-sulfate and -glucuronide derivatives questioning the relevance of multiple reported mechanistic in vitro data on resveratrol. In this study, we compare side by side different physiologically relevant resveratrol metabolites (resveratrol sulfates- and -glucuronides) and their parent compound in their influence on eNOS enzyme activity, endothelial NO release, and intracellular ROS levels. In contrast to resveratrol, none of the tested resveratrol metabolites elevated eNOS enzyme activity and endothelial NO release or affected intracellular ROS levels, leaving the possibility that not tested metabolites are active and able to explain in vivo findings. PMID:25329867

Elevated atmospheric CO2 increases microbial growth rates and enzymes activity in soil

NASA Astrophysics Data System (ADS)

Blagodatskaya, Evgenia; Blagodatsky, Sergey; Dorodnikov, Maxim; Kuzyakov, Yakov

2010-05-01

Increasing the belowground translocation of assimilated carbon by plants grown under elevated CO2 can cause a shift in the structure and activity of the microbial community responsible for the turnover of organic matter in soil. We investigated the long-term effect of elevated CO2 in the atmosphere on microbial biomass and specific growth rates in root-free and rhizosphere soil. The experiments were conducted under two free air carbon dioxide enrichment (FACE) systems: in Hohenheim and Braunschweig, as well as in the intensively managed forest mesocosm of the Biosphere 2 Laboratory (B2L) in Oracle, AZ. Specific microbial growth rates (μ) were determined using the substrate-induced respiration response after glucose and/or yeast extract addition to the soil. We evaluated the effect of elevated CO2 on b-glucosidase, chitinase, phosphatase, and sulfatase to estimate the potential enzyme activity after soil amendment with glucose and nutrients. For B2L and both FACE systems, up to 58% higher μ were observed under elevated vs. ambient CO2, depending on site, plant species and N fertilization. The μ-values increased linearly with atmospheric CO2 concentration at all three sites. The effect of elevated CO2 on rhizosphere microorganisms was plant dependent and increased for: Brassica napus=Triticum aestivumelevated CO2 was smoothed on rich vs. simple substrate. So, the r/K strategies ratio can be better revealed by studying growth on simple (glucose) than on rich substrate mixtures (yeast extract). After adding glucose, enzyme activities under elevated CO2 were

Paraoxonase 1 and oxidative stress in paediatric non-alcoholic steatohepatitis.

PubMed

Desai, Sonal; Baker, Susan S; Liu, Wensheng; Moya, Diana A; Browne, Richard W; Mastrandrea, Lucy; Baker, Robert D; Zhu, Lixin

2014-01-01

Non-alcoholic steatohepatitis (NASH) in children is a significant public health concern. Oxidative stress is an important component in the pathophysiology of NASH. Several enzymatic antioxidant mechanisms protect the liver from oxidative injury. Examination of the expression of these enzymes in NASH livers may provide insight on the roles for these antioxidant mechanisms in the pathophysiology of NASH. The mRNA expression of catalase, glutathione peroxidase 1 (GPX1), glutathione reductase (GSR), paraoxonase 1 (PON1) and other reactive oxygen species-related genes was evaluated by microarray and quantitative real-time PCR analyses. The PON1 protein levels were evaluated in liver and serum by Western blot analyses. Serum enzymatic activities of GPX, GSR and PON1 (paraoxonase and arylesterase activities) were examined. NASH livers exhibited elevated mRNA expression of catalase and PON1, but not GPX1 or GSR. No difference in serum GPX or GSR activity was detected between NASH patients and controls. Elevated expression of PON1 mRNA and protein was detected in NASH livers, but serum PON1 protein and activities were not elevated. Elevated expression of catalase and PON1 suggests protective roles for these antioxidants in NASH livers. Given the importance of oxidative stress in the pathophysiology of NASH, future studies focusing on these enzymes could identify important targets for therapeutic or preventive interventions for NASH patients. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Activation by nitric oxide of an oxidative-stress response that defends Escherichia coli against activated macrophages.

PubMed Central

Nunoshiba, T; deRojas-Walker, T; Wishnok, J S; Tannenbaum, S R; Demple, B

1993-01-01

Nitric oxide is a free radical (NO) formed biologically through the oxidation of L-arginine by nitric oxide synthases. NO is produced transiently in mammalian cells for intercellular signaling and in copious quantities to cause cytostasis and cytotoxicity. In the latter situation, NO is a deliberate cytotoxic product of activated macrophages, along with other reactive oxygen species such as hydrogen peroxide (H2O2) and superoxide (O2-). Escherichia coli has a complex set of responses to H2O2 and O2- that involves approximately 80 inducible proteins; we wondered whether these bacteria might induce analogous defenses against nitric oxide. We show here that a multigene system controlled by the redox-sensitive transcriptional regulator SoxR is activated by NO in vivo. This induction confers bacterial resistance to activated murine macrophages with kinetics that parallel the production of NO by these cells. Elimination of specific SoxR-regulated genes diminishes the resistance of these bacteria to the cytotoxic macrophages. The required functions include manganese-containing superoxide dismutase, endonuclease IV (a DNA-repair enzyme for oxidative damage), and micF, an antisense regulator of the outer membrane porin OmpF. These results demonstrate that SoxR is a sensor for cellular exposure to NO, and that the soxRS response system may contribute to bacterial virulence. PMID:8234347

Nitric oxide ameliorates the damaging effects of oxidative stress induced by iron deficiency in cyanobacterium Anabaena 7120.

PubMed

Kaushik, Manish Singh; Srivastava, Meenakshi; Srivastava, Alka; Singh, Anumeha; Mishra, Arun Kumar

2016-11-01

In cyanobacterium Anabaena 7120, iron deficiency leads to oxidative stress with unavoidable consequences. Nitric oxide reduces pigment damage and supported the growth of Anabaena 7120 in iron-deficient conditions. Elevation in nitric oxide accumulation and reduced superoxide radical production justified the role of nitric oxide in alleviating oxidative stress in iron deficiency. Increased activities of antioxidative enzymes and higher levels of ROS scavengers (ascorbate, glutathione and thiol) in iron deficiency were also observed in the presence of nitric oxide. Nitric oxide also supported the membrane integrity of Anabaena cells and reduces protein and DNA damage caused by oxidative stress induced by iron deficiency. Results suggested that nitric oxide alleviates the damaging effects of oxidative stress induced by iron deficiency in cyanobacterium Anabaena 7120.

Indium tin oxide thin film strain gages for use at elevated temperatures

NASA Astrophysics Data System (ADS)

Luo, Qing

A robust ceramic thin film strain gage based on indium-tin-oxide (ITO) has been developed for static and dynamic strain measurements in advanced propulsion systems at temperatures up to 1400°C. These thin film sensors are ideally suited for in-situ strain measurement in harsh environments such as those encountered in the hot sections of gas turbine engines. A novel self-compensation scheme was developed using thin film platinum resistors placed in series with the active strain element (ITO) to minimize the thermal effect of strain or apparent strain. A mathematical model as well as design rules were developed for the self-compensated circuitry using this approach and close agreement between the model and actual static strain results has been achieved. High frequency dynamic strain tests were performed at temperatures up to 500°C and at frequencies up to 2000Hz to simulate conditions that would be encountered during engine vibration fatigue. The results indicated that the sensors could survive extreme test conditions while maintaining sensitivity. A reversible change in sign of the piezoresistive response from -G to +G was observed in the vicinity of 950°C, suggesting that the change carrier responsible for conduction in the ITO gage had been converted from a net "n-carrier" to a net "p-carrier" semiconductor. Electron spectroscopy for chemical analysis (ESCA) of the ITO films suggested they experienced an interfacial reaction with the Al2O3 substrate at 1400°C. It is likely that oxygen uptake from the substrate is responsible for stabilizing the ITO films to elevated temperatures through the interfacial reaction. Thermo gravimetric analysis of ITO films on alumina at elevated temperatures showed no sublimation of ITO films at temperature up to 1400°C. The surface morphology of ITO films heated to 800, 1200 and 1400°C were also evaluated by atomic force microscopy (AFM). A linear current-voltage (I--V) characteristic indicated that the contact interface

Basal levels of metabolic activity are elevated in Genetic Absence Epilepsy Rats from Strasbourg (GAERS): measurement of regional activity of cytochrome oxidase and lactate dehydrogenase by histochemistry.

PubMed

Dufour, Franck; Koning, Estelle; Nehlig, Astrid

2003-08-01

The Genetic Absence Epilepsy Rats from Strasbourg (GAERS) are considered an isomorphic, predictive, and homologous model of human generalized absence epilepsy. It is characterized by the expression of spike-and-wave discharges in the thalamus and cortex. In this strain, basal regional rates of cerebral glucose utilization measured by the quantitative autoradiographic [(14)C]2-deoxyglucose technique display a widespread consistent increase compared to a selected strain of genetically nonepileptic rats (NE). In order to verify whether these high rates of glucose metabolism are paralleled by elevated activities of the enzymes of the glycolytic and tricarboxylic acid cycle pathways, we measured by histochemistry the regional activity of the two key enzymes of glucose metabolism, lactate dehydrogenase (LDH) for the anaerobic pathway and cytochrome oxidase (CO) for the aerobic pathway coupled to oxidative phosphorylation. CO and LDH activities were significantly higher in GAERS than in NE rats in 24 and 28 of the 30 brain regions studied, respectively. The differences in CO and LDH activity between both strains were widespread, affected all brain systems studied, and ranged from 12 to 63%. The data of the present study confirm the generalized increase in cerebral glucose metabolism in GAERS, occurring both at the glycolytic and at the oxidative step. However, they still do not allow us to understand why the ubiquitous mutation(s) generates spike-and-wave discharges only in the thalamocortical circuit.

Oxidation of cefalexin by thermally activated persulfate: Kinetics, products, and antibacterial activity change.

PubMed

Qian, Yajie; Xue, Gang; Chen, Jiabin; Luo, Jinming; Zhou, Xuefei; Gao, Pin; Wang, Qi

2018-05-03

While the widely used β-lactam antibiotics, such as cephalosporins, are known to be susceptible to oxidation by sulfate radical (SO 4 - ), comprehensive study about SO 4 - -induced oxidation of cephalosporins is still limited, such as the impact of water matrices, and the structure and antibacterial activity of transformation products. Herein, the oxidation of cefalexin (CFX), a most frequently detected cephalosporin, was systematically investigated by thermally activated persulfate (PS). CFX oxidation followed pseudo-first-order kinetics, and SO 4 - dominantly contributed to the overall oxidation of CFX. The impact of water matrices, such as Cl - , HCO 3 - and natural organic matter, on CFX degradation was predicted using a pseudo-steady-state kinetic model. The secondary reactive species, such as chlorine and carbonate radicals, were found to contribute to CFX degradation. Product analysis indicated oxidation of CFX to six products (molecular weight of 363), with two stereoisomeric sulfoxides as the primary oxidation products. It was thus suggested that the primary amine on the side chain, and the thioether sulfur and double bond on the six-membered ring were the reactive sites of CFX towards SO 4 - oxidation. Antibacterial activity assessment showed that the biological activity of CFX solution was significantly diminished after treatment by the thermally activated PS. Copyright © 2018 Elsevier B.V. All rights reserved.

Serum prolidase activity and oxidative status in Helicobacter pylori infection.

PubMed

Aslan, Mehmet; Nazligul, Yasar; Horoz, Mehmet; Bolukbas, Cengiz; Bolukbas, Fusun F; Aksoy, Nurten; Celik, Hakim; Erel, Ozcan

2007-01-01

During the course of Helicobacter pylori infection, increased oxidative stress plays an important role in the pathogenesis of gastroduodenal mucosal inflammation, which can cause gastric mucosal atrophy that characterized by the replacement of the gastric mucosal glands by collagen fibers. In the present study, we aimed to determine serum prolidase activity and oxidative status, and to find out if there is any association between serum prolidase activity and oxidative status in H. pylori infection. Forty H. pylori-positive and 32 H. pylori-negative subjects were enrolled. Serum prolidase activity was measured spectrophotometrically. Oxidative status was determined using total antioxidant capacity and total oxidant status measurement and calculation of oxidative stress index. Total antioxidant capacity level was lower in H. pylori-positive group than H. pylori-negative group (p<0.001), whereas total oxidant status, oxidative stress index and prolidase activity were higher (all p<0.05). Significant correlation was observed between serum prolidase activity, and total antioxidant capacity, total oxidant status and oxidative stress index (p<0.01, r=-0.367; p<0.05, r=0.283; p<0.01, r=0.379; respectively) in H. pylori-positive subjects. H. pylori infection may be associated with increased oxidative stress and increased serum prolidase activity. Increased oxidative stress seems to be associated with increased serum prolidase activity and this association may help to provide a better understanding about the pathogenesis of H. pylori infection.

Investigating Endothelial Activation and Oxidative Stress in relation to Glycaemic Control in a Multiethnic Population

PubMed Central

Brady, E. M.; Webb, D. R.; Morris, D. H.; Khunti, K.; Talbot, D. S. C.; Sattar, N.; Davies, M. J.

2012-01-01

Aim. An exploration of ethnic differences in measures of oxidative stress and endothelial activation in relation to known cardiovascular risk factors within South Asians (SA) and White Europeans (WE) residing in the UK. Methods. 202 participants within a UK multiethnic population provided biomedical and anthropometric data. Human urinary 2,3-dinor-8-iso-prostaglandin-F1α and plasma ICAM-1 were quantified as measures of oxidative stress and endothelial activation, respectively. Results. 2,3-Dinor-8-iso-prostaglandin-F1α levels were significantly higher in the SA group compared to WE group (10.36 (95% CI: 9.09, 11.79) versus 8.46 (7.71, 9.29), P = 0.021) after adjustment for age, gender, smoking status, body weight, HbA1c, and medication. Oxidative stress was positively associated with HbA1c (β = 1.08, 95% CI:1.02, 1.14, P = 0.009), fasting (β = 1.06, 95% CI: 1.02, 1.10, P = 0.002), and 2 hr glucose (β = 1.02, 95% CI: 1.00, 1.04, P = 0.052). In each adjusted model, SA continued to have elevated levels of oxidative stress compared to WE. ICAM-1 levels were significantly higher in the composite IGR group compared to the normoglycaemic group (P < 0.001). No ethnic differences in ICAM-1 were observed. Conclusion. These results suggest that SA are more susceptible to the detrimental effects of hyperglycaemia-induced oxidative stress at lower blood glucose thresholds than WE. Further research into the potential mechanisms involved is warranted. PMID:23304116

Antibacterial activity of graphite, graphite oxide, graphene oxide, and reduced graphene oxide: membrane and oxidative stress.

PubMed

Liu, Shaobin; Zeng, Tingying Helen; Hofmann, Mario; Burcombe, Ehdi; Wei, Jun; Jiang, Rongrong; Kong, Jing; Chen, Yuan

2011-09-27

Health and environmental impacts of graphene-based materials need to be thoroughly evaluated before their potential applications. Graphene has strong cytotoxicity toward bacteria. To better understand its antimicrobial mechanism, we compared the antibacterial activity of four types of graphene-based materials (graphite (Gt), graphite oxide (GtO), graphene oxide (GO), and reduced graphene oxide (rGO)) toward a bacterial model-Escherichia coli. Under similar concentration and incubation conditions, GO dispersion shows the highest antibacterial activity, sequentially followed by rGO, Gt, and GtO. Scanning electron microscope (SEM) and dynamic light scattering analyses show that GO aggregates have the smallest average size among the four types of materials. SEM images display that the direct contacts with graphene nanosheets disrupt cell membrane. No superoxide anion (O(2)(•-)) induced reactive oxygen species (ROS) production is detected. However, the four types of materials can oxidize glutathione, which serves as redox state mediator in bacteria. Conductive rGO and Gt have higher oxidation capacities than insulating GO and GtO. Results suggest that antimicrobial actions are contributed by both membrane and oxidation stress. We propose that a three-step antimicrobial mechanism, previously used for carbon nanotubes, is applicable to graphene-based materials. It includes initial cell deposition on graphene-based materials, membrane stress caused by direct contact with sharp nanosheets, and the ensuing superoxide anion-independent oxidation. We envision that physicochemical properties of graphene-based materials, such as density of functional groups, size, and conductivity, can be precisely tailored to either reducing their health and environmental risks or increasing their application potentials. © 2011 American Chemical Society

Transcriptional profiling reveals elevated CO2 and elevated O3 alter resistance of soybean (Glycine max) to Japanese beetles (Popillia japonica).

PubMed

Casteel, Clare L; O'Neill, Bridget F; Zavala, Jorge A; Bilgin, Damla D; Berenbaum, May R; Delucia, Evan H

2008-04-01

The accumulation of CO2 and O3 in the troposphere alters phytochemistry which in turn influences the interactions between plants and insects. Using microarray analysis of field-grown soybean (Glycine max), we found that the number of transcripts in the leaves affected by herbivory by Japanese beetles (Popillia japonica) was greater when plants were grown under elevated CO2, elevated O3 and the combination of elevated CO2 plus elevated O3 than when grown in ambient atmosphere. The effect of herbivory on transcription diminished strongly with time (<1% of genes were affected by herbivory after 3 weeks), and elevated CO2 interacted more strongly with herbivory than elevated O3. The majority of transcripts affected by elevated O3 were related to antioxidant metabolism. Constitutive levels and the induction by herbivory of key transcripts associated with defence and hormone signalling were down-regulated under elevated CO2; 1-aminocyclopropane-1-carboxylate (ACC) synthase, lipoxygenase (LOX), allene oxide synthase (AOS), allene oxide cyclase (AOC), chalcone synthase (CHS), polyphenol oxidase (PPO) and cysteine protease inhibitor (CystPI) were lower in abundance compared with levels under ambient conditions. By suppressing the ability to mount an effective defence, elevated CO2 may decrease resistance of soybean to herbivory.

Role of RuO2(100) in surface oxidation and CO oxidation catalysis on Ru(0001).

PubMed

Flege, Jan Ingo; Lachnitt, Jan; Mazur, Daniel; Sutter, Peter; Falta, Jens

2016-01-07

We have studied the oxidation of the Ru(0001) surface by in situ microscopy during exposure to NO2, an efficient source of atomic oxygen, at elevated temperatures. In a previous investigation [Flege et al., Phys. Rev. B: Condens. Matter Mater. Phys., 2008, 78, 165407], at O coverages exceeding 1 monolayer, using the combination of intensity-voltage (I(V)) low-energy electron microscopy (LEEM) and multiple scattering calculations for the (00) beam in the very-low-energy range (E≤ 50 eV) we identified three surface components during the initial Ru oxidation: a (1 × 1)-O chemisorption phase, the RuO2(110) oxide phase, and a surface oxide structure characterized by a trilayer O-Ru-O stacking. Here, we use dark-field LEEM imaging and micro-illumination low-energy electron diffraction in the range of 100 to 400 eV to show that this trilayer phase is actually a RuO2(100)-(1 × 1) phase with possibly mixed O and Ru surface terminations. This identification rationalizes the thermodynamic stability of this phase at elevated temperatures and is consistent with the observation of catalytic activity of the phase in CO oxidation.

Effect of elevated CO2 on chlorpyriphos degradation and soil microbial activities in tropical rice soil.

PubMed

Adak, Totan; Munda, Sushmita; Kumar, Upendra; Berliner, J; Pokhare, Somnath S; Jambhulkar, N N; Jena, M

2016-02-01

Impact of elevated CO2 on chlorpyriphos degradation, microbial biomass carbon, and enzymatic activities in rice soil was investigated. Rice (variety Naveen, Indica type) was grown under four conditions, namely, chambered control, elevated CO2 (550 ppm), elevated CO2 (700 ppm) in open-top chambers and open field. Chlorpyriphos was sprayed at 500 g a.i. ha(-1) at maximum tillering stage. Chlorpyriphos degraded rapidly from rice soils, and 88.4% of initially applied chlorpyriphos was lost from the rice soil maintained under elevated CO2 (700 ppm) by day 5 of spray, whereas the loss was 80.7% from open field rice soil. Half-life values of chlorpyriphos under different conditions ranged from 2.4 to 1.7 days with minimum half-life recorded with two elevated CO2 treatments. Increased CO2 concentration led to increase in temperature (1.2 to 1.8 °C) that played a critical role in chlorpyriphos persistence. Microbial biomass carbon and soil enzymatic activities specifically, dehydrogenase, fluorescien diacetate hydrolase, urease, acid phosphatase, and alkaline phosphatase responded positively to elevated CO2 concentrations. Generally, the enzyme activities were highly correlated with each other. Irrespective of the level of CO2, short-term negative influence of chlorpyriphos was observed on soil enzymes till day 7 of spray. Knowledge obtained from this study highlights that the elevated CO2 may negatively influence persistence of pesticide but will have positive effects on soil enzyme activities.

Associations of Metabolic Syndrome, Elevated C-Reactive Protein, and Physical Activity in U.S. Adolescents.

PubMed

Williams, Bethany D; Richardson, Michael R; Johnson, Tammie M; Churilla, James R

2017-12-01

The aim was to estimate the prevalence of metabolic syndrome (MetS) criteria, elevated C-reactive protein (CRP), and physical activity (PA) as well as the odds of MetS criteria in those active versus inactive utilizing a representative sample of U.S. adolescents. The study sample (n = 676) included male and female adolescent (12-17 years) participants in the 2007-2010 National Health and Nutrition Examination Survey. The criteria analyzed were based on a modified definition of MetS using the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Current adult cut points were used to determine elevated CRP. Activity was estimated using reported days per week and minutes per day of moderate/vigorous PA. The MetS criteria with the highest and lowest overall prevalence estimates were elevated fasting glucose and elevated blood pressure (20.7% [95% confidence interval, 17.02-24.38] and 5.7% [95% confidence interval, 3.70-7.70], respectively). The prevalence of elevated CRP was 7.1% (6.3% and 7.8% in males and females, respectively; p = .42). The prevalence of insufficient PA was 75.0%. Odds of low high-density lipoprotein cholesterol were significantly lower in active adolescents when compared with inactive adolescents (odds ratio = .39, p < .05). In a representative sample of U.S. adolescents, elevated fasting glucose is the most prevalent MetS criterion. One out of five U.S. adolescents has elevated fasting glucose, and three out four do not meet the daily federal PA recommendations. Adolescents meeting the federal PA recommendation demonstrate approximately 60% lower odds of having low high-density lipoprotein cholesterol. Copyright © 2017 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

Process for preparing active oxide powders

DOEpatents

Berard, Michael F.; Hunter, Jr., Orville; Shiers, Loren E.; Dole, Stephen L.; Scheidecker, Ralph W.

1979-02-20

An improved process for preparing active oxide powders in which cation hydroxide gels, prepared in the conventional manner are chemically dried by alternately washing the gels with a liquid organic compound having polar characteristics and a liquid organic compound having nonpolar characteristics until the mechanical water is removed from the gel. The water-free cation hydroxide is then contacted with a final liquid organic wash to remove the previous organic wash and speed drying. The dried hydroxide treated in the conventional manner will form a highly sinterable active oxide powder.

Insulin sensitivity is related to fat oxidation and protein kinase C activity in children with acute burn injury

PubMed Central

Cree, Melanie G.; Zwetsloot, Jennifer J.; Herndon, David N.; Newcomer, Bradley R.; Fram, Ricki Y.; Angel, Carlos; Green, Justin M.; Dohm, Gerald L.; Sun, Dayoung; Aarsland, Asle; Wolfe, Robert R.

2014-01-01

Objective Impaired fatty acid oxidation occurs with type 2 diabetes and is associated with accumulations of intracellular lipids, which may increase diacylglycerol, stimulate protein kinase C activity and inactivate insulin signaling. Glucose and fat metabolism are altered in burn patients, but have never been related to intracellular lipids or insulin signaling. Methods Thirty children sustaining >40% total body surface area burns were studied acutely with glucose and palmitate tracer infusions and a hyper-insulinemic euglycemic clamp. Muscle triglyceride, diacylglycerol, fatty acyl CoA and insulin signaling were measured. Liver and muscle triglyceride levels were measured with magnetic resonance spectroscopy. Muscle samples from healthy children were controls for diacylglycerol concentrations. Results Insulin sensitivity was reduced and correlated with whole body palmitate β-oxidation (P=0.004). Muscle insulin signaling was not stimulated by hyper-insulinemia. Tissue triglyceride concentrations and activated protein kinase C-β were elevated, whereas the concentration of diacylglycerol was similar to the controls. Free fatty acid profiles of muscle triglyceride did not match diacylglycerol. Conclusions Insulin resistance following burn injury is accompanied by decreased insulin signaling and increased protein kinase C-β activation. The best metabolic predictor of insulin resistance in burned patients was palmitate oxidation. PMID:18535477

Elevated-Temperature Tribology of Metallic Materials

DOE Office of Scientific and Technical Information (OSTI.GOV)

Blau, Peter Julian

The wear of metals and alloys takes place in many forms, and the type of wear that dominates in each instance is influenced by the mechanics of contact, material properties, the interfacial temperature, and the surrounding environment. The control of elevated-temperature friction and wear is important for applications like internal combustion engines, aerospace propulsion systems, and metalworking equipment. The progression of interacting, often synergistic processes produces surface deformation, subsurface damage accumulation, the formation of tribolayers, and the creation of free particles. Reaction products, particularly oxides, play a primary role in debris formation and microstructural evolution. Chemical reactions are known tomore » be influenced by the energetic state of the exposed surfaces, and that surface energy is in turn affected by localized deformation and fracture. At relatively low temperatures, work-hardening can occur beneath tribo-contacts, but exposure to high temperatures can modify the resultant defect density and grain structure to affect the mechanisms of re-oxidation. As research by others has shown, the rate of wear at elevated temperatures can either be enhanced or reduced, depending on contact conditions and nature of oxide layer formation. Furthermore, the thermodynamic driving force for certain chemical reactions is moderated by kinetics and microstructure. The role of deformation, oxidation, and tribo-corrosion in the elevated temperature tribology of metallic alloys will be exemplified by three examples involving sliding wear, single-point abrasion, and repetitive impact plus slip.« less

Passive stretch reduces calpain activity through nitric oxide pathway in unloaded soleus muscles.

PubMed

Xu, Peng-Tao; Li, Quan; Sheng, Juan-Juan; Chang, Hui; Song, Zhen; Yu, Zhi-Bin

2012-08-01

Unloading in spaceflight or long-term bed rest induces to pronounced atrophy of anti-gravity skeletal muscles. Passive stretch partially resists unloading-induced atrophy of skeletal muscle, but the mechanism remains elusive. The aims of this study were to investigate the hypotheses that stretch tension might increase protein level of neuronal nitric oxide synthase (nNOS) in unloaded skeletal muscle, and then nNOS-derived NO alleviated atrophy of skeletal muscle by inhibiting calpain activity. The tail-suspended rats were used to unload rat hindlimbs for 2 weeks, at the same time, left soleus muscle was stretched by applying a plaster cast to fix the ankle at 35° dorsiflexion. Stretch partially resisted atrophy and inhibited the decreased protein level and activity of nNOS in unloaded soleus muscles. Unloading increased frequency of calcium sparks and elevated intracellular resting and caffeine-induced Ca(2+) concentration ([Ca(2+)]i) in unloaded soleus muscle fibers. Stretch reduced frequency of calcium sparks and restored intracellular resting and caffeine-induced Ca(2+) concentration to control levels in unloaded soleus muscle fibers. The increased protein level and activity of calpain as well as the higher degradation of desmin induced by unloading were inhibited by stretch in soleus muscles. In conclusion, these results suggest that stretch can preserve the stability of sarcoplasmic reticulum Ca(2+) release channels which prevents the elevated [Ca(2+)]i by means of keeping nNOS activity, and then the enhanced protein level and activity of calpain return to control levels in unloaded soleus muscles. Therefore, stretch can resist in part atrophy of unloaded soleus muscles.

Nanostructured manganese oxides as highly active water oxidation catalysts: a boost from manganese precursor chemistry.

PubMed

Menezes, Prashanth W; Indra, Arindam; Littlewood, Patrick; Schwarze, Michael; Göbel, Caren; Schomäcker, Reinhard; Driess, Matthias

2014-08-01

We present a facile synthesis of bioinspired manganese oxides for chemical and photocatalytic water oxidation, starting from a reliable and versatile manganese(II) oxalate single-source precursor (SSP) accessible through an inverse micellar molecular approach. Strikingly, thermal decomposition of the latter precursor in various environments (air, nitrogen, and vacuum) led to the three different mineral phases of bixbyite (Mn2 O3 ), hausmannite (Mn3 O4 ), and manganosite (MnO). Initial chemical water oxidation experiments using ceric ammonium nitrate (CAN) gave the maximum catalytic activity for Mn2 O3 and MnO whereas Mn3 O4 had a limited activity. The substantial increase in the catalytic activity of MnO in chemical water oxidation was demonstrated by the fact that a phase transformation occurs at the surface from nanocrystalline MnO into an amorphous MnOx (1oxidizing agent. Photocatalytic water oxidation in the presence of [Ru(bpy)3 ](2+) (bpy=2,2'-bipyridine) as a sensitizer and peroxodisulfate as an electron acceptor was carried out for all three manganese oxides including the newly formed amorphous MnOx . Both Mn2 O3 and the amorphous MnOx exhibit tremendous enhancement in oxygen evolution during photocatalysis and are much higher in comparison to so far known bioinspired manganese oxides and calcium-manganese oxides. Also, for the first time, a new approach for the representation of activities of water oxidation catalysts has been proposed by determining the amount of accessible manganese centers. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Stimulating ammonia oxidizing bacteria (AOB) activity drives the ammonium oxidation rate in a constructed wetland (CW).

PubMed

Su, Yu; Wang, Weidong; Wu, Di; Huang, Wei; Wang, Mengzi; Zhu, Guibing

2018-05-15

An integrated approach to document high ammonium oxidation rate in Guanjinggang constructed wetland (GJG-CW) was performed and the results showed that the substantial ammonium oxidation rate could be obtained by enhancing Ammonia Oxidizing Bacteria (AOB) activity rather than Ammonia Oxidizing Archaea (AOA) activity. In the plant-bed/ditch system, ditch center and plant-bed fringe were two active zones for NH 4 + -N removal with ammonium oxidation rate peaking at 2.98±0.04 and 2.15±0.02mgNkg -1 d -1 , respectively. The enhanced AOB activity were achieved by increasing water level fluctuations, extending hydraulic retention time (HRT) and stimulating substrate availability, which subsequently enhanced NH 4 + -N removal by 34.06% in GJG-CW. However, the high AOB activity was not correlated with high AOB abundance, but was instead mostly determined by specific AOB taxa, particularly Nitrosomonas, which dominated in the active AOB. The increased cell-specific AOA activity and high AOA diversity were also achieved using those engineering measures. Although the AOA activity decreased overall with extended HRT and increased NH 4 + -N contents in GJG-CW, AOA still played a major role on ammonium oxidation in plant-bed soil. The study illustrated that artificially enhancing AOB activity and certain species in anthropogenically polluted water ecosystems would be an effective strategy to improve NH 4 + -N removal. Copyright © 2017 Elsevier B.V. All rights reserved.

Effect of elevated CO2 on degradation of azoxystrobin and soil microbial activity in rice soil.

PubMed

Manna, Suman; Singh, Neera; Singh, V P

2013-04-01

An experiment was conducted in open-top chambers (OTC) to study the effect of elevated CO2 (580 ± 20 μmol mol(-1)) on azoxystrobin degradation and soil microbial activities. Results indicated that elevated CO2 did not have any significant effect on the persistence of azoxystrobin in rice-planted soil. The half-life values for the azoxystrobin in rice soils were 20.3 days in control (rice grown at ambient CO2 outdoors), 19.3 days in rice grown under ambient CO2 atmosphere in OTC, and 17.5 days in rice grown under elevated CO2 atmosphere in OTC. Azoxystrobin acid was recovered as the only metabolite of azoxystrobin, but it did not accumulate in the soil/water and was further metabolized. Elevated CO2 enhanced soil microbial biomass (MBC) and alkaline phosphatase activity of soil. Compared with rice grown at ambient CO2 (both outdoors and in OTC), the soil MBC at elevated CO2 increased by twofold. Elevated CO2 did not affect dehydrogenase, fluorescein diacetate, and acid phosphatase activity. Azoxystrobin application to soils, both ambient and elevated CO2, inhibited alkaline phosphates activity, while no effect was observed on other enzymes. Slight increase (1.8-2 °C) in temperature inside OTC did not affect microbial parameters, as similar activities were recorded in rice grown outdoors and in OTC at ambient CO2. Higher MBC in soil at elevated CO2 could be attributed to increased carbon availability in the rhizosphere via plant metabolism and root secretion; however, it did not significantly increase azoxystrobin degradation, suggesting that pesticide degradation was not the result of soil MBC alone. Study suggested that increased CO2 levels following global warming might not adversely affect azoxystrobin degradation. However, global warming is a continuous and cumulative process, therefore, long-term studies are necessary to get more realistic assessment of global warming on fate of pesticide.

Oxidation of Ethylene Glycol by a Salt-Requiring Bacterium

PubMed Central

Caskey, William H.; Taber, Willard A.

1981-01-01

Bacterium T-52, cultured on ethylene glycol, readily oxidized glycolate and glyoxylate and exhibited elevated activities of ethylene glycol dehydrogenase and glycolate oxidase. Labeled glyoxylate was identified in reaction mixtures containing [14C]-ethylene glycol, but no glycolate was detected. The most likely pathway of ethylene glycol catabolism by bacterium T-52 is sequential oxidation to glycolate and glyoxylate. PMID:16345810

Oxidative Stress and Inflammation Differentially Elevated in Objective Versus Habitual Subjective Reduced Sleep Duration in Obstructive Sleep Apnea.

PubMed

DeMartino, Theresanne; Ghoul, Rawad El; Wang, Lu; Bena, James; Hazen, Stanley L; Tracy, Russel; Patel, Sanjay R; Auckley, Dennis; Mehra, Reena

2016-07-01

Data have demonstrated adverse health effects of sleep deprivation. We postulate that oxidative stress and systemic inflammation biomarkers will be elevated in relation to short-term and long-term sleep duration reduction. We analyzed data from the baseline examination of a randomized controlled trial involving participants with moderate to severe obstructive sleep apnea (OSA). Baseline polysomnography provided the total sleep time (PSG-TST, primary predictor); self-reported habitual sleep duration (SR-HSD) data was collected. Morning measures of oxidative stress and systemic inflammation included: myeloperoxidase (MPO, pmol/L), oxidized low-density lipoprotein (ox-LDL, U/L), F2-isoprostane (ng/mg), paraoxonase 1 (PON1, nmol·min(-1)·mL(-1)), and aryl esterase (μmol·min(-1)·mL(-1)). Linear models adjusted for age, sex, race, body mass index (BMI), cardiovascular disease (CVD), smoking, statin/anti-inflammatory medications, and apnea-hypopnea index were utilized (beta estimates and 95% confidence intervals). One hundred forty-seven participants comprised the final analytic sample; they were overall middle-aged (51.0 ± 11.7 y), obese (BMI = 37.3 ± 8.1 kg/m(2)), and 17% had CVD. Multivariable models demonstrated a significant inverse association of PSG-TST and MPO (β [95% CI] = -20.28 [-37.48, -3.08], P = 0.021), i.e., 20.3 pmol/L MPO reduction per hour increase PSG-TST. Alternatively, a significant inverse association with ox-LDL and SR-HSD was observed (β [95% CI] = 0.98 [0.96, 0.99], P = 0.027), i.e., 2% ox-LDL reduction per hour increase SR-HSD. Even after consideration of obesity and OSA severity, inverse significant findings were observed such that reduced PSG-TST was associated with elevated MPO levels and SR-HSD with ox-LDL, suggesting differential up-regulation of oxidative stress and pathways of inflammation in acute versus chronic sleep curtailment. NIH clinical trials registry number NCT00607893. © 2016 Associated Professional Sleep Societies, LLC.

Hysteresis in the Active Oxidation of SiC

NASA Technical Reports Server (NTRS)

Jacobson, Nathan S.; Harder, Bryan J.; Myers, Dwight L.

2011-01-01

Si and SiC show both passive oxidation behavior where a protective film of SiO2 forms and active oxidation behavior where a volatile suboxide SiO(g) forms. The active-to-passive and passive-to-active oxidation transitions are explored for both Si and SiC. Si shows a dramatic difference between the P(O2) for the two transitions of 10-4 bar. The active-to-passive transition is controlled by the condition for SiO2/Si equilibrium and the passive-to-active transition is controlled by the decomposition of SiO2. In the case of SiC, the P(O2) for these transitions are much closer. The active-to-passive transition appears to be controlled by the condition for SiO2/SiC equilibrium. The passive-to-active transition appears to be controlled by the interfacial reaction of SiC and SiO2 and subsequent generation of gases at the interface which leads to scale breakdown.

Vitamin D3-induced hypercalcemia increases carbon tetrachloride-induced hepatotoxicity through elevated oxidative stress in mice

PubMed Central

Usuda, Haruki; Miura, Nobuhiko; Fukuishi, Nobuyuki; Nonogaki, Tsunemasa; Onosaka, Satomi

2017-01-01

The aim of this study was to determine whether calcium potentiates acute carbon tetrachloride (CCl4) -induced toxicity. Elevated calcium levels were induced in mice by pre-treatment with cholecalciferol (vitamin D3; V.D3), a compound that has previously been shown to induce hypercalcemia in human and animal models. As seen previously, mice injected with CCl4 exhibited increased plasma levels of alanine aminotransferase, aspartate aminotransferase, and creatinine; transient body weight loss; and increased lipid peroxidation along with decreased total antioxidant power, glutathione, ATP, and NADPH. Pre-treatment of these animals with V.D3 caused further elevation of the values of these liver functional markers without altering kidney functional markers; continued weight loss; a lower lethal threshold dose of CCl4; and enhanced effects on lipid peroxidation and total antioxidant power. In contrast, exposure to V.D3 alone had no effect on plasma markers of liver or kidney damage or on total antioxidant power or lipid peroxidation. The potentiating effect of V.D3 was positively correlated with elevation of hepatic calcium levels. Furthermore, direct injection of CaCl2 also enhanced CCl4-induced hepatic injury. Since CaCl2 induced hypercalcemia transiently (within 3 h of injection), our results suggest that calcium enhances the CCl4-induced hepatotoxicity at an early stage via potentiation of oxidative stress. PMID:28448545

[Effects of elevated ozone concentrations on enzyme activities and organic acids content in wheat rhizospheric soil.

PubMed

Yin, Wei Qin; Jing, Hao Qi; Wang, Ya Bo; Wei, Si Yu; Sun, Yue; Wang, Sheng Sen; Wang, Xuai Zhi

2018-02-01

The elevated concentration of tropospheric ozone (O 3 ) is an important global climate change driver, with adverse impacts on soil ecological environment and crop growth. In this study, a pot experiment was carried out in an open top chamber (OTC), to investigate the effects of elevated ozone concentration on soil enzyme activities (catalase, polyphenol oxidase, dehydrogenase and invertase), organic acids contents (oxalic acid, citric acid and malic acid) at different growth stages (tillering, jointing, heading and ripening stages) of wheat, and combined with the rhizospheric soil physicochemical properties and plant root characteristics to analyze the underlying reasons. The results showed that, elevated ozone concentration increased soil catalase, polyphenol oxidase, dehydrogenase and invertase activities at wheat ripening period to different degrees, with the effects on the activities of catalase and polyphenol oxidase being statistically significant. At the heading stage, activities of dehydrogenase and invertase were significantly increased by up to 76.7%. At the ripening stage, elevated ozone concentration significantly increased the content of citric acid and malic acid and redox potential (Eh) in rhizospheric soil, but reduced soil pH, electrical conductivity, total carbon and nitrogen. For root characteristics, elevated ozone concentrations significantly reduced the wheat root biomass, total root length and root surface area but increased the average root diameter.

Evidence of acrylamide induced oxidative stress and neurotoxicity in Drosophila melanogaster - its amelioration with spice active enrichment: relevance to neuropathy.

PubMed

Prasad, Sathya N; Muralidhara

2012-10-01

Acrylamide (ACR) intoxication in its monomeric form leads to neuronal damage in both experimental animals and humans. Oxidative stress is one of the principle mechanisms related to the neurotoxicity of ACR exposure. Hence, the present study aimed to recapitulate the potential of ACR to cause oxidative stress and neurotoxic effects in Drosophila melanogaster. Exposure of adult male flies (Oregon K strain) to ACR (1-10 mM, 7 d) in the diet resulted in a concentration and time dependent mortality, while the survivors exhibited significant locomotor deficits. Further, ACR exposure (1-5 mM, 3 d) caused robust oxidative stress as evidenced by markedly elevated levels of reactive oxygen species and hypdroperoxides in head/body regions. Enhanced lipid peroxidation, perturbations in the activities of antioxidant enzymes accompanied with depletion of reduced glutathione levels in head region at high concentrations suggested induction of oxidative stress. Further, marked diminution in the activities of complexes I-III, Succinic dehydrogenase, with concomitant reduction in MTT suggested the propensity of ACR to impair mitochondrial function. Furthermore, ACR-induced neurotoxic effects were discernible in terms of diminished ATPase activity, enhanced activity of acetylcholinesterase and dopamine depletion. In a satellite study, employing a co-exposure paradigm, we tested the propensity of spice actives namely eugenol (EU) and isoeugenol (IE) to ameliorate ACR-induced neurotoxicity. EU/IE enriched diet offered marked protection against ACR-induced mortality, locomotor dysfunctions and oxidative stress. Furthermore, the spice actives prevented the depletion of reduced GSH levels, maintained the activity of AChE enzyme and dopamine levels in head region. Collectively, these findings clearly demonstrate that ACR induced neurotoxicity in Drosophila may be mediated through oxidative stress mechanisms and the potential of spice actives to abrogate the condition. These data suggest

Protective activity of Panduratin A against Thioacetamide-induced oxidative damage: demonstration with in vitro experiments using WRL-68 liver cell line

PubMed Central

2013-01-01

Background Chalcone Panduratin A (PA) has been known for its antioxidant property, but its merits against oxidative damage in liver cells has yet to be investigated. Hence, the paper aimed at accomplishing this task with normal embryonic cell line WRL-68. Methods PA was isolated from Boesenbergia rotunda rhizomes and its 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging and ferric reducing power (FRAP) activities were measured in comparison with that of the standard reference drug Silymarin (SI). Oxidative damage was induced by treating the cells with 0.04 g/ml of toxic thioacetamide for 60 minutes followed by treatment with 1, 10 and 100 μg/ml concentrations of either PA or SI. The severities of oxidative stress in the control and experimental groups of cells were measured by Malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Results PA exhibited an acceptable DPPH scavenging and FRAP activities close to that of Silymarin. Treating the injured cells with PA significantly reduced the MDA level and increased the cell viability, comparable to SI. The activities of SOD, CAT and GPx were significantly elevated in the PA-treated cells in a dose dependent manner and again similar to SI. Conclusion Collectively, data suggested that PA has capacity to protect normal liver cells from oxidative damage, most likely via its antioxidant scavenging ability. PMID:24156366

Involvement of catalase in the protective benefits of metformin in mice with oxidative liver injury.

PubMed

Dai, Jie; Liu, Mingwei; Ai, Qing; Lin, Ling; Wu, Kunwei; Deng, Xinyu; Jing, Yuping; Jia, Mengying; Wan, Jingyuan; Zhang, Li

2014-06-05

Metformin is a commonly used anti-diabetic drug with AMP-activated protein kinase (AMPK)-dependent hypoglycemic activities. Recent studies have revealed its anti-inflammatory and anti-oxidative properties. In the present study, the anti-oxidative potential of metformin and its potential mechanisms were investigated in a mouse model with carbon tetrachloride (CCl₂)-induced severe oxidative liver injury. Our results showed that treatment with metformin significantly attenuated CCl₂-induced elevation of serum aminotransferases and hepatic histological abnormalities. The alleviated liver injury was associated with decreased hepatic contents of oxidized glutathione (GSSG) and malondialdehyde (MDA). In addition, metformin treatment dose-dependently enhanced the activities of catalase (CAT) and decreased CCl₄-induced elevation of hepatic H₂O₂ levels, but it had no obvious effects on the protein level of CAT. We also found that metformin increased the level of phosphorylated AMP-activated protein kinase (AMPK), but treatment with AMPK activator AICAR had no obvious effects on CAT activity. A molecular docking analysis indicated that metformin might interact with CAT via hydrogen bonds. These data suggested that metformin effectively alleviated CCl₄-induced oxidative liver injury in mice and these hepatoprotective effects might be associated with CAT. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Oxidative stress and anti-oxidant enzyme activities in the trophocytes and fat cells of queen honeybees (Apis mellifera).

PubMed

Hsieh, Yu-Shan; Hsu, Chin-Yuan

2013-08-01

Trophocytes and fat cells of queen honeybees have been used for delayed cellular senescence studies, but their oxidative stress and anti-oxidant enzyme activities with advancing age are unknown. In this study, we assayed reactive oxygen species (ROS) and anti-oxidant enzymes in the trophocytes and fat cells of young and old queens. Young queens had lower ROS levels, lower superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, and higher thioredoxin reductase (TR) activity compared to old queens. These results show that oxidative stress and anti-oxidant enzyme activities in trophocytes and fat cells increase with advancing age in queens and suggest that an increase in oxidative stress and a consequent increase in stress defense mechanisms are associated with the longevity of queen honeybees.

Chronic Oxidative Stress, Mitochondrial Dysfunction, Nrf2 Activation and Inflammation in the Hippocampus Accompany Heightened Systemic Inflammation and Oxidative Stress in an Animal Model of Gulf War Illness

PubMed Central

Shetty, Geetha A.; Hattiangady, Bharathi; Upadhya, Dinesh; Bates, Adrian; Attaluri, Sahithi; Shuai, Bing; Kodali, Maheedhar; Shetty, Ashok K.

2017-01-01

Memory and mood dysfunction are the key symptoms of Gulf war illness (GWI), a lingering multi-symptom ailment afflicting >200,000 veterans who served in the Persian Gulf War-1. Research probing the source of the disease has demonstrated that concomitant exposures to anti-nerve gas agent pyridostigmine bromide (PB), pesticides, and war-related stress are among the chief causes of GWI. Indeed, exposures to GWI-related chemicals (GWIR-Cs) and mild stress in animal models cause memory and mood impairments alongside reduced neurogenesis and chronic low-level inflammation in the hippocampus. In the current study, we examined whether exposure to GWIR-Cs and stress causes chronic changes in the expression of genes related to increased oxidative stress, mitochondrial dysfunction, and inflammation in the hippocampus. We also investigated whether GWI is linked with chronically increased activation of Nrf2 (a master regulator of antioxidant response) in the hippocampus, and inflammation and enhanced oxidative stress at the systemic level. Adult male rats were exposed daily to low-doses of PB and pesticides (DEET and permethrin), in combination with 5 min of restraint stress for 4 weeks. Analysis of the hippocampus performed 6 months after the exposure revealed increased expression of many genes related to oxidative stress response and/or antioxidant activity (Hmox1, Sepp1, and Srxn1), reactive oxygen species metabolism (Fmo2, Sod2, and Ucp2) and oxygen transport (Ift172 and Slc38a1). Furthermore, multiple genes relevant to mitochondrial respiration (Atp6a1, Cox6a1, Cox7a2L, Ndufs7, Ndufv1, Lhpp, Slc25a10, and Ucp1) and neuroinflammation (Nfkb1, Bcl6, Csf2, IL6, Mapk1, Mapk3, Ngf, N-pac, and Prkaca) were up-regulated, alongside 73–88% reduction in the expression of anti-inflammatory genes IL4 and IL10, and nuclear translocation and increased expression of Nrf2 protein. These hippocampal changes were associated with elevated levels of pro-inflammatory cytokines and chemokines

Preparation, characterization and antibacterial activity of oxidized κ-carrageenan.

PubMed

Zhu, Mingjin; Ge, Liming; Lyu, Yongbo; Zi, Yaxin; Li, Xinying; Li, Defu; Mu, Changdao

2017-10-15

The oxidized κ-carrageenans with different oxidation levels were prepared through the hydrogen peroxide and copper sulfate redox system. The oxidation level of oxidized κ-carrageenan was successfully controlled by adjusting the dosage of hydrogen peroxide. The results showed that the microtopography of oxidized κ-carrageenan changed from rough granules to smooth flakes, mainly resulting from the easily melting property of oxidized κ-carrageenan induced by introduced carboxyl and aldehyde groups. Especially, the antibacterial activity of oxidized κ-carrageenans against Gram-positive bacteria (Staphylococcus aureus and Listeria monocytogenes) and Gram-negative bacteria (Escherichia coli and Pseudomonas aeruginosa) was systematically investigated. The results showed that the oxidized κ-carrageenan could damage the bacterial cell wall and cytoplasmic membrane and suppress the growth of both Gram-positive and Gram-negative bacteria. The oxidized κ-carrageenan possessed broad-spectrum antibacterial activity, which may be used as a new antibacterial agent. Copyright © 2017 Elsevier Ltd. All rights reserved.

Increased Activity of Rhizosphere and Hyphosphere Enzymes under Elevated CO2 in a Loblolly Pine Stand

NASA Astrophysics Data System (ADS)

Meier, I.; Phillips, R.

2012-12-01

The stimulatory effect of elevated atmospheric CO2 under global climate change on forest productivity has been predicted to decrease over time as pools of available N in soil become depleted, but empirical support for such progressive N limitation has been lacking. Increased N acquisition from soil depleted in inorganic nitrogen requires stimulation of the microbial processing of organic N, possibly through increasing C supply to soil by plant roots or mycorrhizal hyphae. Increases in (mycorr)rhizosphere C fluxes could stimulate microbes to produce extra-cellular enzymes that release N from SOM, feeding back from soil microsites to ecosystem-scale processes. We investigated the influence of elevated CO2 on root exudation and soil enzyme activity at the Duke Forest FACE site, USA, where loblolly pine (Pinus taeda L.) stands have been exposed to elevated CO2 for 14 years and N fertilization for five years. In each plot, root boxes containing acetate windows were installed in 2008. Two years after installation, we collected soils adjacent to root tips (the rhizosphere), hyphal tips (the hyphosphere) and bulk soil. We measured in situ root exudation rates from intact pine roots. Study objectives were to analyze (i) the influence of atmospheric CO2 on root exudation and extra-cellular enzyme activities, (ii) the influence of soil N availability in regulating these activities, and (iii) the relationship between the activities of enzymes involved in N cycling in soils and gross N transformations at soil microsites. Elevated atmospheric CO2 significantly increased the activity of β-1-4-N-acetylglucosaminidase (NAG) in the rhizosphere by almost 2.5 times (39 to 95 nmol h-1 g-1), and 1.6fold in the hyphosphere relative to ambient plots. NAG is an enzyme involved in the degradation of chitin from the cell walls of soil organisms, releasing absorbable forms of nitrogen. The activity of peroxidase, which degrades aromatic C compounds of SOM, increased significantly in the

Testosterone Deficiency Causes Endothelial Dysfunction via Elevation of Asymmetric Dimethylarginine and Oxidative Stress in Castrated Rats.

PubMed

Kataoka, Tomoya; Hotta, Yuji; Maeda, Yasuhiro; Kimura, Kazunori

2017-12-01

damage to the corpus cavernosum, resulting in erectile dysfunction. Kataoka T, Hotta Y, Maeda Y, Kimura K. Testosterone Deficiency Causes Endothelial Dysfunction via Elevation of Asymmetric Dimethylarginine and Oxidative Stress in Castrated Rats. J Sex Med 2017;14:1540-1548. Copyright © 2017 International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.

Disparate effects of oxidation on plasma acyltransferase activities: inhibition of cholesterol esterification but stimulation of transesterification of oxidized phospholipids.

PubMed

Subbaiah, P V; Liu, M

1996-05-31

Oxidation of lipoproteins results in the formation of several polar phospholipids with pro-inflammatory and pro-atherogenic properties. To examine the possible role of lecithin/cholesterol acyltransferase (LCAT) in the metabolism of these oxidized phospholipids, we oxidized whole plasma with either Cu(2+) or a free-radical generator, and determined the various activities of LCAT. Oxidation caused a reduction in plasma phosphatidylcholine (PC), an increase in a short-chain polar PC (SCP-PC), and an inhibition of the transfer of long-chain acyl groups to cholesterol (LCAT activity) or to lyso PC (lysolecithin acyltransferase (LAT) I activity). However, the transfer of short-chain acyl groups from SCP-PC to lyso PCLAT II activity) was stimulated several fold, in direct correlation with the degree of oxidation. LAT II activity was not stimulated by oxidation in LCAT-deficient plasma, showing that it is carried out by LCAT. Oxidized normal plasma exhibited low LCAT activity even in the presence of exogenous proteoliposome substrate, indicating that the depletion of substrate PC was not responsible for the loss of activity. Oxidation of isolated LDL or HDL abolished their ability to support LCAT and LAT I activities of exogenous enzyme, but promoted the LAT II activity. Purified LCAT lost its LCAT and LAT I functions, but not its LAT II function, when oxidized in vitro. These results show that while oxidation of plasma causes a loss of LCAT's ability to transfer long-chain acyl groups, its ability to transfer short-chain acyl groups, from SCP-PC is retained, and even stimulated, suggesting that LCAT may have a physiological role in the metabolism of oxidized PC in plasma.

Generation and Biological Activities of Oxidized Phospholipids

PubMed Central

Oskolkova, Olga V.; Birukov, Konstantin G.; Levonen, Anna-Liisa; Binder, Christoph J.; Stöckl, Johannes

2010-01-01

Abstract Glycerophospholipids represent a common class of lipids critically important for integrity of cellular membranes. Oxidation of esterified unsaturated fatty acids dramatically changes biological activities of phospholipids. Apart from impairment of their structural function, oxidation makes oxidized phospholipids (OxPLs) markers of “modified-self” type that are recognized by soluble and cell-associated receptors of innate immunity, including scavenger receptors, natural (germ line-encoded) antibodies, and C-reactive protein, thus directing removal of senescent and apoptotic cells or oxidized lipoproteins. In addition, OxPLs acquire novel biological activities not characteristic of their unoxidized precursors, including the ability to regulate innate and adaptive immune responses. Effects of OxPLs described in vitro and in vivo suggest their potential relevance in different pathologies, including atherosclerosis, acute inflammation, lung injury, and many other conditions. This review summarizes current knowledge on the mechanisms of formation, structures, and biological activities of OxPLs. Furthermore, potential applications of OxPLs as disease biomarkers, as well as experimental therapies targeting OxPLs, are described, providing a broad overview of an emerging class of lipid mediators. Antioxid. Redox Signal. 12, 1009–1059. PMID:19686040

Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome During Apoptosis

PubMed Central

Shimada, Kenichi; Crother, Timothy R.; Karlin, Justin; Dagvadorj, Jargalsaikhan; Chiba, Norika; Chen, Shuang; Ramanujan, V. Krishnan; Wolf, Andrea J.; Vergnes, Laurent; Ojcius, David M.; Rentsendorj, Altan; Vargas, Mario; Guerrero, Candace; Wang, Yinsheng; Fitzgerald, Katherine A.; Underhill, David M.; Town, Terrence; Arditi, Moshe

2012-01-01

SUMMARY We report that in the presence of signal 1 (NF-κB), the NLRP3 inflammasome was activated by mitochondrial apoptotic signaling that licensed production of interleukin-1β (IL-1β). NLRP3 secondary signal activators such as ATP induced mitochondrial dysfunction and apoptosis, resulting in release of oxidized mitochondrial DNA (mtDNA) into the cytosol, where it bound to and activated the NLRP3 inflammasome. The anti-apoptotic protein Bcl-2 inversely regulated mitochondrial dysfunction and NLRP3 inflammasome activation. Mitochondrial DNA directly induced NLRP3 inflammasome activation, because macrophages lacking mtDNA had severely attenuated IL-1β production, yet still underwent apoptosis. Both binding of oxidized mtDNA to the NLRP3 inflammasome and IL-1β secretion could be competitively inhibited by the oxidized nucleoside, 8-OH-dG. Thus, our data reveal that oxidized mtDNA released during programmed cell death causes activation of the NLRP3 inflammasome. These results provide a missing link between apoptosis and inflammasome activation, via binding of cytosolic oxidized mtDNA to the NLRP3 inflammasome. PMID:22342844

Zinc oxide nanoparticles decrease the expression and activity of plasma membrane calcium ATPase, disrupt the intracellular calcium homeostasis in rat retinal ganglion cells.

PubMed

Guo, Dadong; Bi, Hongsheng; Wang, Daoguang; Wu, Qiuxin

2013-08-01

Zinc oxide nanoparticle is one of the most important materials with diverse applications. However, it has been reported that zinc oxide nanoparticles are toxic to organisms, and that oxidative stress is often hypothesized to be an important factor in cytotoxicity mediated by zinc oxide nanoparticles. Nevertheless, the mechanism of toxicity of zinc oxide nanoparticles has not been completely understood. In this study, we investigated the cytotoxic effect of zinc oxide nanoparticles and the possible molecular mechanism involved in calcium homeostasis mediated by plasma membrane calcium ATPase in rat retinal ganglion cells. Real-time cell electronic sensing assay showed that zinc oxide nanoparticles could exert cytotoxic effect on rat retinal ganglion cells in a concentration-dependent manner; flow cytometric analysis indicated that zinc oxide nanoparticles could lead to cell damage by inducing the overproduction of reactive oxygen species. Furthermore, zinc oxide nanoparticles could also apparently decrease the expression level and their activity of plasma membrane calcium ATPase, which finally disrupt the intracellular calcium homeostasis and result in cell death. Taken together, zinc oxide nanoparticles could apparently decrease the plasma membrane calcium ATPase expression, inhibit their activity, cause the elevated intracellular calcium ion level and disrupt the intracellular calcium homeostasis. Further, the disrupted calcium homeostasis will trigger mitochondrial dysfunction, generate excessive reactive oxygen species, and finally initiate cell death. Thus, the disrupted calcium homeostasis is involved in the zinc oxide nanoparticle-induced rat retinal ganglion cell death. Copyright © 2013 Elsevier Ltd. All rights reserved.

Enhanced oxidation resistance of active nanostructures via dynamic size effect

DOE Office of Scientific and Technical Information (OSTI.GOV)

Liu, Yun; Yang, Fan; Zhang, Yi

A major challenge limiting the practical applications of nanomaterials is that the activities of nanostructures (NSs) increase with reduced size, often sacrificing their stability in the chemical environment. Under oxidative conditions, NSs with smaller sizes and higher defect densities are commonly expected to oxidize more easily, since high-concentration defects can facilitate oxidation by enhancing the reactivity with O 2 and providing a fast channel for oxygen incorporation. Here, using FeO NSs as an example, we show to the contrary, that reducing the size of active NSs can drastically increase their oxidation resistance. A maximum oxidation resistance is found for FeOmore » NSs with dimensions below 3.2 nm. Rather than being determined by the structure or electronic properties of active sites, the enhanced oxidation resistance originates from the size-dependent structural dynamics of FeO NSs in O 2. We find this dynamic size effect to govern the chemical properties of active NSs.« less

Enhanced oxidation resistance of active nanostructures via dynamic size effect

DOE PAGES

Liu, Yun; Yang, Fan; Zhang, Yi; ...

2017-02-22

A major challenge limiting the practical applications of nanomaterials is that the activities of nanostructures (NSs) increase with reduced size, often sacrificing their stability in the chemical environment. Under oxidative conditions, NSs with smaller sizes and higher defect densities are commonly expected to oxidize more easily, since high-concentration defects can facilitate oxidation by enhancing the reactivity with O 2 and providing a fast channel for oxygen incorporation. Here, using FeO NSs as an example, we show to the contrary, that reducing the size of active NSs can drastically increase their oxidation resistance. A maximum oxidation resistance is found for FeOmore » NSs with dimensions below 3.2 nm. Rather than being determined by the structure or electronic properties of active sites, the enhanced oxidation resistance originates from the size-dependent structural dynamics of FeO NSs in O 2. We find this dynamic size effect to govern the chemical properties of active NSs.« less

Plant responses to elevated atmospheric CO/sub 2/ with emphasis on belowground processes

DOE Office of Scientific and Technical Information (OSTI.GOV)

Norby, R.J.; Luxmoore, R.J.; O'Neill, E.G.

1984-12-01

Consideration of the interrelationships between carbon, water, and nutrient pathways in soil-plant systems has led to the hypothesis that stimulation of root and rhizosphere processes by elevated levels of CO/sub 2/ will increase nutrient availability and lead to an increase in plant growth. Several experiments were conducted to investigate the effects of CO/sub 2/ concentration on carbon allocation, root exudation, nitrogen utilization, and microbial responses, as well as overall plant growth and nutrient utilization. Increases in the growth of yellow-poplar (Liriodendron tulipifera L.) seedlings in response to elevated CO/sub 2/ were demonstrated even when the plants were under apparent nutrientmore » limitation in a forest soil. The proportion of photosynthetically fixed carbon that was allocated to the roots of yellow-poplar and hazel alder (Alnus serrulata (Ait.) Willd.) seedlings was greater at 700 ppM CO/sub 2/ than at ambient CO/sub 2/. Exudation of carbon from yellow-poplar roots also tended to be higher in elevated CO/sub 2/. Responses of rhizosphere microbial populations to elevated CO/sub 2/ were inconsistent, but there was a trend toward relatively fewer ammonium oxidizers, nitrite oxidizers, and phosphate solubilizers in the rhizosphere population of yellow-poplar seedlings grown in 700 ppM CO/sub 2/ compared to that of seedlings grown in ambient CO/sub 2/. Other observed trends included increased nodulation and nitrogenase activity and decreased nitrate reductase activity in hazel alder seedlings in elevated CO/sub 2/. Net uptake of some essential plant nutrients, aluminum, and other trace metals by Virginia pine (Pinus virginiana Mill.) increased with increasing CO/sub 2/ concentration. There was less leaching of some nutrients from soil-plant systems with Virginia pine and yellow-poplar seedlings but increased leaching of zinc. 123 references, 16 figures, 17 tables.« less

Effect of high-intensity intermittent swimming training on fatty acid oxidation enzyme activity in rat skeletal muscle.

PubMed

Terada, Shin; Tabata, Izumi; Higuchi, Mitsuru

2004-02-01

We previously reported that high-intensity exercise training significantly increased citrate synthase (CS) activity, a marker of oxidative enzyme, in rat skeletal muscle to a level equaling that attained after low-intensity prolonged exercise training (Terada et al., J Appl Physiol 90: 2019-2024, 2001). Since mitochondrial oxidative enzymes and fatty acid oxidation (FAO) enzymes are often increased simultaneously, we assessed the effect of high-intensity intermittent swimming training on FAO enzyme activity in rat skeletal muscle. Male Sprague-Dawley rats (3 to 4 weeks old) were assigned to a 10-day period of high-intensity intermittent exercise training (HIT), low-intensity prolonged exercise training (LIT), or sedentary control conditions. In the HIT group, the rats repeated fourteen 20 s swimming sessions with a weight equivalent to 14-16% of their body weight. Between the exercise sessions, a 10 s pause was allowed. Rats in the LIT group swam 6 h/day in two 3 h sessions separated by 45 min of rest. CS activity in the triceps muscle of rats in the HIT and LIT groups was significantly higher than that in the control rats by 36 and 39%, respectively. Furthermore, 3-beta hydroxyacyl-CoA dehydrogenase (HAD) activity, an important enzyme in the FAO pathway in skeletal muscle, was higher in the two training groups than in the control rats (HIT: 100%, LIT: 88%). No significant difference in HAD activity was observed between the two training groups. In conclusion, the present investigation demonstrated that high-intensity intermittent swimming training elevated FAO enzyme activity in rat skeletal muscle to a level similar to that attained after 6 h of low-intensity prolonged swimming exercise training.

Heterogeneous water oxidation: surface activity versus amorphization activation in cobalt phosphate catalysts.

PubMed

González-Flores, Diego; Sánchez, Irene; Zaharieva, Ivelina; Klingan, Katharina; Heidkamp, Jonathan; Chernev, Petko; Menezes, Prashanth W; Driess, Matthias; Dau, Holger; Montero, Mavis L

2015-02-16

Is water oxidation catalyzed at the surface or within the bulk volume of solid oxide materials? This question is addressed for cobalt phosphate catalysts deposited on inert electrodes, namely crystallites of pakhomovskyite (Co3(PO4)2⋅8 H2O, Pak) and phosphate-containing Co oxide (CoCat). X-ray spectroscopy reveals that oxidizing potentials transform the crystalline Pak slowly (5-8 h) but completely into the amorphous CoCat. Electrochemical analysis supports high-TOF surface activity in Pak, whereas its amorphization results in dominating volume activity of the thereby formed CoCat material. In the directly electrodeposited CoCat, volume catalysis prevails, but not at very low levels of the amorphous material, implying high-TOF catalysis at surface sites. A complete picture of heterogeneous water oxidation requires insight in catalysis at the electrolyte-exposed "outer surface", within a hydrated, amorphous volume phase, and modes and kinetics of restructuring upon operation. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Electrocardiograhic findings resulting in inappropriate cardiac catheterization laboratory activation for ST-segment elevation myocardial infarction

PubMed Central

Shamim, Shariq; McCrary, Justin; Wayne, Lori; Gratton, Matthew

2014-01-01

Background Prompt reperfusion has been shown to improve outcomes in patients with acute ST-segment elevation myocardial infarction (STEMI) with a goal of culprit vessel patency in <90 minutes. This requires a coordinated approach between the emergency medical services (EMS), emergency department (ED) and interventional cardiology. The urgency of this process can contribute to inappropriate cardiac catheterization laboratory (CCL) activations. Objectives One of the major determinants of inappropriate activations has been misinterpretation of the electrocardiogram (ECG) in the patient with acute chest pain. Methods We report the ECG findings for all CCL activations over an 18-month period after the inception of a STEMI program at our institution. Results There were a total of 139 activations with 77 having a STEMI diagnosis confirmed and 62 activations where there was no STEMI. The inappropriate activations resulted from a combination of atypical symptoms and misinterpretation of the ECG (45% due to anterior ST-segment elevation) on patient presentation. The electrocardiographic abnormalities were particularly problematic in African-Americans with left ventricular hypertrophy. Conclusions In this single-center, prospective observational study, nearly half of the inappropriate STEMI activations were due to the misinterpretation of anterior ST-segment elevation and this finding was commonly seen in African-Americans with left ventricular hypertrophy. PMID:25009790

Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis.

PubMed

Shimada, Kenichi; Crother, Timothy R; Karlin, Justin; Dagvadorj, Jargalsaikhan; Chiba, Norika; Chen, Shuang; Ramanujan, V Krishnan; Wolf, Andrea J; Vergnes, Laurent; Ojcius, David M; Rentsendorj, Altan; Vargas, Mario; Guerrero, Candace; Wang, Yinsheng; Fitzgerald, Katherine A; Underhill, David M; Town, Terrence; Arditi, Moshe

2012-03-23

We report that in the presence of signal 1 (NF-κB), the NLRP3 inflammasome was activated by mitochondrial apoptotic signaling that licensed production of interleukin-1β (IL-1β). NLRP3 secondary signal activators such as ATP induced mitochondrial dysfunction and apoptosis, resulting in release of oxidized mitochondrial DNA (mtDNA) into the cytosol, where it bound to and activated the NLRP3 inflammasome. The antiapoptotic protein Bcl-2 inversely regulated mitochondrial dysfunction and NLRP3 inflammasome activation. Mitochondrial DNA directly induced NLRP3 inflammasome activation, because macrophages lacking mtDNA had severely attenuated IL-1β production, yet still underwent apoptosis. Both binding of oxidized mtDNA to the NLRP3 inflammasome and IL-1β secretion could be competitively inhibited by the oxidized nucleoside 8-OH-dG. Thus, our data reveal that oxidized mtDNA released during programmed cell death causes activation of the NLRP3 inflammasome. These results provide a missing link between apoptosis and inflammasome activation, via binding of cytosolic oxidized mtDNA to the NLRP3 inflammasome. Copyright © 2012 Elsevier Inc. All rights reserved.

A potential biomarker for fatigue: Oxidative stress and anti-oxidative activity.

PubMed

Fukuda, Sanae; Nojima, Junzo; Motoki, Yukari; Yamaguti, Kouzi; Nakatomi, Yasuhito; Okawa, Naoko; Fujiwara, Kazumi; Watanabe, Yasuyoshi; Kuratsune, Hirohiko

2016-07-01

We sought to determine whether oxidative stress and anti-oxidative activity could act as biomarkers that discriminate patients with chronic fatigue syndrome (CFS) from healthy volunteers at acute and sub-acute fatigue and resting conditions. We calculated the oxidative stress index (OSI) from reactive oxygen metabolites-derived compounds (d-ROMs) and the biological antioxidant potential (BAP). We determined changes in d-ROMs, BAP, and OSI in acute and sub-acute fatigue in two healthy groups, and compared their values at rest between patients with CFS (diagnosed by Fukuda 1994 criteria) and another group of healthy controls. Following acute fatigue in healthy controls, d-ROMs and OSI increased, and BAP decreased. Although d-ROMs and OSI were significantly higher after sub-acute fatigue, BAP did not decrease. Resting condition yielded higher d-ROMs, higher OSI, and lower BAP in patients with CFS than in healthy volunteers, but lower d-ROMs and OSI when compared with sub-acute controls. BAP values did not significantly differ between patients with CFS and controls in the sub-acute condition. However, values were significantly higher than in the resting condition for controls. Thus, measured of oxidative stress (d-ROMS) and anti-oxidative activity (BAP) might be useful for discriminating acute, sub-acute, and resting fatigue in healthy people from patients with CFS, or for evaluating fatigue levels in healthy people. Copyright © 2016 Elsevier B.V. All rights reserved.

Lipid homeostasis and inflammatory activation are disturbed in classically activated macrophages with peroxisomal β-oxidation deficiency.

PubMed

Geric, Ivana; Tyurina, Yulia Y; Krysko, Olga; Krysko, Dmitri V; De Schryver, Evelyn; Kagan, Valerian E; Van Veldhoven, Paul P; Baes, Myriam; Verheijden, Simon

2018-03-01

Macrophage activation is characterized by pronounced metabolic adaptation. Classically activated macrophages show decreased rates of mitochondrial fatty acid oxidation and oxidative phosphorylation and acquire a glycolytic state together with their pro-inflammatory phenotype. In contrast, alternatively activated macrophages require oxidative phosphorylation and mitochondrial fatty acid oxidation for their anti-inflammatory function. Although it is evident that mitochondrial metabolism is regulated during macrophage polarization and essential for macrophage function, little is known on the regulation and role of peroxisomal β-oxidation during macrophage activation. In this study, we show that peroxisomal β-oxidation is strongly decreased in classically activated bone-marrow-derived macrophages (BMDM) and mildly induced in alternatively activated BMDM. To examine the role of peroxisomal β-oxidation in macrophages, we used Mfp2 -/- BMDM lacking the key enzyme of this pathway. Impairment of peroxisomal β-oxidation in Mfp2 -/- BMDM did not cause lipid accumulation but rather an altered distribution of lipid species with very-long-chain fatty acids accumulating in the triglyceride and phospholipid fraction. These lipid alterations in Mfp2 -/- macrophages led to decreased inflammatory activation of Mfp2 -/- BMDM and peritoneal macrophages evidenced by impaired production of several inflammatory cytokines and chemokines, but did not affect anti-inflammatory polarization. The disturbed inflammatory responses of Mfp2 -/- macrophages did not affect immune cell infiltration, as mice with selective elimination of MFP2 from myeloid cells showed normal monocyte and neutrophil influx upon challenge with zymosan. Together, these data demonstrate that peroxisomal β-oxidation is involved in fine-tuning the phenotype of macrophages, probably by influencing the dynamic lipid profile during macrophage polarization. © 2017 John Wiley & Sons Ltd.

Cerebral cortical neurons with activity linked to central neurogenic spontaneous and evoked elevations in cerebral blood flow

NASA Technical Reports Server (NTRS)

Golanov, E. V.; Reis, D. J.

1996-01-01

We recorded neurons in rat cerebral cortex with activity relating to the neurogenic elevations in regional cerebral blood flow (rCBF) coupled to stereotyped bursts of EEG activity, burst-cerebrovascular wave complexes, appearing spontaneously or evoked by electrical stimulation of rostral ventrolateral medulla (RVL) or fastigial nucleus (FN). Of 333 spontaneously active neurons only 15 (5%), in layers 5-6, consistently (P < 0.05, chi-square) increased their activity during the earliest potential of the complex, approximately 1.3 s before the rise of rCBF, and during the minutes-long elevation of rCBF elicited by 10 s of stimulation of RVL or FN. The results indicate the presence of a small population of neurons in deep cortical laminae whose activity correlates with neurogenic elevations of rCBF. These neurons may function to transduce afferent neuronal signals into vasodilation.

Uniform 2 nm gold nanoparticles supported on iron oxides as active catalysts for CO oxidation reaction: structure-activity relationship

NASA Astrophysics Data System (ADS)

Guo, Yu; Gu, Dong; Jin, Zhao; Du, Pei-Pei; Si, Rui; Tao, Jing; Xu, Wen-Qian; Huang, Yu-Ying; Senanayake, Sanjaya; Song, Qi-Sheng; Jia, Chun-Jiang; Schüth, Ferdi

2015-03-01

Uniform Au nanoparticles (~2 nm) with narrow size-distribution (standard deviation: 0.5-0.6 nm) supported on both hydroxylated (Fe_OH) and dehydrated iron oxide (Fe_O) have been prepared by either deposition-precipitation (DP) or colloidal-deposition (CD) methods. Different structural and textural characterizations were applied to the dried, calcined and used gold-iron oxide samples. Transmission electron microscopy (TEM) and high-resolution TEM (HRTEM) showed high homogeneity in the supported Au nanoparticles. The ex situ and in situ X-ray absorption fine structure (XAFS) characterization monitored the electronic and short-range local structure of active gold species. The synchrotron-based in situ X-ray diffraction (XRD), together with the corresponding temperature-programmed reduction by hydrogen (H2-TPR), indicated a structural evolution of the iron-oxide supports, correlating to their reducibility. An inverse order of catalytic activity between DP (Au/Fe_OH < Au/Fe_O) and CD (Au/Fe_OH > Au/Fe_O) was observed. Effective gold-support interaction results in a high activity for gold nanoparticles, locally generated by the sintering of dispersed Au atoms on the oxide support in the DP synthesis, while a hydroxylated surface favors the reactivity of externally introduced Au nanoparticles on Fe_OH support for the CD approach. This work reveals why differences in the synthetic protocol translate to differences in the catalytic performance of Au/FeOx catalysts with very similar structural characteristics in CO oxidation.

Uniform 2 nm gold nanoparticles supported on iron oxides as active catalysts for CO oxidation reaction: Structure-activity relationship

DOE PAGES

Guo, Yu; Senanayake, Sanjaya; Gu, Dong; ...

2015-01-12

Uniform Au nanoparticles (~2 nm) with narrow size-distribution (standard deviation: 0.5–0.6 nm) supported on both hydroxylated (Fe_OH) and dehydrated iron oxide (Fe_O) have been prepared by either deposition-precipitation (DP) or colloidal-deposition (CD) methods. Different structural and textural characterizations were applied to the dried, calcined and used gold-iron oxide samples. The transmission electron microscopy (TEM) and high-resolution TEM (HRTEM) described the high homogeneity in the supported Au nanoparticles. The ex-situ and in-situ X-ray absorption fine structure (XAFS) characterization monitored the electronic and short-range local structure of active gold species. The synchrotron-based in-situ X-ray diffraction (XRD), together with the corresponding temperature-programmed reductionmore » by hydrogen (H₂-TPR), indicated a structural evolution of the iron-oxide supports, correlating to their reducibility. An inverse order of catalytic activity between DP (Au/Fe_OH < Au/Fe_O) and CD (Au/Fe_OH > Au/Fe_O) was observed. Effective gold-support interaction results in a high activity for gold nanoparticles, locally generated by the sintering of dispersed Au atoms on the oxide support in the DP synthesis, while a hydroxylated surface favors the reactivity of externally introduced Au nanoparticles on Fe_OH support for the CD approach. This work reveals why differences in the synthetic protocol translate to differences in the catalytic performance of Au/FeO x catalysts with very similar structural characteristics in CO oxidation.« less

Oxidative stress in deep scattering layers: Heat shock response and antioxidant enzymes activities of myctophid fishes thriving in oxygen minimum zones

NASA Astrophysics Data System (ADS)

Lopes, Ana Rita; Trübenbach, Katja; Teixeira, Tatiana; Lopes, Vanessa M.; Pires, Vanessa; Baptista, Miguel; Repolho, Tiago; Calado, Ricardo; Diniz, Mário; Rosa, Rui

2013-12-01

Diel vertical migrators, such as myctophid fishes, are known to encounter oxygen minimum zones (OMZ) during daytime in the Eastern Pacific Ocean and, therefore, have to cope with temperature and oxidative stress that arise while ascending to warmer, normoxic surface waters at night-time. The aim of this study was to investigate the antioxidant defense strategies and heat shock response (HSR) in two myctophid species, namely Triphoturus mexicanus and Benthosema panamense, at shallow and warm surface waters (21 kPa, 20-25 °C) and at hypoxic, cold (≤1 kPa, 10 °C) mesopelagic depths. More specifically, we quantified (i) heat shock protein concentrations (HSP70/HSC70) (ii) antioxidant enzyme activities [including superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST)], and (iii) lipid peroxidation [malondialdehyde (MDA) levels]. HSP70/HSC70 levels increased in both myctophid species at warmer, well-oxygenated surface waters probably to prevent cellular damage (oxidative stress) due to increased oxygen demand under elevated temperatures and reactive oxygen species (ROS) formation. On the other hand, CAT and GST activities were augmented under hypoxic conditions, probably as preparatory response to a burst of oxyradicals during the reoxygenation phase (while ascending). SOD activity decreased under hypoxia in B. panamense, but was kept unchanged in T. mexicanus. MDA levels in B. panamense did not change between the surface and deep-sea conditions, whereas T. mexicanus showed elevated MDA and HSP70/HSC70 concentrations at warmer surface waters. This indicated that T. mexicanus seems to be not so well tuned to temperature and oxidative stress associated to diel vertical migrations. The understanding of such physiological strategies that are linked to oxygen deprivation and reoxygenation phases may provide valuable information about how different species might respond to the impacts of environmental stressors (e.g. expanding mesopelagic hypoxia

Inhibition of neutral sphingomyelinase decreases elevated levels of inducible nitric oxide synthase and apoptotic cell death in ocular hypertensive rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

Aslan, Mutay, E-mail: mutayaslan@akdeniz.edu.tr; Basaranlar, Goksun; Unal, Mustafa

Endoplasmic reticulum (ER) stress and excessive nitric oxide production via induction of inducible nitric oxide synthase (NOS2) have been implicated in the pathogenesis of neuronal retinal cell death in ocular hypertension. Neutral sphingomyelinase (N-SMase)/ceramide pathway can regulate NOS2 expression, hence this study determined the role of selective neutral sphingomyelinase (N-SMase) inhibition on retinal NOS2 levels, ER stress, apoptosis and visual evoked potentials (VEPs) in a rat model of elevated intraocular pressure (EIOP). NOS2 expression and retinal protein nitration were significantly greater in EIOP and significantly decreased with N-SMase inhibition. A significant increase was observed in retinal ER stress markers pPERK,more » CHOP and GRP78 in EIOP, which were not significantly altered by N-SMase inhibition. Retinal TUNEL staining showed increased apoptosis in all EIOP groups; however N-SMase inhibition significantly decreased the percent of apoptotic cells in EIOP. Caspase-3, -8 and -9 activities were significantly increased in EIOP and returned to baseline levels following N-SMase inhibition. Latencies of all VEP components were significantly prolonged in EIOP and shortened following N-SMase inhibition. Data confirm the role of nitrative injury in EIOP and highlight the protective effect of N-SMase inhibition in EIOP via down-regulation of NOS2 levels and nitrative stress. - Highlights: • Inhibition of N-SMase decreases NOS2 levels in ocular hypertension. • Inhibition of N-SMase decreases protein nitration in ocular hypertension. • Inhibition of N-SMase decreases caspase activation in ocular hypertension. • Inhibition of N-SMase decreases apoptosis in ocular hypertension.« less

The inhibition of inducible nitric oxide synthase and oxidative stress by agmatine attenuates vascular dysfunction in rat acute endotoxemic model.

PubMed

El-Awady, Mohammed S; Nader, Manar A; Sharawy, Maha H

2017-10-01

Vascular dysfunction leading to hypotension is a major complication in patients with septic shock. Inducible nitric oxide synthase (iNOS) together with oxidative stress play an important role in development of vascular dysfunction in sepsis. Searching for an endogenous, safe and yet effective remedy was the chief goal for this study. The current study investigated the effect of agmatine (AGM), an endogenous metabolite of l-arginine, on sepsis-induced vascular dysfunction induced by lipopolysaccharides (LPS) in rats. AGM pretreatment (10mg/kg, i.v.) 1h before LPS (5mg/kg, i.v.) prevented the LPS-induced mortality and elevations in serum creatine kinase-MB isoenzyme (CK-MB) activity, lactate dehydrogenase (LDH) activity, C-reactive protein (CRP) level and total nitrite/nitrate (NOx) level after 24h from LPS injection. The elevation in aortic lipid peroxidation illustrated by increased malondialdehyde (MDA) content and the decrease in aortic glutathione (GSH) and superoxide dismutase (SOD) were also ameliorated by AGM. Additionally, AGM prevented LPS-induced elevation in mRNA expression of iNOS, while endothelial NOS (eNOS) mRNA was not affected. Furthermore AGM prevented the impaired aortic contraction to KCl and phenylephrine (PE) and endothelium-dependent relaxation to acetylcholine (ACh) without affecting endothelium-independent relaxation to sodium nitroprusside (SNP). AGM may represent a potential endogenous therapeutic candidate for sepsis-induced vascular dysfunction through its inhibiting effect on iNOS expression and oxidative stress. Copyright © 2017 Elsevier B.V. All rights reserved.

Constitutively elevated salicylic acid levels alter photosynthesis and oxidative state but not growth in transgenic populus.

PubMed

Xue, Liang-Jiao; Guo, Wenbing; Yuan, Yinan; Anino, Edward O; Nyamdari, Batbayar; Wilson, Mark C; Frost, Christopher J; Chen, Han-Yi; Babst, Benjamin A; Harding, Scott A; Tsai, Chung-Jui

2013-07-01

Salicylic acid (SA) has long been implicated in plant responses to oxidative stress. SA overproduction in Arabidopsis thaliana leads to dwarfism, making in planta assessment of SA effects difficult in this model system. We report that transgenic Populus tremula × alba expressing a bacterial SA synthase hyperaccumulated SA and SA conjugates without negative growth consequences. In the absence of stress, endogenously elevated SA elicited widespread metabolic and transcriptional changes that resembled those of wild-type plants exposed to oxidative stress-promoting heat treatments. Potential signaling and oxidative stress markers azelaic and gluconic acids as well as antioxidant chlorogenic acids were strongly coregulated with SA, while soluble sugars and other phenylpropanoids were inversely correlated. Photosynthetic responses to heat were attenuated in SA-overproducing plants. Network analysis identified potential drivers of SA-mediated transcriptome rewiring, including receptor-like kinases and WRKY transcription factors. Orthologs of Arabidopsis SA signaling components NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 and thioredoxins were not represented. However, all members of the expanded Populus nucleoredoxin-1 family exhibited increased expression and increased network connectivity in SA-overproducing Populus, suggesting a previously undescribed role in SA-mediated redox regulation. The SA response in Populus involved a reprogramming of carbon uptake and partitioning during stress that is compatible with constitutive chemical defense and sustained growth, contrasting with the SA response in Arabidopsis, which is transient and compromises growth if sustained.

Reduction of nitric oxide and DNA/RNA oxidation products are associated with active disease in systemic lupus erythematosus patients.

PubMed

Iriyoda, T M V; Stadtlober, N; Lozovoy, M A B; Delongui, F; Costa, N T; Reiche, E M V; Dichi, I; Simão, A N C

2017-09-01

The aims of the present study were to evaluate biomarkers of oxidative and nitrosative stress in systemic lupus erythematosus (SLE) patients, in particular products of DNA/RNA oxidative damage and their correlation with disease activity. This study included 188 controls and 203 patients; 153 with inactive SLE (SLEDAI < 6) and 50 with active SLE (SLEDAI ≥ 6) without renal impairment. Oxidative stress was assessed by tert-butyl hydroperoxide-initiated by chemiluminescence, advanced oxidation protein products (AOPP), total radical-trapping antioxidant parameter (TRAP), nitric oxide metabolites (NOx), and DNA/RNA oxidation products. Patients with SLE showed increased oxidative stress, as demonstrated by the augmentation of lipid hydroperoxides ( p < 0.0001) and AOPP ( p < 0.001) and reduced total antioxidant capacity ( p < 0.0001), without differences between patients with active disease and in remission. NOx levels and DNA/RNA oxidation products were inversely and independently associated with disease activity ( p < 0.0001 and p = 0.021, respectively), regardless of BMI and prednisone use. The linear regression analysis showed that about 5% of the SLEDAI score can be explained by the levels of DNA/RNA oxidation products ( r 2 :0.051; p = 0.002) and about 9% of this score by the levels of NOx ( r 2 :0.091; p < 0.0001). This study provides evidence for an inverse association between serum NOx levels and DNA/RNA oxidation products and SLE disease activity, suggesting that oxidative/nitrosative stress markers may be useful in evaluating SLE disease activity and progression of the disease.

High concentration of branched-chain amino acids promotes oxidative stress, inflammation and migration of human peripheral blood mononuclear cells via mTORC1 activation.

PubMed

Zhenyukh, Olha; Civantos, Esther; Ruiz-Ortega, Marta; Sánchez, Maria Soledad; Vázquez, Clotilde; Peiró, Concepción; Egido, Jesús; Mas, Sebastián

2017-03-01

Leucine, isoleucine and valine are essential aminoacids termed branched-chain amino acids (BCAA) due to its aliphatic side-chain. In several pathological and physiological conditions increased BCAA plasma concentrations have been described. Elevated BCAA levels predict insulin resistance development. Moreover, BCAA levels higher than 2mmol/L are neurotoxic by inducing microglial activation in maple syrup urine disease. However, there are no studies about the direct effects of BCAA in circulating cells. We have explored whether BCAA could promote oxidative stress and pro-inflammatory status in peripheral blood mononuclear cells (PBMCs) obtained from healthy donors. In cultured PBMCs, 10mmol/L BCAA increased the production of reactive oxygen species (ROS) via both NADPH oxidase and the mitochondria, and activated Akt-mTOR signalling. By using several inhibitors and activators of these molecular pathways we have described that mTOR activation by BCAA is linked to ROS production and mitochondrial dysfunction. BCAA stimulated the activation of the redox-sensitive transcription factor NF-κB, which resulted in the release of pro-inflammatory molecules, such as interleukin-6, tumor necrosis factor-α, intracellular adhesion molecule-1 or CD40L, and the migration of PBMCs. In conclusion, elevated BCAA blood levels can promote the activation of circulating PBMCs, by a mechanism that involving ROS production and NF-κB pathway activation. These data suggest that high concentrations of BCAA could exert deleterious effects on circulating blood cells and therefore contribute to the pro-inflammatory and oxidative status observed in several pathophysiological conditions. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

Methanosarcinaceae and Acetate-Oxidizing Pathways Dominate in High-Rate Thermophilic Anaerobic Digestion of Waste-Activated Sludge

PubMed Central

Ho, Dang P.; Jensen, Paul D.

2013-01-01

This study investigated the process of high-rate, high-temperature methanogenesis to enable very-high-volume loading during anaerobic digestion of waste-activated sludge. Reducing the hydraulic retention time (HRT) from 15 to 20 days in mesophilic digestion down to 3 days was achievable at a thermophilic temperature (55°C) with stable digester performance and methanogenic activity. A volatile solids (VS) destruction efficiency of 33 to 35% was achieved on waste-activated sludge, comparable to that obtained via mesophilic processes with low organic acid levels (<200 mg/liter chemical oxygen demand [COD]). Methane yield (VS basis) was 150 to 180 liters of CH4/kg of VSadded. According to 16S rRNA pyrotag sequencing and fluorescence in situ hybridization (FISH), the methanogenic community was dominated by members of the Methanosarcinaceae, which have a high level of metabolic capability, including acetoclastic and hydrogenotrophic methanogenesis. Loss of function at an HRT of 2 days was accompanied by a loss of the methanogens, according to pyrotag sequencing. The two acetate conversion pathways, namely, acetoclastic methanogenesis and syntrophic acetate oxidation, were quantified by stable carbon isotope ratio mass spectrometry. The results showed that the majority of methane was generated by nonacetoclastic pathways, both in the reactors and in off-line batch tests, confirming that syntrophic acetate oxidation is a key pathway at elevated temperatures. The proportion of methane due to acetate cleavage increased later in the batch, and it is likely that stable oxidation in the continuous reactor was maintained by application of the consistently low retention time. PMID:23956388

LDL oxidation by platelets propagates platelet activation via an oxidative stress-mediated mechanism.

PubMed

Carnevale, Roberto; Bartimoccia, Simona; Nocella, Cristina; Di Santo, Serena; Loffredo, Lorenzo; Illuminati, Giulio; Lombardi, Elisabetta; Boz, Valentina; Del Ben, Maria; De Marco, Luigi; Pignatelli, Pasquale; Violi, Francesco

2014-11-01

Platelets generate oxidized LDL (ox-LDL) via NOX2-derived oxidative stress. We investigated if once generated by activated platelets ox-LDL can propagate platelet activation. Experiments were performed in platelets from healthy subjects (HS), hyper-cholesterolemic patients and patients with NOX2 hereditary deficiency. Agonist-stimulated platelets from HS added with LDL were associated with a dose-dependent increase of reactive oxidant species and ox-LDL. Agonist-stimulated platelets from HS added with a fixed dose of LDL (57.14 μmol/L) or added with homogenized human atherosclerotic plaque showed enhanced ox-LDL formation (approximately +50% and +30% respectively), which was lowered by a NOX2 inhibitor (approximately -35% and -25% respectively). Compared to HS, ox-LDL production was more pronounced in agonist-stimulated platelet rich plasma (PRP) from hyper-cholesterolemic patients but was almost absent in PRP from NOX2-deficient patients. Platelet aggregation and 8-iso-PGF2α-ΙΙΙ formation increased in LDL-treated washed platelets (+42% and +53% respectively) and PRP (+31% and +53% respectively). Also, LDL enhanced platelet-dependent thrombosis at arterial shear rate (+33%) but did not affect platelet activation in NOX2-deficient patients. Platelet activation by LDL was significantly inhibited by CD36 or LOX1 blocking peptides, two ox-LDL receptor antagonists, or by a NOX2 inhibitor. LDL-added platelets showed increased p38MAPK (+59%) and PKC (+51%) phosphorylation, p47(phox) translocation to platelet membrane (+34%) and NOX2 activation (+30%), which were inhibited by ox-LDL receptor antagonists. Platelets oxidize LDL, which in turn amplify platelet activation via specific ox-LDL receptors; both effects are mediated by NOX2 activation. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Effect of diabetes and elevated glucose on nitric oxide-mediated neurotransmission in rat anococcygeus muscle.

PubMed Central

Way, K. J.; Reid, J. J.

1995-01-01

1. Nitric oxide (NO)-mediated neurotransmission is impaired in anococcygeus muscle from 8-week streptozotocin-induced diabetic rats. This study investigated the effects of insulin treatment, and the duration of diabetes on this impairment. In addition, the effect of in vitro exposure to elevated glucose has been investigated on NO-mediated relaxations, in muscles from untreated rats. 2. Relaxant responses to field stimulation (0.5-5 Hz, 10s train), sodium nitroprusside (SNP; 5 and 10 nM) and NO (1 and 3 microM) were significantly impaired in anococcygeus muscles from 8-week diabetic rats, compared to responses from control rats. Insulin treatment (5 u Lente day-1, s.c.) of diabetic rats prevented the development of this impairment. 3. Consistent with findings in 8-week diabetic rats, relaxation induced by field stimulation, SNP and NO were attenuated in tissues from 2-week and 4-week diabetic rats compared to corresponding control responses, whereas relaxations to papaverine (3 and 10 microM) were not reduced. In contrast, diabetes of 3-days duration did not affect relaxations to field stimulation, SNP or NO. 4. Incubation of anococcygeus muscles from untreated rats in medium containing elevated glucose (44.1 mM) for 6 h, significantly impaired relaxations to field stimulation compared to responses obtained after normal glucose (11.1 mM) incubation. Relaxations to SNP and to NO were not affected by 6 h exposure to elevated glucose. Similarly, incubation in hyperosmolar solutions containing mannose or sucrose for 6 h, impaired relaxations to field stimulation, but not to SNP or NO.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7582450

Elevated temperature altered photosynthetic products in wheat seedlings and organic compounds and biological activity in rhizopshere soil under cadmium stress.

PubMed

Jia, Xia; Zhao, YongHua; Wang, WenKe; He, Yunhua

2015-09-23

The objective of this study was to investigate the effects of slightly elevated atmospheric temperature in the spring on photosynthetic products in wheat seedlings and on organic compounds and biological activity in rhizosphere soil under cadmium (Cd) stress. Elevated temperature was associated with increased soluble sugars, reducing sugars, starch, and total sugars, and with decreased amino acids in wheat seedlings under Cd stress. Elevated temperature improved total soluble sugars, free amino acids, soluble phenolic acids, and organic acids in rhizosphere soil under Cd stress. The activity of amylase, phenol oxidase, invertase, β-glucosidase, and l-asparaginase in rhizosphere soil was significantly improved by elevated temperature under Cd stress; while cellulase, neutral phosphatase, and urease activity significantly decreased. Elevated temperature significantly improved bacteria, fungi, actinomycetes, and total microorganisms abundance and fluorescein diacetate activity under Cd stress. In conclusion, slightly elevated atmospheric temperature in the spring improved the carbohydrate levels in wheat seedlings and organic compounds and biological activity in rhizosphere soil under Cd stress in the short term. In addition, elevated atmospheric temperature in the spring stimulated available Cd by affecting pH, DOC, phenolic acids, and organic acids in rhizosphere soil, which resulted in the improvement of the Cd uptake by wheat seedlings.

Elevated temperature altered photosynthetic products in wheat seedlings and organic compounds and biological activity in rhizopshere soil under cadmium stress

PubMed Central

Jia, Xia; Zhao, YongHua; Wang, WenKe; He, Yunhua

2015-01-01

The objective of this study was to investigate the effects of slightly elevated atmospheric temperature in the spring on photosynthetic products in wheat seedlings and on organic compounds and biological activity in rhizosphere soil under cadmium (Cd) stress. Elevated temperature was associated with increased soluble sugars, reducing sugars, starch, and total sugars, and with decreased amino acids in wheat seedlings under Cd stress. Elevated temperature improved total soluble sugars, free amino acids, soluble phenolic acids, and organic acids in rhizosphere soil under Cd stress. The activity of amylase, phenol oxidase, invertase, β-glucosidase, and l-asparaginase in rhizosphere soil was significantly improved by elevated temperature under Cd stress; while cellulase, neutral phosphatase, and urease activity significantly decreased. Elevated temperature significantly improved bacteria, fungi, actinomycetes, and total microorganisms abundance and fluorescein diacetate activity under Cd stress. In conclusion, slightly elevated atmospheric temperature in the spring improved the carbohydrate levels in wheat seedlings and organic compounds and biological activity in rhizosphere soil under Cd stress in the short term. In addition, elevated atmospheric temperature in the spring stimulated available Cd by affecting pH, DOC, phenolic acids, and organic acids in rhizosphere soil, which resulted in the improvement of the Cd uptake by wheat seedlings. PMID:26395070

Elevated temperature altered photosynthetic products in wheat seedlings and organic compounds and biological activity in rhizopshere soil under cadmium stress

NASA Astrophysics Data System (ADS)

Jia, Xia; Zhao, Yonghua; Wang, Wenke; He, Yunhua

2015-09-01

The objective of this study was to investigate the effects of slightly elevated atmospheric temperature in the spring on photosynthetic products in wheat seedlings and on organic compounds and biological activity in rhizosphere soil under cadmium (Cd) stress. Elevated temperature was associated with increased soluble sugars, reducing sugars, starch, and total sugars, and with decreased amino acids in wheat seedlings under Cd stress. Elevated temperature improved total soluble sugars, free amino acids, soluble phenolic acids, and organic acids in rhizosphere soil under Cd stress. The activity of amylase, phenol oxidase, invertase, β-glucosidase, and L-asparaginase in rhizosphere soil was significantly improved by elevated temperature under Cd stress; while cellulase, neutral phosphatase, and urease activity significantly decreased. Elevated temperature significantly improved bacteria, fungi, actinomycetes, and total microorganisms abundance and fluorescein diacetate activity under Cd stress. In conclusion, slightly elevated atmospheric temperature in the spring improved the carbohydrate levels in wheat seedlings and organic compounds and biological activity in rhizosphere soil under Cd stress in the short term. In addition, elevated atmospheric temperature in the spring stimulated available Cd by affecting pH, DOC, phenolic acids, and organic acids in rhizosphere soil, which resulted in the improvement of the Cd uptake by wheat seedlings.

Anti-acetylcholinesterase and Antioxidant Activities of Inhaled Juniper Oil on Amyloid Beta (1-42)-Induced Oxidative Stress in the Rat Hippocampus.

PubMed

Cioanca, Oana; Hancianu, Monica; Mihasan, Marius; Hritcu, Lucian

2015-05-01

Juniper volatile oil is extracted from Juniperus communis L., of the Cupressaceae family, also known as common juniper. Also, in aromatherapy the juniper volatile oil is used against anxiety, nervous tension and stress-related conditions. In the present study, we identified the effects of the juniper volatile oil on amyloid beta (1-42)-induced oxidative stress in the rat hippocampus. Rats received a single intracerebroventricular injection of amyloid beta (1-42) (400 pmol/rat) and then were exposed to juniper volatile oil (200 μl, either 1 or 3 %) for controlled 60 min period, daily, for 21 continuous days. Also, the antioxidant activity in the hippocampus was assessed using superoxide dismutase, glutathione peroxidase and catalase specific activities, the total content of the reduced glutathione, protein carbonyl and malondialdehyde levels. Additionally, the acetylcholinesterase activity in the hippocampus was assessed. The amyloid beta (1-42)-treated rats exhibited the following: increase of the acetylcholinesterase, superoxide dismutase and catalase specific activities, decrease of glutathione peroxidase specific activity and the total content of the reduced glutathione along with an elevation of malondialdehyde and protein carbonyl levels. Inhalation of the juniper volatile oil significantly decreases the acetylcholinesterase activity and exhibited antioxidant potential. These findings suggest that the juniper volatile oil may be a potential candidate for the development of therapeutic agents to manage oxidative stress associated with Alzheimer's disease through decreasing the activity of acetylcholinesterase and anti-oxidative mechanism.

Elevated Mitochondrial Reactive Oxygen Species and Cellular Redox Imbalance in Human NADPH-Oxidase-Deficient Phagocytes

PubMed Central

Sundqvist, Martina; Christenson, Karin; Björnsdottir, Halla; Osla, Veronica; Karlsson, Anna; Dahlgren, Claes; Speert, David P.; Fasth, Anders; Brown, Kelly L.; Bylund, Johan

2017-01-01

Chronic granulomatous disease (CGD) is caused by mutations in genes that encode the NADPH-oxidase and result in a failure of phagocytic cells to produce reactive oxygen species (ROS) via this enzyme system. Patients with CGD are highly susceptible to infections and often suffer from inflammatory disorders; the latter occurs in the absence of infection and correlates with the spontaneous production of inflammatory cytokines. This clinical feature suggests that NADPH-oxidase-derived ROS are not required for, or may even suppress, inflammatory processes. Experimental evidence, however, implies that ROS are in fact required for inflammatory cytokine production. By using a myeloid cell line devoid of a functional NADPH-oxidase and primary CGD cells, we analyzed intracellular oxidants, signs of oxidative stress, and inflammatory cytokine production. Herein, we demonstrate that phagocytes lacking a functional NADPH-oxidase, namely primary CGD phagocytes and a gp91phox-deficient cell line, display elevated levels of ROS derived from mitochondria. Accordingly, these cells, despite lacking the major source of cellular ROS, display clear signs of oxidative stress, including an induced expression of antioxidants and altered oxidation of cell surface thiols. These observed changes in redox state were not due to abnormalities in mitochondrial mass or membrane integrity. Finally, we demonstrate that increased mitochondrial ROS enhanced phosphorylation of ERK1/2, and induced production of IL8, findings that correlate with previous observations of increased MAPK activation and inflammatory cytokine production in CGD cells. Our data show that elevated baseline levels of mitochondria-derived oxidants lead to the counter-intuitive observation that CGD phagocytes are under oxidative stress and have enhanced MAPK signaling, which may contribute to the elevated basal production of inflammatory cytokines and the sterile inflammatory manifestations in CGD. PMID:29375548

Oxidative stress-mediated antibacterial activity of graphene oxide and reduced graphene oxide in Pseudomonas aeruginosa.

PubMed

Gurunathan, Sangiliyandi; Han, Jae Woong; Dayem, Ahmed Abdal; Eppakayala, Vasuki; Kim, Jin-Hoi

2012-01-01

Graphene holds great promise for potential use in next-generation electronic and photonic devices due to its unique high carrier mobility, good optical transparency, large surface area, and biocompatibility. The aim of this study was to investigate the antibacterial effects of graphene oxide (GO) and reduced graphene oxide (rGO) in Pseudomonas aeruginosa. In this work, we used a novel reducing agent, betamercaptoethanol (BME), for synthesis of graphene to avoid the use of toxic materials. To uncover the impacts of GO and rGO on human health, the antibacterial activity of two types of graphene-based material toward a bacterial model P. aeruginosa was studied and compared. The synthesized GO and rGO was characterized by ultraviolet-visible absorption spectroscopy, particle-size analyzer, X-ray diffraction, scanning electron microscopy and Raman spectroscopy. Further, to explain the antimicrobial activity of graphene oxide and reduced graphene oxide, we employed various assays, such as cell growth, cell viability, reactive oxygen species generation, and DNA fragmentation. Ultraviolet-visible spectra of the samples confirmed the transition of GO into graphene. Dynamic light-scattering analyses showed the average size among the two types of graphene materials. X-ray diffraction data validated the structure of graphene sheets, and high-resolution scanning electron microscopy was employed to investigate the morphologies of prepared graphene. Raman spectroscopy data indicated the removal of oxygen-containing functional groups from the surface of GO and the formation of graphene. The exposure of cells to GO and rGO induced the production of superoxide radical anion and loss of cell viability. Results suggest that the antibacterial activities are contributed to by loss of cell viability, induced oxidative stress, and DNA fragmentation. The antibacterial activities of GO and rGO against P. aeruginosa were compared. The loss of P. aeruginosa viability increased in a dose- and

Oxidative stress-mediated antibacterial activity of graphene oxide and reduced graphene oxide in Pseudomonas aeruginosa

PubMed Central

Gurunathan, Sangiliyandi; Han, Jae Woong; Dayem, Ahmed Abdal; Eppakayala, Vasuki; Kim, Jin-Hoi

2012-01-01

Background Graphene holds great promise for potential use in next-generation electronic and photonic devices due to its unique high carrier mobility, good optical transparency, large surface area, and biocompatibility. The aim of this study was to investigate the antibacterial effects of graphene oxide (GO) and reduced graphene oxide (rGO) in Pseudomonas aeruginosa. In this work, we used a novel reducing agent, betamercaptoethanol (BME), for synthesis of graphene to avoid the use of toxic materials. To uncover the impacts of GO and rGO on human health, the antibacterial activity of two types of graphene-based material toward a bacterial model P. aeruginosa was studied and compared. Methods The synthesized GO and rGO was characterized by ultraviolet-visible absorption spectroscopy, particle-size analyzer, X-ray diffraction, scanning electron microscopy and Raman spectroscopy. Further, to explain the antimicrobial activity of graphene oxide and reduced graphene oxide, we employed various assays, such as cell growth, cell viability, reactive oxygen species generation, and DNA fragmentation. Results Ultraviolet-visible spectra of the samples confirmed the transition of GO into graphene. Dynamic light-scattering analyses showed the average size among the two types of graphene materials. X-ray diffraction data validated the structure of graphene sheets, and high-resolution scanning electron microscopy was employed to investigate the morphologies of prepared graphene. Raman spectroscopy data indicated the removal of oxygen-containing functional groups from the surface of GO and the formation of graphene. The exposure of cells to GO and rGO induced the production of superoxide radical anion and loss of cell viability. Results suggest that the antibacterial activities are contributed to by loss of cell viability, induced oxidative stress, and DNA fragmentation. Conclusion The antibacterial activities of GO and rGO against P. aeruginosa were compared. The loss of P

[Atherosclerosis, oxidative stress and physical activity. Review].

PubMed

Calderón, Juan Camilo; Fernández, Ana Zita; María de Jesús, Alina Isabel

2008-09-01

Atherosclerosis and related diseases have emerged as the leading cause of morbidity and mortality in the western world and, therefore, as a problem of public health. Free radicals and reactive oxygen species have been suggested to be part of the pathophysiology of these diseases. It is well known that physical activity plays an important role as a public health measure by reducing the risk of developing atherosclerosis-related cardiovascular events in the general population. It is also known that physical activity increases in some tissues, the reactive oxygen species production. In this review the atherosclerosis-oxidative stress-physical activity relationship is focused on the apparent paradox by which physical activity reduces atherosclerosis and cardiovascular risk in parallel with the activation of an apparently damaging mechanism which is an increased oxidative stress. A hypothesis including the experimental and clinical evidence is presented to explain the aforementioned paradox.

Oxidative Stress and NLRP3-Inflammasome Activity as Significant Drivers of Diabetic Cardiovascular Complications: Therapeutic Implications

PubMed Central

Sharma, Arpeeta; Tate, Mitchel; Mathew, Geetha; Vince, James E.; Ritchie, Rebecca H.; de Haan, Judy B.

2018-01-01

It is now increasingly appreciated that inflammation is not limited to the control of pathogens by the host, but rather that sterile inflammation which occurs in the absence of viral or bacterial pathogens, accompanies numerous disease states, none more so than the complications that arise as a result of hyperglycaemia. Individuals with type 1 or type 2 diabetes mellitus (T1D, T2D) are at increased risk of developing cardiac and vascular complications. Glucose and blood pressure lowering therapies have not stopped the advance of these morbidities that often lead to fatal heart attacks and/or stroke. A unifying mechanism of hyperglycemia-induced cellular damage was initially proposed to link elevated blood glucose levels with oxidative stress and the dysregulation of metabolic pathways. Pre-clinical evidence has, in most cases, supported this notion. However, therapeutic strategies to lessen oxidative stress in clinical trials has not proved efficacious, most likely due to indiscriminate targeting by antioxidants such as vitamins. Recent evidence now suggests that oxidative stress is a major driver of inflammation and vice versa, with the latest findings suggesting not only a key role for inflammatory pathways underpinning metabolic and haemodynamic dysfunction in diabetes, but furthermore that these perturbations are driven by activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. This review will address these latest findings with an aim of highlighting the interconnectivity between oxidative stress, NLRP3 activation and inflammation as it pertains to cardiac and vascular injury sustained by diabetes. Current therapeutic strategies to lessen both oxidative stress and inflammation will be emphasized. This will be placed in the context of improving the burden of these diabetic complications. PMID:29515457

Activation of peroxisome proliferator-activated receptor-{alpha} enhances fatty acid oxidation in human adipocytes

DOE Office of Scientific and Technical Information (OSTI.GOV)

Lee, Joo-Young; Hashizaki, Hikari; Goto, Tsuyoshi

2011-04-22

Highlights: {yields} PPAR{alpha} activation increased mRNA expression levels of adipocyte differentiation marker genes and GPDH activity in human adipocytes. {yields} PPAR{alpha} activation also increased insulin-dependent glucose uptake in human adipocytes. {yields} PPAR{alpha} activation did not affect lipid accumulation in human adipocytes. {yields} PPAR{alpha} activation increased fatty acid oxidation through induction of fatty acid oxidation-related genes in human adipocytes. -- Abstract: Peroxisome proliferator-activated receptor-{alpha} (PPAR{alpha}) is a key regulator for maintaining whole-body energy balance. However, the physiological functions of PPAR{alpha} in adipocytes have been unclarified. We examined the functions of PPAR{alpha} using human multipotent adipose tissue-derived stem cells as a humanmore » adipocyte model. Activation of PPAR{alpha} by GW7647, a potent PPAR{alpha} agonist, increased the mRNA expression levels of adipocyte differentiation marker genes such as PPAR{gamma}, adipocyte-specific fatty acid-binding protein, and lipoprotein lipase and increased both GPDH activity and insulin-dependent glucose uptake level. The findings indicate that PPAR{alpha} activation stimulates adipocyte differentiation. However, lipid accumulation was not changed, which is usually observed when PPAR{gamma} is activated. On the other hand, PPAR{alpha} activation by GW7647 treatment induced the mRNA expression of fatty acid oxidation-related genes such as CPT-1B and AOX in a PPAR{alpha}-dependent manner. Moreover, PPAR{alpha} activation increased the production of CO{sub 2} and acid soluble metabolites, which are products of fatty acid oxidation, and increased oxygen consumption rate in human adipocytes. The data indicate that activation of PPAR{alpha} stimulates both adipocyte differentiation and fatty acid oxidation in human adipocytes, suggesting that PPAR{alpha} agonists could improve insulin resistance without lipid accumulation in adipocytes. The

Involvement of mitogen-activated protein kinase activation in the signal-transduction pathways of the soya bean oxidative burst.

PubMed Central

Taylor, A T; Kim, J; Low, P S

2001-01-01

The oxidative burst constitutes one of the most rapid defence responses characterized in the Plant Kingdom. We have observed that four distinct elicitors of the soya bean oxidative burst activate kinases of masses approximately 44 kDa and approximately 47 kDa. Evidence that these kinases regulate production of reactive oxygen species include: (i) their rapid activation by oxidative burst elicitors, (ii) their tight temporal correlation between activation/deactivation of the kinases and activation/deactivation of the oxidative burst, (iii) the identical pharmacological profile of kinase activation and oxidant production for 13 commonly used inhibitors, and (iv) the autologous activation of both kinases and oxidant production by calyculin A and cantharidin, two phosphatase inhibitors. Immunological and biochemical studies reveal that the activated 44 kDa and 47 kDa kinases are mitogen-activated protein (MAP) kinase family members. The kinases prefer myelin basic protein as a substrate, and they phosphorylate primarily on threonine residues. The kinases are themselves phosphorylated on tyrosine residues, and this phosphorylation is required for activity. Finally, both kinases are recognized by an antibody against activated MAP kinase immediately after (but not before) cell stimulation by elicitors. Based on these and other observations, a preliminary sequence of signalling steps linking elicitor stimulation, kinase activation and Ca(2+) entry, to initiation of oxidant production, is proposed. PMID:11311144

[Acetylcholine activation of alpha-ketoglutarate oxidation in liver mitochondria].

PubMed

Shostakovskaia, I V; Doliba, N M; Gordiĭ, S K; Babskiĭ, A M; Kondrashova, M N

1986-01-01

Activation of alpha-ketoglutarate oxidation in the rat liver mitochondria takes place 15 and 30 min after intraperitoneal injection of acetyl choline. This mediator in doses of 25, 50 and 100 micrograms per 100 g of body weight causes a pronounced stimulation of phosphorylation respiration rate and calcium capacity of mitochondria with alpha-ketoglutarate oxidation. Acetyl choline is found to have a moderate inhibitory action on oxidation of lower (physiological) concentrations of succinate. Its stimulating action on alpha-ketoglutarate oxidation is associated with activation of M-cholinoreceptors; atropine, a choline-blocker, removes completely this effect. It is supposed that alpha-ketoglutarate and succinate are included into the composition of two reciprocal hormonal-substrate nucleotide systems.

Benefit of azilsartan on blood pressure elevation around rest-to-active phase in spontaneously hypertensive rats.

PubMed

Isegawa, Kengo; Hirooka, Yoshitaka; Kishi, Takuya; Yasukawa, Keiji; Utsumi, Hideo; Sunagawa, Kenji

2015-01-01

Abnormal elevation of blood pressure in early morning (rest-to-active phase) is suggested to cause cardiovascular events. We investigated whether azilsartan (AZL), a novel potent angiotensin receptor blocker, suppresses blood pressure elevation from the light-rest to dark-active phase in spontaneously hypertensive rats (SHRs). AZL has a sustained depressor effect around the rest-to-active phase in SHRs to a greater extent than candesartan (CAN), despite their similar depressor effects for over 24 h. AZL did not cause sympathoexcitation. These results suggest that AZL has a more sustained depressor effect than CAN around the rest-to-active phase in SHRs, and might have advantages for early morning hypertension.

Assessment of anti-oxidant activity of plant extracts using microbial test systems.

PubMed

Oktyabrsky, O; Vysochina, G; Muzyka, N; Samoilova, Z; Kukushkina, T; Smirnova, G

2009-04-01

To evaluate the anti-oxidant properties of extracts from 20 medicinal herbs growing in western Siberia using microbial test systems and different in vitro methods. In vivo anti-oxidant activity of extracts was evaluated for their capacity to protect bacteria, Escherichia coli, against bacteriostatic and bactericidal effects of H(2)O(2) and menadione, and action on anti-oxidant gene expression. In vitro anti-oxidant activity has been examined by a number of methods including: the 1,1-diphenyl-2-picrylhydrazyl radical (DPPH(*))-scavenging assay, chelating activity and capacity to protect plasmid DNA against oxidative damage. In addition, total polyphenol content was determined. The extracts of Fragaria vesca, Rosa majalis, Pentaphylloides fruticosa, Alchemilla vulgaris and Pulmonaria mollis possessed the highest levels of anti-oxidant activity in vivo and in vitro. The protective properties were more closely related to the DPPH(*) radical-scavenging activity, tannin content and action on anti-oxidant gene expression than to other parameters. The extracts of medicinal plants may have anti-oxidant effects on bacteria simultaneously through several different pathways, including direct inhibition of reactive oxygen species, iron chelation and anti-oxidant genes induction. Using microbial test systems, we revealed herbs that may be used as potential sources of natural anti-oxidants.

Smoke Exposure Causes Endoplasmic Reticulum Stress and Lipid Accumulation in Retinal Pigment Epithelium through Oxidative Stress and Complement Activation*

PubMed Central

Kunchithapautham, Kannan; Atkinson, Carl; Rohrer, Bärbel

2014-01-01

Age-related macular degeneration (AMD) is a complex disease caused by genetic and environmental factors, including genetic variants in complement components and smoking. Smoke exposure leads to oxidative stress, complement activation, endoplasmic reticulum (ER) stress, and lipid dysregulation, which have all been proposed to be associated with AMD pathogenesis. Here we examine the effects of smoke exposure on the retinal pigment epithelium (RPE). Mice were exposed to cigarette smoke or filtered air for 6 months. RPE cells grown as stable monolayers were exposed to 5% cigarette smoke extract (CSE). Effects of smoke were determined by biochemical, molecular, and histological measures. Effects of the alternative pathway (AP) of complement and complement C3a anaphylatoxin receptor signaling were analyzed using knock-out mice or specific inhibitors. ER stress markers were elevated after smoke exposure in RPE of intact mice, which was eliminated in AP-deficient mice. To examine this relationship further, RPE monolayers were exposed to CSE. Short term smoke exposure resulted in production and release of complement C3, the generation of C3a, oxidative stress, complement activation on the cell membrane, and ER stress. Long term exposure to CSE resulted in lipid accumulation, and secretion. All measures were reversed by blocking C3a complement receptor (C3aR), alternative complement pathway signaling, and antioxidant therapy. Taken together, our results provide clear evidence that smoke exposure results in oxidative stress and complement activation via the AP, resulting in ER stress-mediated lipid accumulation, and further suggesting that oxidative stress and complement act synergistically in the pathogenesis of AMD. PMID:24711457

Oxidative status and paraoxonase activity in children with asthma.

PubMed

Cakmak, Alpay; Zeyrek, Dost; Atas, Ali; Selek, Sahabettin; Erel, Ozcan

2009-10-01

To compare paraoxonase activity and changes in oxidative status in asthmatic children and healthy children by determining serum paraoxonase activity and total oxidative status, total antioxidant capacity and lipid hydroperoxidation. Forty two asthmatic children were compared with 32 healthy children of similar age and sex. To evaluate the paraoxonase and oxidative status, total antioxidant capacity and lipid hydroperoxidation were examined. Serum paraoxonase activity was evaluated by measuring the rate of paraoxon hydrolosis. Oxidative status was evaluated by the method developed by Erel. Lipid hydroperoxide was measured by an iodometric method. In comparison with the healthy control group, the paraoxonase activity of the asthmatic children was found to be low (163.7 +/- 73.0 (U/L) and 349.2 +/- 153.9 (U/L), P = 0.002) and total oxidant status (9.0 +/- 3.5 micromol H2O2 Eq/L and 13.4 +/- 7.0 micromol H2O2 Eq/L, P =0.002), total antioxidant capacity (5.5 +/- 2.5 micromol Trolox Eq/L and 1.0 +/- 0.6 micromol Trolox Eq/L, P < 0.001), and lipid hydroperoxidation values (9.9 +/- 3.4 micromol H2O2 Eq/L and 4.4 +/- 1.5 micromol H2O2 Eq/L, P < 0.001) were found to be high. The high density lipoprotein (HDL) concentration of the asthmatic children was lower than that in the control group (40.1 +/- 9.2 mg/dl and 54.5 +/- 15.9 mg/dl, P < 0.001) In asthmatic children, when total oxidant status, total antioxidant capacity and lipid hydroperoxidation levels increase, paraoxonase activity decreased.

Oxidative stress and skin diseases: possible role of physical activity.

PubMed

Kruk, Joanna; Duchnik, Ewa

2014-01-01

The skin is the largest body organ that regulates excretion of metabolic waste products, temperature, and plays an important role in body protection against environmental physical and chemical, as well as biological factors. These include agents that may act as oxidants or catalysts of reactions producing reactive oxygen species (ROS), reactive nitrogen species (RNS), and other oxidants in skin cells. An increased amount of the oxidants, exceeding the antioxidant defense system capacity is called oxidative stress, leading to chronic inflammation, which, in turn, can cause collagen fragmentation and disorganization of collagen fibers and skin cell functions, and thus contribute to skin diseases including cancer. Moreover, research suggests that oxidative stress participates in all stages of carcinogenesis. We report here a summary of the present state of knowledge on the role of oxidative stress in pathogenesis of dermatologic diseases, defensive systems against ROS/RNS, and discuss how physical activity may modulate skin diseases through effects on oxidative stress. The data show duality of physical activity actions: regular moderate activity protects against ROS/RNS damage, and endurance exercise with a lack of training mediates oxidative stress. These findings indicate that the redox balance should be considered in the development of new antioxidant strategies linked to the prevention and therapy of skin diseases.

Aqueous Extract of Phyllanthus niruri Leaves Displays In Vitro Antioxidant Activity and Prevents the Elevation of Oxidative Stress in the Kidney of Streptozotocin-Induced Diabetic Male Rats

PubMed Central

Giribabu, Nelli; Rao, Pasupuleti Visweswara; Kumar, Korla Praveen; Muniandy, Sekaran; Swapna Rekha, Somesula; Salleh, Naguib

2014-01-01

P. niruri has been reported to possess antidiabetic and kidney protective effects. In the present study, the phytochemical constituents and in vitro antioxidant activity of P. niruri leaf aqueous extract were investigated together with its effect on oxidative stress and antioxidant enzymes levels in diabetic rat kidney. Results. Treatment of diabetic male rats with P. niruri leaf aqueous extract (200 and 400 mg/kg) for 28 consecutive days prevents the increase in the amount of lipid peroxidation (LPO) product, malondialdehyde (MDA), and the diminution of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity levels in the kidney of diabetic rats. The amount of LPO showed strong negative correlation with SOD, CAT, and GPx activity levels. P. niruri leaf aqueous extract exhibits in vitro antioxidant activity with IC50 slightly lower than ascorbic acid. Phytochemical screening of plant extract indicates the presence of polyphenols. Conclusion. P. niruri leaf extract protects the kidney from oxidative stress induced by diabetes. PMID:24991228

The myeloperoxidase-derived oxidant HOSCN inhibits protein tyrosine phosphatases and modulates cell signalling via the mitogen-activated protein kinase (MAPK) pathway in macrophages

PubMed Central

Lane, Amanda E.; Tan, Joanne T. M.; Hawkins, Clare L.; Heather, Alison K.; Davies, Michael J.

2010-01-01

MPO (myeloperoxidase) catalyses the oxidation of chloride, bromide and thiocyanate by hydrogen peroxide to HOCl (hypochlorous acid), HOBr (hypobromous acid) and HOSCN (hypothiocyanous acid) respectively. Specificity constants indicate that SCN− is a major substrate for MPO. HOSCN is also a major oxidant generated by other peroxidases including salivary, gastric and eosinophil peroxidases. While HOCl and HOBr are powerful oxidizing agents, HOSCN is a less reactive, but more specific, oxidant which targets thiols and especially low pKa species. In the present study we show that HOSCN targets cysteine residues present in PTPs (protein tyrosine phosphatases) with this resulting in a loss of PTP activity for the isolated enzyme, in cell lysates and intact J774A.1 macrophage-like cells. Inhibition also occurs with MPO-generated HOCl and HOBr, but is more marked with MPO-generated HOSCN, particularly at longer incubation times. This inhibition is reversed by dithiothreitol, particularly at early time points, consistent with the reversible oxidation of the active site cysteine residue to give either a cysteine–SCN adduct or a sulfenic acid. Inhibition of PTP activity is associated with increased phosphorylation of p38a and ERK2 (extracellular-signal-regulated kinase 2) as detected by Western blot analysis and phosphoprotein arrays, and results in altered MAPK (mitogen-activated protein kinase) signalling. These data indicate that the highly selective targeting of some protein thiols by HOSCN can result in perturbation of cellular phosphorylation and altered cell signalling. These changes occur with (patho)physiological concentrations of SCN− ions, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage, particularly in smokers who have elevated plasma levels of SCN−. PMID:20528774

Antibacterial Activity of Polymer Coated Cerium Oxide Nanoparticles

PubMed Central

Shah, Vishal; Shah, Shreya; Shah, Hirsh; Rispoli, Fred J.; McDonnell, Kevin T.; Workeneh, Selam; Karakoti, Ajay; Kumar, Amit; Seal, Sudipta

2012-01-01

Cerium oxide nanoparticles have found numerous applications in the biomedical industry due to their strong antioxidant properties. In the current study, we report the influence of nine different physical and chemical parameters: pH, aeration and, concentrations of MgSO4, CaCl2, KCl, natural organic matter, fructose, nanoparticles and Escherichia coli, on the antibacterial activity of dextran coated cerium oxide nanoparticles. A least-squares quadratic regression model was developed to understand the collective influence of the tested parameters on the anti-bacterial activity and subsequently a computer-based, interactive visualization tool was developed. The visualization allows us to elucidate the effect of each of the parameters in combination with other parameters, on the antibacterial activity of nanoparticles. The results indicate that the toxicity of CeO2 NPs depend on the physical and chemical environment; and in a majority of the possible combinations of the nine parameters, non-lethal to the bacteria. In fact, the cerium oxide nanoparticles can decrease the anti-bacterial activity exerted by magnesium and potassium salts. PMID:23110109

Small dense HDLs display potent vasorelaxing activity, reflecting their elevated content of sphingosine-1-phosphate.

PubMed

Perségol, Laurence; Darabi, Maryam; Dauteuille, Carolane; Lhomme, Marie; Chantepie, Sandrine; Rye, Kerry-Anne; Therond, Patrice; Chapman, M John; Salvayre, Robert; Nègre-Salvayre, Anne; Lesnik, Philippe; Monier, Serge; Kontush, Anatol

2018-01-01

The functional heterogeneity of HDL is attributed to its diverse bioactive components. We evaluated whether the vasodilatory effects of HDL differed across HDL subpopulations, reflecting their distinct molecular composition. The capacity of five major HDL subfractions to counteract the inhibitory effects of oxidized LDL on acetylcholine-induced vasodilation was tested in a rabbit aortic rings model. NO production, an essential pathway in endothelium-dependent vasorelaxation, was studied in simian vacuolating virus 40-transformed murine endothelial cells (SVECs). Small dense HDL3 subfractions displayed potent vasorelaxing activity (up to +31% vs. baseline, P < 0.05); in contrast, large light HDL2 did not induce aortic-ring relaxation when compared on a total protein basis. HDL3 particles were enriched with sphingosine-1-phosphate (S1P) (up to 3-fold vs. HDL2), with the highest content in HDL3b and -3c that concomitantly revealed the strongest vasorelaxing properties. NO generation was enhanced by HDL3c in SVECs (1.5-fold, P < 0.01), a phenomenon that was blocked by the S1P receptor antagonist, VPC 23019. S1P-enriched reconstituted HDL (rHDL) was a 1.8-fold ( P < 0.01) more potent vasorelaxant than control rHDL in aortic rings. Small dense HDL3 particles displayed potent protective effects against oxidative stress-associated endothelium dysfunction, potentially reflecting their elevated content of S1P that might facilitate interaction with S1P receptors and ensuing NO generation. Copyright © 2018 by the American Society for Biochemistry and Molecular Biology, Inc.

Electrospun strontium titanata nanofibers incorporated with nickel oxide nanoparticles for improved photocatalytic activities

NASA Astrophysics Data System (ADS)

Alharbi, Abdulaziz; Alarifi, Ibrahim M.; Khan, Waseem S.; Asmatulu, Ramazan

2015-03-01

The inexpensive sources of fossil fuels in the world are limited, and will deplete soon because of the huge demand on the energy and growing economies worldwide. Thus, many research activities have been focused on the non-fossil fuel based energy sources, and this will continue next few decades. Water splitting using photocatalysts is one of the major alternative energy technologies to produce hydrogen directly from water using photon energy of the sun. Numerous solid photocatalysts have been used by researchers for water splitting. In the present study, nickel oxide and strontium titanata were chosen as photocatalysts for water splitting. Poly (vinyl pyrrolidone) (PVP) was incorporated with nickel oxide [Ni2O3] (co-catalyst), while poly (vinyl acetate) (PVAc) was mixed with titanium (IV) isopropoxide [C12H28O4Ti] and strontium nitrate [Sr(NO3)2]. Then, two solutions were electrospun using coaxial electrospinning technique to generate nanoscale fibers incorporated with NiOx nanoparticles. The fibers were then heat treated at elevated temperatures for 2hr in order to transform the strontium titanata and nickel oxide into crystalline form for a better photocatalytic efficiency. The morphology of fibers was characterized via scanning electron microscopy (SEM), while the surface hydrophobicity was determined using water contact angle goniometer. The UV-vis spectrophotometer was also used to determine the band gap energy values of the nanofibers. This study may open up new possibilities to convert water into fuel directly using the novel photocatalysts.

Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways.

PubMed

Morris, Gerwyn; Anderson, George; Maes, Michael

2017-11-01

There is evidence that immune-inflammatory and oxidative and nitrosative stress (O&NS) pathways play a role in the pathophysiology of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). There is also evidence that these neuroimmune diseases are accompanied by hypothalamic-pituitary-adrenal (HPA) axis hypoactivity as indicated by lowered baseline glucocorticoid levels. This paper aims to review the bidirectional communications between immune-inflammatory and O&NS pathways and HPA axis hypoactivity in ME/CFS, considering two possibilities: (a) Activation of immune-inflammatory pathways is secondary to HPA axis hypofunction via attenuated negative feedback mechanisms, or (b) chronic activated immune-inflammatory and O&NS pathways play a causative role in HPA axis hypoactivity. Electronic databases, i.e., PUBMED, Scopus, and Google Scholar, were used as sources for this narrative review by using keywords CFS, ME, cortisol, ACTH, CRH, HPA axis, glucocorticoid receptor, cytokines, immune, immunity, inflammation, and O&NS. Findings show that activation of immune-inflammatory and O&NS pathways in ME/CFS are probably not secondary to HPA axis hypoactivity and that activation of these pathways may underpin HPA axis hypofunction in ME/CFS. Mechanistic explanations comprise increased levels of tumor necrosis factor-α, T regulatory responses with elevated levels of interleukin-10 and transforming growth factor-β, elevated levels of nitric oxide, and viral/bacterial-mediated mechanisms. HPA axis hypoactivity in ME/CFS is most likely a consequence and not a cause of a wide variety of activated immune-inflammatory and O&NS pathways in that illness.

The elevation effect on water-soluble polysaccharides and DPPH free radical scavenging activity of Ganoderma lucidum K

NASA Astrophysics Data System (ADS)

Darsih, C.; Apriyana, W.; Nur Hayati, S.; Taufika Rosyida, V.; Hernawan; Dewi Poeloengasih, C.

2017-02-01

Water soluble polysaccharide is one of the important phytochemical in Ganoderma lucidum K. Phytochemicals in the plants, microorganisms, and plants were affected by internal and external factors. The objective of the research was to evaluate the effect of elevation on the water-soluble polysaccharides and its DPPH radical scavenging activity. We found that the water-polysaccharides in mushroom from Godean (elevation <100 mamsl) (35.28 ± 0.31%) higher than Kaliurang (elevation 800 mamsl) (25.17 ± 1.85%). The DPPH free radical scavenging activity of Ganoderma lucidum K from Godean (IC50 11.5 ± 0.29 mg/mL) higher than Kaliurang (IC50 14.4 ± 0.27%).

Silver nanoparticles anchored reduced graphene oxide for enhanced electrocatalytic activity towards methanol oxidation

NASA Astrophysics Data System (ADS)

Kumar, Sanjeev; Mahajan, Mani; Singh, Rajinder; Mahajan, Aman

2018-02-01

In this report, silver nanoparticles (Ag NPs) anchored reduced graphene oxide (rGO) sheets (rGO/Ag) nanohybrid has been explored as anode material in direct methanol fuel cells (DMFCs). The synthesized rGO/Ag nanohybrid is characterized by XRD, XPS, FTIR spectroscopy and HRTEM techniques. Cyclic voltammograms demonstrate that the rGO/Ag nanohybrid exhibits higher electrocatalytic activity in comparison to rGO sheets for methanol oxidation reaction (MOR). This enhancement is attributed to the synergetic effect produced by the presence of more active sites provided by Ag NPs anchored on a conducting network of large surface area rGO sheets.

Energetic basis of catalytic activity of layered nanophase calcium manganese oxides for water oxidation.

PubMed

Birkner, Nancy; Nayeri, Sara; Pashaei, Babak; Najafpour, Mohammad Mahdi; Casey, William H; Navrotsky, Alexandra

2013-05-28

Previous measurements show that calcium manganese oxide nanoparticles are better water oxidation catalysts than binary manganese oxides (Mn3O4, Mn2O3, and MnO2). The probable reasons for such enhancement involve a combination of factors: The calcium manganese oxide materials have a layered structure with considerable thermodynamic stability and a high surface area, their low surface energy suggests relatively loose binding of H2O on the internal and external surfaces, and they possess mixed-valent manganese with internal oxidation enthalpy independent of the Mn(3+)/Mn(4+) ratio and much smaller in magnitude than the Mn2O3-MnO2 couple. These factors enhance catalytic ability by providing easy access for solutes and water to active sites and facile electron transfer between manganese in different oxidation states.

Elevated pressure causes endothelial dysfunction in mouse carotid arteries by increasing local angiotensin signaling

PubMed Central

Zhao, Yingzi; Flavahan, Sheila; Leung, Susan W.; Xu, Aimin; Vanhoutte, Paul M.

2014-01-01

Experiments were performed to determine whether or not acute exposure to elevated pressure would disrupt endothelium-dependent dilatation by increasing local angiotensin II (ANG II) signaling. Vasomotor responses of mouse-isolated carotid arteries were analyzed in a pressure myograph at a control transmural pressure (PTM) of 80 mmHg. Acetylcholine-induced dilatation was reduced by endothelial denudation or by inhibition of nitric oxide synthase (NG-nitro-l-arginine methyl ester, 100 μM). Transient exposure to elevated PTM (150 mmHg, 180 min) inhibited dilatation to acetylcholine but did not affect responses to the nitric oxide donor diethylamine NONOate. Elevated PTM also increased endothelial reactive oxygen species, and the pressure-induced endothelial dysfunction was prevented by the direct antioxidant and NADPH oxidase inhibitor apocynin (100 μM). The increase in endothelial reactive oxygen species in response to elevated PTM was reduced by the ANG II type 1 receptor (AT1R) antagonists losartan (3 μM) or valsartan (1 μM). Indeed, elevated PTM caused marked expression of angiotensinogen, the precursor of ANG II. Inhibition of ANG II signaling, by blocking angiotensin-converting enzyme (1 μM perindoprilat or 10 μM captopril) or blocking AT1Rs prevented the impaired response to acetylcholine in arteries exposed to 150 mmHg but did not affect dilatation to the muscarinic agonist in arteries maintained at 80 mmHg. After the inhibition of ANG II, elevated pressure no longer impaired endothelial dilatation. In arteries treated with perindoprilat to inhibit endogenous formation of the peptide, exogenous ANG II (0.3 μM, 180 min) inhibited dilatation to acetylcholine. Therefore, elevated pressure rapidly impairs endothelium-dependent dilatation by causing ANG expression and enabling ANG II-dependent activation of AT1Rs. These processes may contribute to the pathogenesis of hypertension-induced vascular dysfunction and organ injury. PMID:25485905

Elevated pressure causes endothelial dysfunction in mouse carotid arteries by increasing local angiotensin signaling.

PubMed

Zhao, Yingzi; Flavahan, Sheila; Leung, Susan W; Xu, Aimin; Vanhoutte, Paul M; Flavahan, Nicholas A

2015-02-15

Experiments were performed to determine whether or not acute exposure to elevated pressure would disrupt endothelium-dependent dilatation by increasing local angiotensin II (ANG II) signaling. Vasomotor responses of mouse-isolated carotid arteries were analyzed in a pressure myograph at a control transmural pressure (PTM) of 80 mmHg. Acetylcholine-induced dilatation was reduced by endothelial denudation or by inhibition of nitric oxide synthase (NG-nitro-L-arginine methyl ester, 100 μM). Transient exposure to elevated PTM (150 mmHg, 180 min) inhibited dilatation to acetylcholine but did not affect responses to the nitric oxide donor diethylamine NONOate. Elevated PTM also increased endothelial reactive oxygen species, and the pressure-induced endothelial dysfunction was prevented by the direct antioxidant and NADPH oxidase inhibitor apocynin (100 μM). The increase in endothelial reactive oxygen species in response to elevated PTM was reduced by the ANG II type 1 receptor (AT1R) antagonists losartan (3 μM) or valsartan (1 μM). Indeed, elevated PTM caused marked expression of angiotensinogen, the precursor of ANG II. Inhibition of ANG II signaling, by blocking angiotensin-converting enzyme (1 μM perindoprilat or 10 μM captopril) or blocking AT1Rs prevented the impaired response to acetylcholine in arteries exposed to 150 mmHg but did not affect dilatation to the muscarinic agonist in arteries maintained at 80 mmHg. After the inhibition of ANG II, elevated pressure no longer impaired endothelial dilatation. In arteries treated with perindoprilat to inhibit endogenous formation of the peptide, exogenous ANG II (0.3 μM, 180 min) inhibited dilatation to acetylcholine. Therefore, elevated pressure rapidly impairs endothelium-dependent dilatation by causing ANG expression and enabling ANG II-dependent activation of AT1Rs. These processes may contribute to the pathogenesis of hypertension-induced vascular dysfunction and organ injury. Copyright © 2015 the American

Oxidative status and serum PON1 activity in beta-thalassemia minor.

PubMed

Selek, Sahbettin; Aslan, Mehmet; Horoz, Mehmet; Gur, Mustafa; Erel, Ozcan

2007-03-01

Paraoxonase-1 (PON1) deficiency is related to increased susceptibility to low density lipoprotein oxidation and development of atherosclerosis. The aim of this study was to investigate paraoxonase and arylesterase activities along with oxidative status parameters, and to find out if there is any increased susceptibility to atherogenesis, which might be reflected with increased oxidative stress and decreased serum PON1 activity in beta-thalassemia minor (BTM) subjects. Thirty-two subjects with BTM and 28 healthy subjects as control were enrolled in the study. Serum paraoxonase and arylesterase activities, lipid hydroperoxide (LOOH) levels, total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined. Serum TAC, paraoxonase and arylesterase activities were significantly lower in BTM subjects than controls (for all p<0.001), while TOS, LOOH levels and OSI were significantly higher (p<0.001, p<0.05 and p<0.001; respectively). In BTM subjects, OSI, TOS, LOOH levels and TAC were significantly correlated with serum paraoxonase (r=-0.245, p<0.05; r=-0.231, p<0.05; r=-0.264, p<0.05 and, r=0.342, p<0.05, respectively) and arylesterase activities (r=-0.332, p<0.05, r=-0.308, p<0.05; r=-0.320, p<0.05 and r=0.443, p<0.05). Additionally, hemoglobin level was also correlated with serum paraoxonase (r=0.501, p<0.001) and arylesterase activities (r=0.501, p<0.001), TAC (r=0.402, p<0.05), TOS (r=-0.274, p<0.05) and OSI (r=-0.352, p<0.05). Oxidative stress is increased, while serum PON1 activity is decreased in BTM subjects. Decrease in PON1 activity seems to be associated with both the degree of oxidative stress and anemia. BTM subjects may be more prone to development of atherogenesis due to low serum PON1 activity.

Polychlorinated biphenyl quinone induces oxidative DNA damage and repair responses: The activations of NHEJ, BER and NER via ATM-p53 signaling axis

DOE Office of Scientific and Technical Information (OSTI.GOV)

Dong, Hui; Shi, Qiong; Song, Xiufang

2015-07-01

Our previous studies demonstrated that polychlorinated biphenyl (PCB) quinone induced oxidative DNA damage in HepG2 cells. To promote genomic integrity, DNA damage response (DDR) coordinates cell-cycle transitions, DNA repair and apoptosis. PCB quinone-induced cell cycle arrest and apoptosis have been documented, however, whether PCB quinone insult induce DNA repair signaling is still unknown. In this study, we identified the activation of DDR and corresponding signaling events in HepG2 cells upon the exposure to a synthetic PCB quinone, PCB29-pQ. Our data illustrated that PCB29-pQ induces the phosphorylation of p53, which was mediated by ataxia telangiectasia mutated (ATM) protein kinase. The observedmore » phosphorylated histone H2AX (γ-H2AX) foci and the elevation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) indicated that DDR was stimulated by PCB29-pQ treatment. Additionally, we found PCB29-pQ activates non-homologous end joining (NHEJ), base excision repair (BER) and nucleotide excision repair (NER) signalings. However, these repair pathways are not error-free processes and aberrant repair of DNA damage may cause the potential risk of carcinogenesis and mutagenesis. - Highlights: • Polychlorinated biphenyl quinone induces oxidative DNA damage in HepG2 cells. • The elevation of γ-H2AX and 8-OHdG indicates the activation of DNA damage response. • ATM-p53 signaling acts as the DNA damage sensor and effector. • Polychlorinated biphenyl quinone activates NHEJ, BER and NER signalings.« less

The Omega-3 Index Is Inversely Associated with Depressive Symptoms among Individuals with Elevated Oxidative Stress Biomarkers123

PubMed Central

Bigornia, Sherman J; Falcón, Luis M; Ordovás, José M; Lai, Chao-Qiang

2016-01-01

Background: Omega-3 (n–3) fatty acid (FA) consumption is thought to improve depressive symptoms. However, current evidence is limited, and whether this association exists among Puerto Ricans, a population burdened by depression, remains uncertain. Objectives: We examined the association between ω-3 FA biomarkers and depressive symptoms as well as the potential influence of oxidative stress. Methods: Baseline and longitudinal analyses were conducted in the Boston Puerto Rican Health Study (n = 787; participants aged 57 ± 0.52 y, 73% women). Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) concentration, a measure of oxidative stress, and erythrocyte FA composition were collected at baseline. We calculated the omega-3 index as the sum of eicosapentaenoic and docosahexaenoic acids, expressed as a percentage of total FAs. Baseline and 2-y depressive symptoms were characterized by using the Center for Epidemiological Studies–Depression Scale (CES-D). Statistical analyses included linear and logistic regression. Results: Urinary 8-OHdG concentration tended to modify the relation between the erythrocyte omega-3 index and baseline CES-D score (P-interaction = 0.10). In stratified analyses, the omega-3 index was inversely associated with CES-D score (β = −1.74, SE = 0.88; P = 0.02) among those in the top quartile of 8-OHdG concentration but not among those in the lower quartiles. The relation between the omega-3 index and CES-D at 2 y was more clearly modified by 8-OHdG concentration (P-interaction = 0.04), where the omega-3 index was inversely associated with CES-D at 2 y, adjusted for baseline (β = −1.66, SE = 0.66; P = 0.02), only among those with elevated 8-OHdG concentrations. Among individuals not taking antidepressant medications and in the top tertile of urinary 8-OHdG concentration, the omega-3 index was associated with significantly lower odds of a CES-D score ≥16 at baseline (OR: 0.72; 95% CI: 0.53, 0.96) but not at 2 y (OR: 0.83; 95% CI: 0.60, 1

Energetic basis of catalytic activity of layered nanophase calcium manganese oxides for water oxidation

PubMed Central

Birkner, Nancy; Nayeri, Sara; Pashaei, Babak; Najafpour, Mohammad Mahdi; Casey, William H.; Navrotsky, Alexandra

2013-01-01

Previous measurements show that calcium manganese oxide nanoparticles are better water oxidation catalysts than binary manganese oxides (Mn3O4, Mn2O3, and MnO2). The probable reasons for such enhancement involve a combination of factors: The calcium manganese oxide materials have a layered structure with considerable thermodynamic stability and a high surface area, their low surface energy suggests relatively loose binding of H2O on the internal and external surfaces, and they possess mixed-valent manganese with internal oxidation enthalpy independent of the Mn3+/Mn4+ ratio and much smaller in magnitude than the Mn2O3-MnO2 couple. These factors enhance catalytic ability by providing easy access for solutes and water to active sites and facile electron transfer between manganese in different oxidation states. PMID:23667149

Candidate's thesis: Platelet-activating factor-induced hearing loss: mediated by nitric oxide?

PubMed

Rhee, Chung-Ku

2003-12-01

Platelet-activating factor (PAF)in middle ear effusion is thought to induce hearing loss. The purpose of this study is to investigate the role of nitric oxide (NO) in the mechanism of PAF-induced hearing loss by studying the effects of PAF application on the round window membrane (RWM) with and without PAF-antagonist NO-blocker. Longitudinal study on randomized guinea pigs using PAF to induce hearing loss. METHODS Guinea pigs were divided into four groups: PBS, PAF, PAF-antagonist, and L-NAME. The PBS group received phosphate buffered saline (PBS) and the PAF groups received 10, 20, and 40 microg of PAF soaked into gelfoam and placed on the RWM. PAF-antagonist (WEB 2170) and NOS inhibitor NG-nitro-l-arginine-methylester (L-NAME) were injected intraperitoneally prior to PAF 20 microg application on the RWM. The following three tests were performed on each animal group: Hearing was tested with an auditory brainstem response (ABR) test over 24 hours. At the end of 24 hours, cochlear hair cells were examined by scanning electron microscopy (SEM) and immunohistochemistry was carried out on the cochlea to test the expression of inducible nitric oxide synthase (iNOS). The PAF group developed significant elevation of ABR threshold and cochlear hair cell damage in the SEM group as compared with the PBS control group. The PAF-antagonist (WEB 2170) and the L-NAME groups did not show significant elevation of ABR threshold and cochlear hair cell damage compared with the group administered PAF 20 microg, but in the PAF-antagonist group, the elevation of ABR threshold was significant compared with that of the PBS control group, whereas it was not significant compared with the PBS group in the L-NAME group. Strong expression of iNOS on cochlea was observed in the PAF group and lighter expression was seen in PBS, WEB 2170, and L-NAME groups. This study demonstrated that PAF placed on the RWM induced hearing loss and cochlear hair cell damage. The PAF-antagonists and L

Elevation of Glucose 6-Phosphate Dehydrogenase Activity Induced by Amplified Insulin Response in Low Glutathione Levels in Rat Liver

PubMed Central

Taniguchi, Misako; Mori, Nobuko; Iramina, Chizuru

2016-01-01

Weanling male Wistar rats were fed on a 10% soybean protein isolate (SPI) diet for 3 weeks with or without supplementing 0.3% sulfur-containing amino acids (SAA; methionine or cystine) to examine relationship between glutathione (GSH) levels and activities of NADPH-producing enzymes, glucose 6-phosphate dehydrogenase (G6PD) and malic enzyme (ME), in the liver. Of rats on the 10% SPI diet, GSH levels were lower and the enzyme activities were higher than of those fed on an SAA-supplemented diet. Despite the lower GSH level, γ-glutamylcysteine synthetase (γ-GCS) activity was higher in the 10% SPI group than other groups. Examination of mRNAs of G6PD and ME suggested that the GSH-suppressing effect on enzyme induction occurred prior to and/or at transcriptional levels. Gel electrophoresis of G6PD indicated that low GSH status caused a decrease in reduced form and an increase in oxidized form of the enzyme, suggesting an accelerated turnover rate of the enzyme. In primary cultured hepatocytes, insulin response to induce G6PD activity was augmented in low GSH levels manipulated in the presence of buthionine sulfoximine. These findings indicated that elevation of the G6PD activity in low GSH levels was caused by amplified insulin response for expression of the enzyme and accelerated turnover rate of the enzyme molecule. PMID:27597985

Oxidative stress and hepatic Nox proteins in chronic hepatitis C and hepatocellular carcinoma

PubMed Central

Choi, Jinah; Corder, Nicole L. B.; Koduru, Bhargav; Wang, Yiyan

2014-01-01

Hepatocellular carcinoma (HCC) is the most common liver cancer and a leading cause of cancer-related mortality in the world. Hepatitis C virus (HCV) is a major etiologic agent of HCC. A majority of HCV infections lead to chronic infection that can progress to cirrhosis and eventually, HCC and liver failure. A common pathogenic feature present in HCV infection, and other conditions leading to HCC, is oxidative stress. HCV directly increases superoxide and H2O2 formation in hepatocytes by elevating Nox protein expression and sensitizing mitochondria to reactive oxygen species generation while decreasing glutathione. Nitric oxide synthesis and hepatic iron are also elevated. Furthermore, activation of phagocytic NADPH oxidase 2 (Nox2) of host immune cells is likely to exacerbate oxidative stress in HCV-infected patients. Key mechanisms of HCC include: genome instability, epigenetic regulation, inflammation with chronic tissue injury and sustained cell proliferation, and modulation of cell growth and death. Oxidative stress, or Nox proteins, plays various roles in these mechanisms. Nox proteins also function in hepatic fibrosis, which commonly precedes HCC, and Nox4 elevation by HCV was mediated by transforming growth factor beta. This review summarizes mechanisms of oncogenesis by HCV, highlighting the role of oxidative stress and hepatic Nox enzymes in HCC. PMID:24816297

Assessment of oxidative stress and activities of antioxidant enzymes depicts the negative systemic effect of iron-containing fertilizers and plant phenolic compounds in the desert locust.

PubMed

Renault, David; Dorrah, Moataza A; Mohamed, Amr A; Abdelfattah, Eman A; Bassal, Taha T M

2016-11-01

For herbivore insects, digesting can be somewhat challenging, as the defense mechanisms evolved by plants, including the release of phenolics like the non-protein amino acid L-3,4-dihydroxyphenylalanine (L-DOPA), can cause fitness costs. In addition, industrial and agricultural activities have elevated the amounts of iron that can be found in nature and more particularly FeSO 4 that is used as fertilizer. Traces of iron can enhance the auto-oxidation of L-DOPA, in turn, generating reactive oxygen species (ROS) and consequently oxidative stress in insects. We examined the effects of the ion Fe 2+ (as FeSO 4 ) and L-DOPA on fifth instars of the desert locust Schistocerca gregaria. We measured the level of oxidative damage occurring to macromolecules (proteins and lipids) from midgut and thoracic tissues and assessed the activities of responsive antioxidant enzymes. Injected L-DOPA and redox-active metal iron generated ROS which caused oxidative damages to proteins and lipids to S. gregaria. The protein carbonyls and lipid peroxides present in tissue homogenates were elevated in treated insects. No synergism was observed when L-DOPA was co-injected with Fe 2+ . K m values of superoxide dismutase (SOD), glutathione reductase (GR), and glutathione peroxidase (GPx) were 4.3, 2.6, and 4.0 mM in thoracic muscles and 5.00, 2.43, and 1.66 mM in whole midgut for SOD, GR, and GPx, respectively, and 8.3 and 3.43 M for catalase (CAT) in the two tissues, respectively. These results suggest higher affinities of GPx and CAT to H 2 O 2 in midgut than in muscles. The time-course changes in activities of antioxidant enzymes and amounts of protein carbonyls and lipid peroxides showed fluctuating patterns, suggesting complex interactions among macromolecules, L-DOPA and FeSO 4 , and their degradation products. Our results demonstrated the stressful effects of L-DOPA and FeSO 4 , proving that iron-containing fertilizers are pollutants that can strongly affect S. gregaria.

Maternal active or passive smoking causes oxidative stress in placental tissue.

PubMed

Aycicek, Ali; Varma, Mustafa; Ahmet, Koc; Abdurrahim, Kocyigit; Erel, Ozcan

2011-05-01

The aim of this study was to assess the influence of active and passive maternal smoking on placenta total oxidant/antioxidant status in term infants. The levels of cord blood total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were measured in samples of fetal placental tissue, cord blood, and the maternal peripheral blood serum and from 19 mothers who were active smokers, 19 who were passive smokers, and 22 who were nonsmokers (not exposed to active or passive smoking). The pregnancies were between 37 and 40 weeks' gestation, were uncomplicated, and the infants were delivered vaginally. Birth weight and head circumference in the active smokers were significantly (P < 0.001) lower than those in the controls. Placenta, cord blood, and the maternal peripheral TAC levels were significantly lower in the active smokers compared with the controls (P < 0.001), while TOS and OSI levels were significantly higher in the active and passive smokers than in the controls (P < 0.001). A positive significant correlation was found between active maternal smoking and placenta TOS and OSI levels (P < 0.016), and a significant negative correlation was found between number of cigarettes exposed to and birthweight and head circumference (P < 0.05). In conclusion, active or passive maternal smoking is associated with important alterations in oxidant and antioxidant balance in fetal placental tissue and causes potent oxidative stress.

Microfluidic electrochemical sensor for on-line monitoring of aerosol oxidative activity.

PubMed

Sameenoi, Yupaporn; Koehler, Kirsten; Shapiro, Jeff; Boonsong, Kanokporn; Sun, Yele; Collett, Jeffrey; Volckens, John; Henry, Charles S

2012-06-27

Particulate matter (PM) air pollution has a significant impact on human morbidity and mortality; however, the mechanisms of PM-induced toxicity are poorly defined. A leading hypothesis states that airborne PM induces harm by generating reactive oxygen species in and around human tissues, leading to oxidative stress. We report here a system employing a microfluidic electrochemical sensor coupled directly to a particle-into-liquid sampler (PILS) system to measure aerosol oxidative activity in an on-line format. The oxidative activity measurement is based on the dithiothreitol (DTT) assay, where, after being oxidized by PM, the remaining reduced DTT is analyzed by the microfluidic sensor. The sensor consists of an array of working, reference, and auxiliary electrodes fabricated in a poly(dimethylsiloxane)-based microfluidic device. Cobalt(II) phthalocyanine-modified carbon paste was used as the working electrode material, allowing selective detection of reduced DTT. The electrochemical sensor was validated off-line against the traditional DTT assay using filter samples taken from urban environments and biomass burning events. After off-line characterization, the sensor was coupled to a PILS to enable on-line sampling/analysis of aerosol oxidative activity. Urban dust and industrial incinerator ash samples were aerosolized in an aerosol chamber and analyzed for their oxidative activity. The on-line sensor reported DTT consumption rates (oxidative activity) in good correlation with aerosol concentration (R(2) from 0.86 to 0.97) with a time resolution of approximately 3 min.

Elevated temperature and PCO2 shift metabolic pathways in differentially oxidative tissues of Notothenia rossii.

PubMed

Strobel, Anneli; Leo, Elettra; Pörtner, Hans O; Mark, Felix C

2013-09-01

Mitochondrial plasticity plays a central role in setting the capacity for acclimation of aerobic metabolism in ectotherms in response to environmental changes. We still lack a clear picture if and to what extent the energy metabolism and mitochondrial enzymes of Antarctic fish can compensate for changing temperatures or PCO2 and whether capacities for compensation differ between tissues. We therefore measured activities of key mitochondrial enzymes (citrate synthase (CS), cytochrome c oxidase (COX)) from heart, red muscle, white muscle and liver in the Antarctic fish Notothenia rossii after warm- (7°C) and hypercapnia- (0.2kPa CO2) acclimation vs. control conditions (1°C, 0.04kPa CO2). In heart, enzymes showed elevated activities after cold-hypercapnia acclimation, and a warm-acclimation-induced upward shift in thermal optima. The strongest increase in enzyme activities in response to hypercapnia occurred in red muscle. In white muscle, enzyme activities were temperature-compensated. CS activity in liver decreased after warm-normocapnia acclimation (temperature-compensation), while COX activities were lower after cold- and warm-hypercapnia exposure, but increased after warm-normocapnia acclimation. In conclusion, warm-acclimated N. rossii display low thermal compensation in response to rising energy demand in highly aerobic tissues, such as heart and red muscle. Chronic environmental hypercapnia elicits increased enzyme activities in these tissues, possibly to compensate for an elevated energy demand for acid-base regulation or a compromised mitochondrial metabolism, that is predicted to occur in response to hypercapnia exposure. This might be supported by enhanced metabolisation of liver energy stores. These patterns reflect a limited capacity of N. rossii to reorganise energy metabolism in response to rising temperature and PCO2. © 2013.

Influence of support material on the electrocatalytic activity of nickel oxide nanoparticles for urea electro-oxidation reaction.

PubMed

Abdel Hameed, R M; Medany, Shymaa S

2018-03-01

Nickel oxide nanoparticles were deposited on different carbon supports including activated Vulcan XC-72R carbon black (NiO/AC), multi-walled carbon nanotubes (NiO/MWCNTs), graphene (NiO/Gr) and graphite (NiO/Gt) through precipitation step followed by calcination at 400 °C. To determine the crystalline structure and morphology of prepared electrocatalysts, X-ray diffraction (XRD) and transmission electron microscopy (TEM) were employed. The electrocatalytic activity of NiO/carbon support electrocatalysts was investigated towards urea electro-oxidation reaction in NaOH solution using cyclic voltammetry, chronoamperometry and electrochemical impedance spectroscopy. Urea oxidation peak current density was increased in the following order: NiO/AC < NiO/MWCNTs < NiO/Gr < NiO/Gt. Chronoamperometry test also showed an increased steady state oxidation current density for NiO/Gt in comparison to other electrocatalysts. The increased activity and stability of NiO/Gt electrocatalyst encourage the application of graphite as an efficient and cost-saving support to carry metal nanoparticles for urea electro-oxidation reaction. Copyright © 2017 Elsevier Inc. All rights reserved.

Cathinone, an active principle of Catha edulis, accelerates oxidative stress in the limbic area of swiss albino mice.

PubMed

Safhi, Mohammed M; Alam, Mohammad Firoz; Hussain, Sohail; Hakeem Siddiqui, Mohammed Abdul; Khuwaja, Gulrana; Jubran Khardali, Ibrahim Abdu; Al-Sanosi, Rashad Mohammed; Islam, Fakhrul

2014-10-28

Cathinone hydrochloride is an active principle of the khat plant (Catha edulis) that produces pleasurable and stimulating effects in khat chewers. To the best of our knowledge no data of cathinone on oxidative stress in limbic areas of mice is available. This is the first study of cathinone on oxidative stress in limbic areas of the brain in Swiss albino male mice. The animals were divided into four groups. Group-I was the control group and received vehicle, while groups-II to IV received (-)-cathinone hydrochloride (0.125, 0.25 and 0.5 mg/kg body wt., i.p.) once daily for 15 days. The level of lipid peroxidation (LPO) was elevated dose-dependently and was significant (p<0.05, p<0.01) with doses of 0.25 and 0.5mg/kg body wt. of cathinone as compared to control group. In contrast, the content of reduced glutathione (GSH) was decreased significantly (p<0.01, p<0.001) with doses of 0.25 and 0.5mg/kg body wt. of cathinone as compared to control group. The activity of antioxidant enzymes (GPx, GR, GST, CAT, and SOD) was also decreased dose-dependently: the decreased activity of GPx, GR, catalase and SOD was significant with doses of 0.25 and 0.5 mg of cathinone as compared to control group, while the activity of GST was decreased dose-dependently and was significant with 0.5mg of cathinone as compared to control group. The results indicate that the cathinone generated oxidative stress hampered antioxidant enzymes, glutathione and lipid peroxidation. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

REPEATED REDUCTIVE AND OXIDATIVE TREATMENTS ON GRANULAR ACTIVATED CARBON

EPA Science Inventory

Fenton oxidation and Fenton oxidation preceded by reduction solutions were applied to granular activated carbon (GAC) to chemically regenerate the adsorbent. No adsorbate was present on the GAC so physicochemical effects from chemically aggressive regeneration of the carbon coul...

The role of FOXO and PPAR transcription factors in diet-mediated inhibition of PDC activation and carbohydrate oxidation during exercise in humans and the role of pharmacological activation of PDC in overriding these changes.

PubMed

Constantin-Teodosiu, Dumitru; Constantin, Despina; Stephens, Francis; Laithwaite, David; Greenhaff, Paul L

2012-05-01

High-fat feeding inhibits pyruvate dehydrogenase complex (PDC)-controlled carbohydrate (CHO) oxidation, which contributes to muscle insulin resistance. We aimed to reveal molecular changes underpinning this process in resting and exercising humans. We also tested whether pharmacological activation of PDC overrides these diet-induced changes. Healthy males consumed a control diet (CD) and on two further occasions an isocaloric high-fat diet (HFD). After each diet, subjects cycled for 60 min after intravenous infusion with saline (CD and HFD) or dichloroacetate (HFD+DCA). Quadriceps muscle biopsies obtained before and after 10 and 60 min of exercise were used to estimate CHO use, PDC activation, and mRNAs associated with insulin, fat, and CHO signaling. Compared with CD, HFD increased resting pyruvate dehydrogenase kinase 2 (PDK2), PDK4, forkhead box class O transcription factor 1 (FOXO1), and peroxisome proliferator-activated receptor transcription factor α (PPARα) mRNA and reduced PDC activation. Exercise increased PDC activation and whole-body CHO use in HFD, but to a lower extent than in CD. Meanwhile PDK4 and FOXO1, but not PPARα or PDK2, mRNA remained elevated. HFD+DCA activated PDC throughout and restored whole-body CHO use during exercise. FOXO1 appears to play a role in HFD-mediated muscle PDK4 upregulation and inhibition of PDC and CHO oxidation in humans. Also, pharmacological activation of PDC restores HFD-mediated inhibition of CHO oxidation during exercise.

Aerobic exercise training improves oxidative stress and ubiquitin proteasome system activity in heart of spontaneously hypertensive rats.

PubMed

de Andrade, Luiz Henrique Soares; de Moraes, Wilson Max Almeida Monteiro; Matsuo Junior, Eduardo Hiroshi; de Orleans Carvalho de Moura, Elizabeth; Antunes, Hanna Karen Moreira; Montemor, Jairo; Antonio, Ednei Luiz; Bocalini, Danilo Sales; Serra, Andrey Jorge; Tucci, Paulo José Ferreira; Brum, Patricia Chakur; Medeiros, Alessandra

2015-04-01

The activity of the ubiquitin proteasome system (UPS) and the level of oxidative stress contribute to the transition from compensated cardiac hypertrophy to heart failure in hypertension. Moreover, aerobic exercise training (AET) is an important therapy for the treatment of hypertension, but its effects on the UPS are not completely known. The aim of this study was to evaluate the effect of AET on UPS's activity and oxidative stress level in heart of spontaneously hypertensive rats (SHR). A total of 53 Wistar and SHR rats were randomly divided into sedentary and trained groups. The AET protocol was 5×/week in treadmill for 13 weeks. Exercise tolerance test, non-invasive blood pressure measurement, echocardiographic analyses, and left ventricle hemodynamics were performed during experimental period. The expression of ubiquitinated proteins, 4-hydroxynonenal (4-HNE), Akt, phospho-Akt(ser473), GSK3β, and phospho-GSK3β(ser9) were analyzed by western blotting. The evaluation of lipid hydroperoxide concentration was performed using the xylenol orange method, and the proteasomal chymotrypsin-like activity was measured by fluorimetric assay. Sedentary hypertensive group presented cardiac hypertrophy, unaltered expression of total Akt, phospho-Akt, total GSK3β and phospho-GSK3β, UPS hyperactivity, increased lipid hydroperoxidation as well as elevated expression of 4-HNE but normal cardiac function. In contrast, AET significantly increased exercise tolerance, decreased resting systolic blood pressure and heart rate in hypertensive animals. In addition, the AET increased phospho-Akt expression, decreased phospho-GSK3β, and did not alter the expression of total Akt, total GSK3β, and ubiquitinated proteins, however, significantly attenuated 4-HNE levels, lipid hydroperoxidation, and UPS's activity toward normotensive group levels. Our results provide evidence for the main effect of AET on attenuating cardiac ubiquitin proteasome hyperactivity and oxidative stress in SHR

High basal metabolic rate does not elevate oxidative stress during reproduction in laboratory mice.

PubMed

Brzęk, Paweł; Książek, Aneta; Ołdakowski, Łukasz; Konarzewski, Marek

2014-05-01

Increased oxidative stress (OS) has been suggested as a physiological cost of reproduction. However, previous studies reported ambiguous results, with some even showing a reduction of oxidative damage during reproduction. We tested whether the link between reproduction and OS is mediated by basal metabolic rate (BMR), which has been hypothesized to affect both the rate of radical oxygen species production and antioxidative capacity. We studied the effect of reproduction on OS in females of laboratory mice divergently selected for high (H-BMR) and low (L-BMR) BMR, previously shown to differ with respect to parental investment. Non-reproducing L-BMR females showed higher oxidative damage to lipids (quantified as the level of malondialdehyde in internal organ tissues) and DNA (quantified as the level of 8-oxodG in blood serum) than H-BMR females. Reproduction did not affect oxidative damage to lipids in either line; however, it reduced damage to DNA in L-BMR females. Reproduction increased catalase activity in liver (significantly stronger in L-BMR females) and decreased it in kidneys. We conclude that the effect of reproduction on OS depends on the initial variation in BMR and varies between studied internal organs and markers of OS.

Elevated atmospheric CO2 affected photosynthetic products in wheat seedlings and biological activity in rhizosphere soil under cadmium stress.

PubMed

Jia, Xia; Liu, Tuo; Zhao, Yonghua; He, Yunhua; Yang, Mingyan

2016-01-01

The objective of this study was to investigate the effects of elevated CO2 (700 ± 23 μmol mol(-1)) on photosynthetic products in wheat seedlings and on organic compounds and biological activity in rhizosphere soil under cadmium (Cd) stress. Elevated CO2 was associated with decreased quantities of reducing sugars, starch, and soluble amino acids, and with increased quantities of soluble sugars, total sugars, and soluble proteins in wheat seedlings under Cd stress. The contents of total soluble sugars, total free amino acids, total soluble phenolic acids, and total organic acids in the rhizosphere soil under Cd stress were improved by elevated CO2. Compared to Cd stress alone, the activity of amylase, phenol oxidase, urease, L-asparaginase, β-glucosidase, neutral phosphatase, and fluorescein diacetate increased under elevated CO2 in combination with Cd stress; only cellulase activity decreased. Bacterial abundance in rhizosphere soil was stimulated by elevated CO2 at low Cd concentrations (1.31-5.31 mg Cd kg(-1) dry soil). Actinomycetes, total microbial abundance, and fungi decreased under the combined conditions at 5.31-10.31 mg Cd kg(-1) dry soil. In conclusion, increased production of soluble sugars, total sugars, and proteins in wheat seedlings under elevated CO2 + Cd stress led to greater quantities of organic compounds in the rhizosphere soil relative to seedlings grown under Cd stress only. Elevated CO2 concentrations could moderate the effects of heavy metal pollution on enzyme activity and microorganism abundance in rhizosphere soils, thus improving soil fertility and the microecological rhizosphere environment of wheat under Cd stress.

Elevation of Plasma Cell-Free Hemoglobin in Pulmonary Arterial Hypertension

PubMed Central

Janz, David R.; Austin, Eric D.; Bastarache, Julie A.; Wheeler, Lisa A.; Ware, Lorraine B.; Hemnes, Anna R.

2014-01-01

BACKGROUND: Cell-free hemoglobin (CFH) is a potent nitric oxide scavenger associated with poor outcomes in several diseases. Pulmonary arterial hypertension (PAH) is characterized by reduced nitric oxide availability. We hypothesized that CFH would be elevated in PAH and would associate with hemodynamics and clinical outcomes. METHODS: We measured CFH in 200 consecutively evaluated patients with PAH, 16 unaffected bone morphogenetic receptor protein type 2 (BMPR2) mutation carriers, 19 healthy subjects, and 29 patients with pulmonary venous hypertension (PVH). CFH values were tested for association with hemodynamics, time to hospitalization, and death. RESULTS: CFH was elevated in patients with PAH and BMPR2 carriers compared with healthy subjects and patients with PVH (P ≤ .01 all comparisons). There were no differences in CFH across PAH subtypes. CFH modestly correlated with mean pulmonary artery pressure (ρ = 0.16, P = .03) and pulmonary vascular resistance (ρ = 0.21, P = .01) and inversely with cardiac index (ρ = −0.18, P = .02) in patients with PAH. CFH was not associated with hemodynamic response to nitric oxide or death. Patients with the highest CFH levels had increased risk of PAH-related hospitalization when adjusted for age, sex, and PAH cause (hazard ratio, 1.69; 95% CI ,1.08-2.66; P = .02). CONCLUSIONS: CFH is elevated in patients with PAH and BMPR2 carriers compared with healthy subjects and patients with PVH. Elevated CFH levels are independently associated with an increased risk of hospitalization. Further study is required to understand the mechanism of CFH elevation and the potential pathologic contribution of CFH in PAH. PMID:24945582

Paraoxonase Activity and Oxidative Status in Patients with Tinnitus

PubMed Central

Akyüz, Servet; Somuk, Battal Tahsin; Soyalic, Harun; Yılmaz, Beyhan; Taskin, Abdullah; Bilinc, Hasan; Aksoy, Nurten

2016-01-01

Background and Objectives The aim of this study was to investigate serum paraoxanase-1 (PON) activity, total oxidant status (TOS), total antioxidant status (TAS), and the oxidative stress index (OSI) in tinnitus; and to compare the results with data from healthy subjects. Subjects and Methods A total of 114 subjects-54 patients with tinnitus and 60 healthy controls were enrolled in this study. Serum PON activity, TOS, TAS, and OSI levels were measured. Results In the tinnitus group, TAS, and PON were significantly lower than in the control group (p<0.001). However, the TOS, and OSI levels were significantly higher in the tinnitus group than in the control group (p<0.001). Conclusions According to the data obtained from the present study, patients with tinnitus were exposed to potent oxidative stress. Oxidative stress may be the key contributing factor to the pathogenesis of tinnitus. PMID:27144229

Elevated ERK/p90 ribosomal S6 kinase activity underlies audiogenic seizure susceptibility in fragile X mice.

PubMed

Sawicka, Kirsty; Pyronneau, Alexander; Chao, Miranda; Bennett, Michael V L; Zukin, R Suzanne

2016-10-11

Fragile X syndrome (FXS) is the most common heritable cause of intellectual disability and a leading genetic form of autism. The Fmr1 KO mouse, a model of FXS, exhibits elevated translation in the hippocampus and the cortex. ERK (extracellular signal-regulated kinase) and mTOR (mechanistic target of rapamycin) signaling regulate protein synthesis by activating downstream targets critical to translation initiation and elongation and are known to contribute to hippocampal defects in fragile X. Here we show that the effect of loss of fragile X mental retardation protein (FMRP) on these pathways is brain region specific. In contrast to the hippocampus, ERK (but not mTOR) signaling is elevated in the neocortex of fragile X mice. Phosphorylation of ribosomal protein S6, typically a downstream target of mTOR, is elevated in the neocortex, despite normal mTOR activity. This is significant in that S6 phosphorylation facilitates translation, correlates with neuronal activation, and is altered in neurodevelopmental disorders. We show that in fragile X mice, S6 is regulated by ERK via the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by the site of elevated phosphorylation and the finding that ERK inhibition corrects elevated RSK and S6 activity. These findings indicate that signaling networks are altered in the neocortex of fragile X mice such that S6 phosphorylation receives aberrant input from ERK/RSK. Importantly, an RSK inhibitor reduces susceptibility to audiogenic seizures in fragile X mice. Our findings identify RSK as a therapeutic target for fragile X and suggest the therapeutic potential of drugs for the treatment of FXS may vary in a brain-region-specific manner.

KDM5 Interacts with Foxo to Modulate Cellular Levels of Oxidative Stress

PubMed Central

Liu, Xingyin; Greer, Christina; Secombe, Julie

2014-01-01

Increased cellular levels of oxidative stress are implicated in a large number of human diseases. Here we describe the transcription co-factor KDM5 (also known as Lid) as a new critical regulator of cellular redox state. Moreover, this occurs through a novel KDM5 activity whereby it alters the ability of the transcription factor Foxo to bind to DNA. Our microarray analyses of kdm5 mutants revealed a striking enrichment for genes required to regulate cellular levels of oxidative stress. Consistent with this, loss of kdm5 results in increased sensitivity to treatment with oxidizers, elevated levels of oxidized proteins, and increased mutation load. KDM5 activates oxidative stress resistance genes by interacting with Foxo to facilitate its recruitment to KDM5-Foxo co-regulated genes. Significantly, this occurs independently of KDM5's well-characterized demethylase activity. Instead, KDM5 interacts with the lysine deacetylase HDAC4 to promote Foxo deacetylation, which affects Foxo DNA binding. PMID:25329053

Production of the forskolin precursor 11β-hydroxy-manoyl oxide in yeast using surrogate enzymatic activities.

PubMed

Ignea, Codruta; Ioannou, Efstathia; Georgantea, Panagiota; Trikka, Fotini A; Athanasakoglou, Anastasia; Loupassaki, Sofia; Roussis, Vassilios; Makris, Antonios M; Kampranis, Sotirios C

2016-02-26

Several plant diterpenes have important biological properties. Among them, forskolin is a complex labdane-type diterpene whose biological activity stems from its ability to activate adenylyl cyclase and to elevate intracellular cAMP levels. As such, it is used in the control of blood pressure, in the protection from congestive heart failure, and in weight-loss supplements. Chemical synthesis of forskolin is challenging, and production of forskolin in engineered microbes could provide a sustainable source. To this end, we set out to establish a platform for the production of forskolin and related epoxy-labdanes in yeast. Since the forskolin biosynthetic pathway has only been partially elucidated, and enzymes involved in terpene biosynthesis frequently exhibit relaxed substrate specificity, we explored the possibility of reconstructing missing steps of this pathway employing surrogate enzymes. Using CYP76AH24, a Salvia pomifera cytochrome P450 responsible for the oxidation of C-12 and C-11 of the abietane skeleton en route to carnosic acid, we were able to produce the forskolin precursor 11β-hydroxy-manoyl oxide in yeast. To improve 11β-hydroxy-manoyl oxide production, we undertook a chassis engineering effort involving the combination of three heterozygous yeast gene deletions (mct1/MCT1, whi2/WHI2, gdh1/GDH1) and obtained a 9.5-fold increase in 11β-hydroxy-manoyl oxide titers, reaching 21.2 mg L(-1). In this study, we identify a surrogate enzyme for the specific and efficient hydroxylation of manoyl oxide at position C-11β and establish a platform that will facilitate the synthesis of a broad range of tricyclic (8,13)-epoxy-labdanes in yeast. This platform forms a basis for the heterologous production of forskolin and will facilitate the elucidation of subsequent steps of forskolin biosynthesis. In addition, this study highlights the usefulness of using surrogate enzymes for the production of intermediates of complex biosynthetic pathways. The combination of

Increased microglial catalase activity in multiple sclerosis grey matter.

PubMed

Gray, Elizabeth; Kemp, Kevin; Hares, Kelly; Redondo, Julianna; Rice, Claire; Scolding, Neil; Wilkins, Alastair

2014-04-22

Chronic demyelination, on-going inflammation, axonal loss and grey matter neuronal injury are likely pathological processes that contribute to disease progression in multiple sclerosis (MS). Although the precise contribution of each process and their aetiological substrates is not fully known, recent evidence has implicated oxidative damage as a major cause of tissue injury in MS. The degree of tissue injury caused by oxidative molecules, such as reactive oxygen species (ROS), is balanced by endogenous anti-oxidant enzymes which detoxify ROS. Understanding endogenous mechanisms which protect the brain against oxidative injury in MS is important, since enhancing anti-oxidant responses is a major therapeutic strategy for preventing irreversible tissue injury in the disease. Our aims were to determine expression and activity levels of the hydrogen peroxide-reducing enzyme catalase in MS grey matter (GM). In MS GM, a catalase enzyme activity was elevated compared to control GM. We measured catalase protein expression by immune dot-blotting and catalase mRNA by a real-time polymerase chain reaction (RT-PCR). Protein analysis studies showed a strong positive correlation between catalase and microglial marker IBA-1 in MS GM. In addition, calibration of catalase mRNA level with reference to the microglial-specific transcript AIF-1 revealed an increase in this transcript in MS. This was reflected by the extent of HLA-DR immunolabeling in MS GM which was significantly elevated compared to control GM. Collectively, these observations provide evidence that microglial catalase activity is elevated in MS grey matter and may be an important endogenous anti-oxidant defence mechanism in MS. Copyright © 2014 Elsevier B.V. All rights reserved.

Resveratrol induces expression of the slow, oxidative phenotype in mdx mouse muscle together with enhanced activity of the SIRT1-PGC-1α axis.

PubMed

Ljubicic, Vladimir; Burt, Matthew; Lunde, John A; Jasmin, Bernard J

2014-07-01

Slower, more oxidative muscle fibers are more resistant to the dystrophic pathology in Duchenne muscular dystrophy (DMD) patients as well as in the preclinical mdx mouse model of DMD. Therefore, one therapeutic strategy for DMD focuses on promoting expression of the slow, oxidative myogenic program. In the current study, we explored the therapeutic potential of stimulating the slow, oxidative phenotype in mdx mice by feeding 6-wk-old animals with the natural phenol resveratrol (RSV; ~100 mg·kg(-1)·day(-1)) for 6 wk. Sirtuin 1 (SIRT1) activity and protein levels increased significantly, as well as peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) activity, in the absence of alterations in AMPK signaling. These adaptations occurred concomitant with evidence of a fast, glycolytic, to slower, more oxidative fiber type conversion, including mitochondrial biogenesis and increased expression of slower myosin heavy chain isoforms. These positive findings raised the question of whether increased exposure to RSV would result in greater therapeutic benefits. We discovered that an elevated RSV dose of ~500 mg·kg(-1)·day(-1) across a duration of 12 wk was clearly less effective at muscle remodeling in mdx mice. This treatment protocol failed to influence SIRT1 or AMPK signaling and did not result in a shift towards a slower, more oxidative phenotype. Taken together, this study demonstrates that RSV can stimulate SIRT1 and PGC-1α activation, which in turn may promote expression of the slow, oxidative myogenic program in mdx mouse muscle. The data also highlight the importance of selecting an appropriate dosage regimen of RSV to maximize its potential therapeutic effectiveness for future application in DMD patients. Copyright © 2014 the American Physiological Society.

Resveratrol induces expression of the slow, oxidative phenotype in mdx mouse muscle together with enhanced activity of the SIRT1-PGC-1α axis

PubMed Central

Ljubicic, Vladimir; Burt, Matthew; Lunde, John A.

2014-01-01

Slower, more oxidative muscle fibers are more resistant to the dystrophic pathology in Duchenne muscular dystrophy (DMD) patients as well as in the preclinical mdx mouse model of DMD. Therefore, one therapeutic strategy for DMD focuses on promoting expression of the slow, oxidative myogenic program. In the current study, we explored the therapeutic potential of stimulating the slow, oxidative phenotype in mdx mice by feeding 6-wk-old animals with the natural phenol resveratrol (RSV; ∼100 mg·kg−1·day−1) for 6 wk. Sirtuin 1 (SIRT1) activity and protein levels increased significantly, as well as peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) activity, in the absence of alterations in AMPK signaling. These adaptations occurred concomitant with evidence of a fast, glycolytic, to slower, more oxidative fiber type conversion, including mitochondrial biogenesis and increased expression of slower myosin heavy chain isoforms. These positive findings raised the question of whether increased exposure to RSV would result in greater therapeutic benefits. We discovered that an elevated RSV dose of ∼500 mg·kg−1·day−1 across a duration of 12 wk was clearly less effective at muscle remodeling in mdx mice. This treatment protocol failed to influence SIRT1 or AMPK signaling and did not result in a shift towards a slower, more oxidative phenotype. Taken together, this study demonstrates that RSV can stimulate SIRT1 and PGC-1α activation, which in turn may promote expression of the slow, oxidative myogenic program in mdx mouse muscle. The data also highlight the importance of selecting an appropriate dosage regimen of RSV to maximize its potential therapeutic effectiveness for future application in DMD patients. PMID:24760981

Chronic mitochondrial uncoupling treatment prevents acute cold-induced oxidative stress in birds.

PubMed

Stier, Antoine; Massemin, Sylvie; Criscuolo, François

2014-12-01

Endotherms have evolved two major types of thermogenesis that allow them to actively produce heat in response to cold exposure, either through muscular activity (i.e. shivering thermogenesis) or through futile electro-chemical cycles (i.e. non-shivering thermogenesis). Amongst the latter, mitochondrial uncoupling is of key importance because it is suggested to drive heat production at a low cost in terms of oxidative stress. While this has been experimentally shown in mammals, the oxidative stress consequences of cold exposure and mitochondrial uncoupling are clearly less understood in the other class of endotherms, the birds. We compared metabolic and oxidative stress responses of zebra finches chronically treated with or without a chemical mitochondrial uncoupler (2,4-dinitrophenol: DNP), undergoing an acute (24 h) and a chronic (4 weeks) cold exposure (12 °C). We predicted that control birds should present at least a transient elevation of oxidative stress levels in response to cold exposure. This oxidative stress cost should be more pronounced in control birds than in DNP-treated birds, due to their lower basal uncoupling state. Despite similar increase in metabolism, control birds presented elevated levels of DNA oxidative damage in response to acute (but not chronic) cold exposure, while DNP-treated birds did not. Plasma antioxidant capacity decreased overall in response to chronic cold exposure. These results show that acute cold exposure increases oxidative stress in birds. However, uncoupling mitochondrial functioning appears as a putative compensatory mechanism preventing cold-induced oxidative stress. This result confirms previous observations in mice and underlines non-shivering thermogenesis as a putative key mechanism for endotherms in mounting a response to cold at a low oxidative cost.

Mangiferin attenuates oxidative stress induced renal cell damage through activation of PI3K induced Akt and Nrf-2 mediated signaling pathways.

PubMed

Saha, Sukanya; Sadhukhan, Pritam; Sinha, Krishnendu; Agarwal, Namrata; Sil, Parames C

2016-03-01

Mangiferin is a polyphenolic xanthonoid with remarkable antioxidant activity. Oxidative stress plays the key role in tert-butyl hydroperoxide (tBHP) induced renal cell damage. In this scenario, we consider mangiferin, as a safe agent in tBHP induced renal cell death and rationalize its action systematically, in normal human kidney epithelial cells (NKE). NKE cells were exposed to 20 µM mangiferin for 2 h followed by 50 µM tBHP for 18 h. The effect on endogenous ROS production, antioxidant status (antioxidant enzymes and thiols), mitochondrial membrane potential, apoptotic signaling molecules, PI3K mediated signaling cascades and cell cycle progression were examined using various biochemical assays, FACS and immunoblot analyses. tBHP exposure damaged the NKE cells and decreased its viability. It also elevated the intracellular ROS and other oxidative stress-related biomarkers within the cells. However, mangiferin dose dependently, exhibited significant protection against this oxidative cellular damage. Mangiferin inhibited tBHP induced activation of different pro-apoptotic signals and thus protected the renal cells against mitochondrial permeabilization. Further, mangiferin enhanced the expression of cell proliferative signaling cascade molecules, Cyclin d1, NFκB and antioxidant molecules HO-1, SOD2, by PI3K/Akt dependent pathway. However, the inhibitor of PI3K abolished mangiferin's protective activity. Results show Mangiferin maintains the intracellular anti-oxidant status, induces the expression of PI3K and its downstream molecules and shields NKE cells against the tBHP induced cytotoxicity. Mangiferin can be indicated as a therapeutic agent in oxidative stress-mediated renal toxicity. This protective action of mangiferin primarily attributes to its potent antioxidant and antiapoptotic nature.

Structure sensitivity in oxide catalysis: First-principles kinetic Monte Carlo simulations for CO oxidation at RuO 2(111)

DOE PAGES

Wang, Tongyu; Reuter, Karsten

2015-11-24

We present a density-functional theory based kinetic Monte Carlo study of CO oxidation at the (111) facet of RuO 2. We compare the detailed insight into elementary processes, steady-state surface coverages, and catalytic activity to equivalent published simulation data for the frequently studied RuO 2(110) facet. Qualitative differences are identified in virtually every aspect ranging from binding energetics over lateral interactions to the interplay of elementary processes at the different active sites. Nevertheless, particularly at technologically relevant elevated temperatures, near-ambient pressures and near-stoichiometric feeds both facets exhibit almost identical catalytic activity. As a result, these findings challenge the traditional definitionmore » of structure sensitivity based on macroscopically observable turnover frequencies and prompt scrutiny of the applicability of structure sensitivity classifications developed for metals to oxide catalysis.« less

Oxidative Processing Lowers the Ice Nucleation Activity of Birch and Alder Pollen

NASA Astrophysics Data System (ADS)

Gute, Ellen; Abbatt, Jonathan P. D.

2018-02-01

Pollen carry water extractable compounds with ice nucleating (IN) activity. This study investigates whether the hydroxyl radical, as the major atmospheric oxidant, can affect the IN activity of silver birch and grey alder subpollen particles under in-cloud conditions for deposition freezing mode conditions at 234 K. It is found that oxidation increases the supersaturation ratio with respect to ice necessary for the onset of ice nucleation and decreases the fraction of particles which initiate ice nucleation. This reduction of IN activity under equivalent oxidation conditions does not occur with a mineral dust sample (Arizona Test Dust). Chemical analysis of fresh and oxidized pollen material indicates a change of molecular structure with a loss of conjugation and an increase in oxidized functional groups, such as carbonyls. This is the first demonstration that in-cloud oxidation may lower the IN abilities of biological particles such as pollen.

Effect of elevated CO₂ on phosphorus nutrition of phosphate-deficient Arabidopsis thaliana (L.) Heynh under different nitrogen forms.

PubMed

Niu, Yaofang; Chai, Rushan; Dong, Huifen; Wang, Huan; Tang, Caixian; Zhang, Yongsong

2013-01-01

Phosphorus (P) nutrition is always a key issue regarding plants responses to elevated CO(2). Yet it is unclear of how elevated CO(2) affects P uptake under different nitrogen (N) forms. This study investigated the influence of elevated CO(2) (800 µl l(-1)) on P uptake and utilization by Arabidopsis grown in pH-buffered phosphate (P)-deficient (0.5 µM) hydroponic culture supplying with 2mM nitrate (NO(3)(-)) or ammonium (NH(4)(+)). After 7 d treatment, elevated CO(2) enhanced the biomass production of both NO(3)(-)- and NH(4) (+)-fed plants but decreased the P amount absorbed per weight of roots and the P concentration in the shoots of plants supplied with NH(4)(+). In comparison, elevated CO(2) increased the amount of P absorbed per weight of roots, as well as the P concentration in plants and alleviated P deficiency-induced symptoms of plants supplied with NO(3)(-). Elevated CO(2) also increased the root/shoot ratio, total root surface area, and acid phosphatase activity, and enhanced the expression of genes or transcriptional factors involving in P uptake, allocation and remobilization in P deficient plants. Furthermore, elevated CO(2) increased the nitric oxide (NO) level in roots of NO(3)(-)-fed plants but decreased it in NH(4)(+)-fed plants. NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) inhibited plant P acquisition by roots under elevated CO(2). Considering all of these findings, this study concluded that a combination of elevated CO(2) and NO(3)(-) nutrition can induce a set of plant adaptive strategies to improve P status from P-deficient soluble sources and that NO may be a signalling molecule that controls these processes.

Elevated CO2 and salinity are responsible for phenolics-enrichment in two differently pigmented lettuces.

PubMed

Sgherri, Cristina; Pérez-López, Usue; Micaelli, Francesco; Miranda-Apodaca, Jon; Mena-Petite, Amaia; Muñoz-Rueda, Alberto; Quartacci, Mike Frank

2017-06-01

Both salt stress and high CO 2 level, besides influencing secondary metabolism, can affect oxidative status of plants mainly acting in an opposite way with salinity provoking oxidative stress and elevated CO 2 alleviating it. The aim of the present work was to study the changes in the composition of phenolic acids and flavonoids as well as in the antioxidant activity in two differently pigmented lettuce cvs (green or red leaf) when submitted to salinity (200 mM NaCl) or elevated CO 2 (700 ppm) or to their combination in order to evaluate how a future global change can affect lettuce quality. Following treatments, the red cv. always maintained higher levels of antioxidant secondary metabolites as well as antioxidant activity, proving to be more responsive to altered environmental conditions than the green one. Overall, these results suggest that the application of moderate salinity or elevated CO 2 , alone or in combination, can induce the production of some phenolics that increase the health benefits of lettuce. In particular, moderate salinity was able to induce the synthesis of the flavonoids quercetin, quercetin-3-O-glucoside, quercetin-3-O-glucuronide and quercitrin. Phenolics-enrichment as well as a higher antioxidant capacity were also observed under high CO 2 with the red lettuce accumulating cyanidin, free chlorogenic acid, conjugated caffeic and ferulic acid as well as quercetin, quercetin-3-O-glucoside, quercetin-3-O-glucuronide, luteolin-7-O-glucoside, rutin, quercitrin and kaempferol. When salinity was present in combination with elevated CO 2 , reduction in yield was prevented and a higher presence of phenolic compounds, in particular luteolin, was observed compared to salinity alone. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Markers of oxidative stress and erythrocyte antioxidant enzyme activity in older men and women with differing physical activity.

PubMed

Rowiński, Rafał; Kozakiewicz, Mariusz; Kędziora-Kornatowska, Kornelia; Hübner-Woźniak, Elżbieta; Kędziora, Józef

2013-11-01

The aim of the present study was to examine the relationship between markers of oxidative stress and erythrocyte antioxidant enzyme activity and physical activity in older men and women. The present study included 481 participants (233 men and 248 women) in the age group 65-69 years (127 men and 125 women) and in the age group 90 years and over (106 men and 123 women). The classification of respondents by physical activity was based on answers to the question if, in the past 12 months, they engaged in any pastimes which require physical activity. The systemic oxidative stress status was assessed by measuring plasma iso-PGF2α and protein carbonyl concentration as well as erythrocyte antioxidant enzymes activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR). The concentration of plasma iso-PGF2α and protein carbonyls (CP) was lower in groups of younger men and women compared to the respective older groups. In all examined groups, physical activity resulted in decrease of these oxidative stress markers and simultaneously caused adaptive increase in the erythrocyte SOD activity. Additionally, in active younger men CAT, GPx, and GR activities were higher than in sedentary ones. In conclusion, oxidative stress increase is age-related, but physical activity can reduce oxidative stress markers and induce adaptive increase in the erythrocyte antioxidant enzyme activity, especially SOD, even in old and very old men and women. © 2013.

Synthesis-Structure-Activity Relationships in Co3O4 Catalyzed CO Oxidation

NASA Astrophysics Data System (ADS)

Mingle, Kathleen; Lauterbach, Jochen

2018-05-01

In this work, a statistical design and analysis platform was used to develop cobalt oxide based oxidation catalysts prepared via one pot metal salt reduction. An emphasis was placed upon understanding the effects of synthesis conditions, such as heating regimen and Co2+ concentration on the metal salt reduction mechanism, the resultant nanomaterial properties (i.e. size, crystal structure, and crystal faceting), and the catalytic activity in CO oxidation. This was accomplished by carrying out XRD, TEM, and FTIR studies on synthesis intermediates and products. Additionally, high-throughput experimentation was employed to study the performance of Co3O4 oxidation catalysts over a wide range of reaction conditions using a 16-channel fixed bed reactor equipped with a parallel infrared imaging system. Specifically, Co3O4 nanomaterials of varying properties were evaluated for their performance as CO oxidation catalysts. Figure-of-merits including light-off temperatures and activation energies were measured and mapped back to the catalyst properties and synthesis conditions. Statistical analysis methods were used to elucidate significant property-activity relationships as well as the design rules relevant in the synthesis of active catalysts. It was found that CO oxidation light off temperatures could be decreased to <90°C by utilizing the discovered synthesis-structure-activity relationships.

Immune activity elevates energy expenditure of house sparrows: a link between direct and indirect costs?

PubMed Central

Martin, Lynn B; Scheuerlein, Alex; Wikelski, Martin

2003-01-01

The activation of an immune response is beneficial for organisms but may also have costs that affect fitness. Documented immune costs include those associated with acquisition of special nutrients, as well as immunopathology or autoimmunity. Here, we test whether an experimental induction of the immune system with a non-pathological stimulant can elevate energy turnover in passerine birds. We injected phytohaemagglutinin (PHA), a commonly used mitogen that activates the cell-mediated immune response, into the wing web of house sparrows, Passer domesticus. We then examined energetic costs resulting from this immune activity and related those costs to other physiological activities. We found that PHA injection significantly elevated resting metabolic rate (RMR) of challenged sparrows relative to saline controls. We calculated the total cost of this immune activity to be ca. 4.20 kJ per day (29% RMR), which is equivalent to the cost of production of half of an egg (8.23 kJ egg(-1)) in this species. We suggest that immune activity in wild passerines increases energy expenditure, which in turn may influence important life-history characteristics such as clutch size, timing of breeding or the scheduling of moult. PMID:12590753

Oxidative Burst of Circulating Neutrophils Following Traumatic Brain Injury in Human

PubMed Central

Liao, Yiliu; Liu, Peng; Guo, Fangyuan; Zhang, Zhi-Yuan; Zhang, Zhiren

2013-01-01

Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes, particularly focusing on neutrophils, from TBI subjects and control subjects with general trauma from 6 hours to 2 weeks following injury, comparing with values from uninjured subjects. We observed increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP, dramatically increased circulating leukocyte counts and elevated expression of TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a systemic inflammatory response following TBI. Our data further showed increased free radical production in leukocyte homogenates and elevated expression of key oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91phox) in circulating leukocytes, indicating an intense induction of oxidative burst following TBI, which is significantly greater than that in control subjects with general trauma. Furthermore, flow cytometry assay proved neutrophils as the largest population in circulation after TBI and showed significantly up-regulated oxidative activity and suppressed phagocytosis rate for circulating neutrophils following brain trauma. It suggests that the highly activated neutrophils might play an important role in the secondary damage, even outside the injured brain. Taken together, the potent systemic inflammatory response induced by TBI, especially the intensively increase oxidative activity of circulating leukocytes, mainly neutrophils, may lead to a systemic damage, dysfunction/damage of bystander tissues/organs and even further exacerbate secondary local damage. Controlling these pathophysiological processes may be a promising therapeutic strategy and will protect unaffected organs and the

Honey Supplementation in Spontaneously Hypertensive Rats Elicits Antihypertensive Effect via Amelioration of Renal Oxidative Stress

PubMed Central

Erejuwa, Omotayo O.; Sulaiman, Siti A.; Ab Wahab, Mohd S.; Sirajudeen, Kuttulebbai N. S.; Salleh, Salzihan; Gurtu, Sunil

2012-01-01

Oxidative stress is implicated in the pathogenesis and/or maintenance of elevated blood pressure in hypertension. This study investigated the effect of honey on elevated systolic blood pressure (SBP) in spontaneously hypertensive rats (SHR). It also evaluated the effect of honey on the amelioration of oxidative stress in the kidney of SHR as a possible mechanism of its antihypertensive effect. SHR and Wistar Kyoto (WKY) rats were randomly divided into 2 groups and administered distilled water or honey by oral gavage once daily for 12 weeks. The control SHR had significantly higher SBP and renal malondialdehyde (MDA) levels than did control WKY. The mRNA expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione S-transferase (GST) were significantly downregulated while total antioxidant status (TAS) and activities of GST and catalase (CAT) were higher in the kidney of control SHR. Honey supplementation significantly reduced SBP and MDA levels in SHR. Honey significantly reduced the activities of GST and CAT while it moderately but insignificantly upregulated the Nrf2 mRNA expression level in the kidney of SHR. These results indicate that Nrf2 expression is impaired in the kidney of SHR. Honey supplementation considerably reduces elevated SBP via amelioration of oxidative stress in the kidney of SHR. PMID:22315654

Honey supplementation in spontaneously hypertensive rats elicits antihypertensive effect via amelioration of renal oxidative stress.

PubMed

Erejuwa, Omotayo O; Sulaiman, Siti A; Ab Wahab, Mohd S; Sirajudeen, Kuttulebbai N S; Salleh, Salzihan; Gurtu, Sunil

2012-01-01

Oxidative stress is implicated in the pathogenesis and/or maintenance of elevated blood pressure in hypertension. This study investigated the effect of honey on elevated systolic blood pressure (SBP) in spontaneously hypertensive rats (SHR). It also evaluated the effect of honey on the amelioration of oxidative stress in the kidney of SHR as a possible mechanism of its antihypertensive effect. SHR and Wistar Kyoto (WKY) rats were randomly divided into 2 groups and administered distilled water or honey by oral gavage once daily for 12 weeks. The control SHR had significantly higher SBP and renal malondialdehyde (MDA) levels than did control WKY. The mRNA expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione S-transferase (GST) were significantly downregulated while total antioxidant status (TAS) and activities of GST and catalase (CAT) were higher in the kidney of control SHR. Honey supplementation significantly reduced SBP and MDA levels in SHR. Honey significantly reduced the activities of GST and CAT while it moderately but insignificantly upregulated the Nrf2 mRNA expression level in the kidney of SHR. These results indicate that Nrf2 expression is impaired in the kidney of SHR. Honey supplementation considerably reduces elevated SBP via amelioration of oxidative stress in the kidney of SHR.

Gender differences between muscle activation and onset timing of the four subdivisions of trapezius during humerothoracic elevation.

PubMed

Szucs, Kimberly A; Borstad, John D

2013-12-01

The aim of this study was to provide a description of gender differences of the normal muscle activation patterns of the four subdivisions of the trapezius (clavicular, descending, transverse, ascending) during arm elevation. Surface EMG was collected from these four subdivisions from twenty-two healthy subjects (12 females, 10 males) during arm elevation in the scapular plane. Percent activation (RMS) of each subdivision was compared between genders across arm angles and elevation phase and onset time of each subdivision was compared between genders. Females demonstrated significantly higher % activation levels for each subdivision (p<.05), except transverse trapezius (p=.36). A statistically significant difference for onset time was observed between gender for the descending trapezius, with a slower onset time for females (p<.05). Findings from this study support the theory that subdivisions within descending trapezius are preferentially activated and demonstrate that gender differences are present within the fourth subdivision of trapezius. As subjects were without shoulder pathology, the observed gender differences may be explained by normal motor control variations. However, as coordinated activation of trapezius is required for normal shoulder motion, it is recommended to include all four subdivisions of trapezius and address gender differences in future studies. Copyright © 2013 Elsevier B.V. All rights reserved.

Triiodothyronine activates lactate oxidation without impairing fatty acid oxidation and improves weaning from extracorporeal membrane oxygenation.

PubMed

Kajimoto, Masaki; Ledee, Dolena R; Xu, Chun; Kajimoto, Hidemi; Isern, Nancy G; Portman, Michael A

2014-01-01

Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. It has previously been shown that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. METHODS AND RESULTS: Nineteen immature piglets (9.1-15.3 kg) were separated into 3 groups with ECMO (6.5 h) and wean: normal circulation (Group-C); transient coronary occlusion (10 min) for ischemia-reperfusion (IR) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon ((13)C)-labeled lactate, medium-chain and long-chain FAs, was infused as oxidative substrates. Substrate fractional contribution (FC) to the citric acid cycle was analyzed by(13)C-nuclear magnetic resonance. ECMO depressed circulating T3 levels to 40% of the baseline at 4 h and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [adenosine triphosphate]/[adenosine diphosphate] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. T3 releases inhibition of lactate oxidation following IR injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning.

Effects of far infrared rays irradiated from ceramic material (BIOCERAMIC) on psychological stress-conditioned elevated heart rate, blood pressure, and oxidative stress-suppressed cardiac contractility.

PubMed

Leung, Ting-Kai; Chen, Chien-Ho; Tsai, Shih-Ying; Hsiao, George; Lee, Chi-Ming

2012-10-31

The present study examined the effects of BIOCERAMIC on psychological stress-conditioned elevated heart rate, blood pressure and oxidative stress-suppressed cardiac contractility using in vivo and in vitro animal models. We investigated the effects of BIOCERAMIC on the in vivo cardiovascular hemodynamic parameters of rats by monitoring their heart rates, systolic blood pressure, mean blood pressure and diastolic blood pressure. Thereafter, we assayed its effects on the heart rate in an isolated frog heart with and without adrenaline stimulation, and on cardiac contractility under oxidative stress. BIOCERAMIC caused significant decreases in heart rates and systolic and mean blood pressure in the stress-conditioned heart rate rat models (P < 0.05), as well as in the experimental models of an isolated frog heart with and without adrenaline stimulation (P < 0.05), and normalized cardiac contractility under oxidative stress (P < 0.05). BIOCERAMIC may, therefore, normalize the effects of psychological stress and oxidative stress conditions.

Lung injury-dependent oxidative status and chymotrypsin-like activity of skeletal muscles in hamsters with experimental emphysema.

PubMed

Tonon, Jair; Cecchini, Alessandra Lourenço; Brunnquell, Cláudia Roberta; Bernardes, Sara Santos; Cecchini, Rubens; Guarnier, Flávia Alessandra

2013-01-23

Peripheral skeletal muscle is altered in patients suffering from emphysema and chronic obstructive pulmonary disease (COPD). Oxidative stress have been demonstrated to participate on skeletal muscle loss of several states, including disuse atrophy, mechanical ventilation, and chronic diseases. No evidences have demonstrated the occurance in a severity manner. We evaluated body weight, muscle loss, oxidative stress, and chymotrypsin-like proteolytic activity in the gastrocnemius muscle of emphysemic hamsters. The experimental animals had 2 different severities of lung damage from experimental emphysema induced by 20 mg/mL (E20) and 40 mg/mL (E40) papain. The severity of emphysema increased significantly in E20 (60.52 ± 2.8, p < 0.05) and E40 (52.27 ± 4.7; crossed the alveolar intercepts) groups. As compared to the control group, there was a reduction on body (171.6 ± 15.9 g) and muscle weight (251.87 ± 24.87 mg) in the E20 group (157.5 ± 10.3 mg and 230.12 ± 23.52 mg, for body and muscle weight, respectively), which was accentuated in the E40 group (137.4 ± 7.2 g and 197.87 ± 10.49 mg, for body and muscle weight, respectively). Additionally, the thiobarbituric acid reactive substances (TBARS), tert-butyl hydroperoxide-initiated chemiluminescence (CL), carbonylated proteins, and chymotrypsin-like proteolytic activity were elevated in the E40 group as compared to the E20 group (p < 0.05 for all comparisons). The severity of emphysema significantly correlated with the progressive increase in CL (r = -0.95), TBARS (r = -0.98), carbonyl proteins (r = -0.99), and chymotrypsin-like proteolytic activity (r = -0.90). Furthermore, augmentation of proteolytic activity correlated significantly with CL (r = 0.97), TBARS (r = 0.96), and carbonyl proteins (r = 0.91). Taken together, the results of the present study suggest that muscle atrophy observed in this model of emphysema is mediated by increased muscle chymotrypsin-like activity, with possible involvement of

Structure sensitivity in oxide catalysis: First-principles kinetic Monte Carlo simulations for CO oxidation at RuO{sub 2}(111)

DOE Office of Scientific and Technical Information (OSTI.GOV)

Wang, Tongyu; Reuter, Karsten, E-mail: karsten.reuter@ch.tum.de; SUNCAT Center for Interface Science and Catalysis, SLAC National Accelerator Laboratory and Stanford University, 443 Via Ortega, Stanford, California 94035-4300

2015-11-28

We present a density-functional theory based kinetic Monte Carlo study of CO oxidation at the (111) facet of RuO{sub 2}. We compare the detailed insight into elementary processes, steady-state surface coverages, and catalytic activity to equivalent published simulation data for the frequently studied RuO{sub 2}(110) facet. Qualitative differences are identified in virtually every aspect ranging from binding energetics over lateral interactions to the interplay of elementary processes at the different active sites. Nevertheless, particularly at technologically relevant elevated temperatures, near-ambient pressures and near-stoichiometric feeds both facets exhibit almost identical catalytic activity. These findings challenge the traditional definition of structure sensitivitymore » based on macroscopically observable turnover frequencies and prompt scrutiny of the applicability of structure sensitivity classifications developed for metals to oxide catalysis.« less

Elevation of Glutathione as a Therapeutic Strategy in Alzheimer Disease

PubMed Central

Pocernich, Chava B.; Butterfield, D. Allan

2011-01-01

Oxidative stress has been associated with the onset and progression of mild cognitive impairment (MCI) and Alzheimer disease (AD). AD and MCI brain and plasma display extensive oxidative stress as indexed by protein oxidation, lipid peroxidation, free radical formation, DNA oxidation, and decreased antioxidants. The most abundant endogenous antioxidant, glutathione, plays a significant role in combating oxidative stress. The ratio of oxidized to reduced glutathione is utilized as a measure of intensity of oxidative stress. Antioxidants have long been considered as an approach to slow down AD progression. In this review, we focus on the elevation on glutathione through N-acytl-cysteine (NAC) and γ-glutamylcysteine ethyl ester (GCEE) as a potential therapeutic approach for Alzheimer disease. PMID:22015471

Pharmacologic activation of peroxisome proliferator-activating receptor-α accelerates hepatic fatty acid oxidation in neonatal pigs

PubMed Central

Shim, Kwanseob; Jacobi, Sheila; Odle, Jack; Lin, Xi

2018-01-01

Up-regulation of peroxisome proliferator-activating receptor-α (PPARα) and increasing fatty acid oxidation are important for reducing pre-weaning mortality of pigs. We examined the time-dependent regulatory effects of PPARα activation via oral postnatal clofibrate administration (75 mg/(kg-BW·d) for up to 7 days) on mitochondrial and peroxisomal fatty acid oxidation in pigs, a species with limited hepatic fatty acid oxidative capacity due to low ketogenesis. Hepatic oxidation was increased by 44-147% (depending on fatty acid chain-length) and was attained after only 4 days of clofibrate treatment. Acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase I (CPTI) activities accelerated in parallel. The increase in CPTI activity was accompanied by a rapid reduction in the sensitivity of CPTI to malonyl-CoA inhibition. The mRNA abundance of CPTI and ACO, as well as peroxisomal keto-acyl-CoA thiolase (KetoACoA) and mitochondrial malonyl-CoA decarboxylase (MCD), also were augmented greatly. However, the increase in ACO activity and MCD expression were different from CPTI, and significant interactions were observed between postnatal age and clofibrate administration. Furthermore, the expression of acetyl-CoA carboxylase β (ACCβ) decreased with postnatal age and clofibrate had no effect on its expression. Collectively these results demonstrate that the expression of PPARα target genes and the increase in fatty acid oxidation induced by clofibrate are time- and age-dependent in the liver of neonatal pigs. Although the induction patterns of CPTI, MCD, ACO, KetoACoA, and ACCβ are different during the early postnatal period, 4 days of exposure to clofibrate were sufficient to robustly accelerate fatty acid oxidation.

Activated Rho Kinase Mediates Diabetes-Induced Elevation of Vascular Arginase Activation and Contributes to Impaired Corpora Cavernosa Relaxation: Possible Involvement of p38 MAPK Activation

PubMed Central

Nunes, Kenia P.; Yao, Lin; Liao, James K.; Webb, R. Clinton; Caldwell, Ruth B.; Caldwell, R. William

2013-01-01

Introduction Activated RhoA/Rho kinase (ROCK) has been implicated in diabetes-induced erectile dysfunction. Earlier studies have demonstrated involvement of ROCK pathway in the activation of arginase in endothelial cells. However, signaling pathways activated by ROCK in the penis remain unclear. Aim We tested whether ROCK and p38 MAPK are involved in the elevation of arginase activity and subsequent impairment of corpora cavernosal (CC) relaxation in diabetes. Methods Eight weeks after streptozotocin-induced diabetes, vascular functional studies, arginase activity assay, and protein expression of RhoA, ROCK, phospho-p38 MAPK, p38 MAPK, phospho-MYPT-1Thr850, MYPT-1 and arginase levels were assessed in CC tissues from nondiabetic wild type (WT), diabetic (D) WT (WT + D), partial ROCK 2+/− knockout (KO), and ROCK 2+/− KO + D mice. Main Outcome Measures The expression of RhoA, ROCK 1 and 2, phosphorylation of MYPT-1Thr850 and p38 MAPK, arginase activity/expression, endothelial- and nitrergic-dependent relaxation of CC was assayed. Results Diabetes significantly reduced maximum relaxation (Emax) to both endothelium-dependent acetylcholine (WT + D: Emax; 61 ± 4% vs. WT: Emax; 75 ± 2%) and nitrergic nerve stimulation. These effects were associated with increased expression of active RhoA, ROCK 2, phospho-MYPT-1Thr850, phospho-p38 MAPK, arginase II, and activity of corporal arginase (1.6-fold) in WT diabetic CC. However, this impairment in CC of WT + D mice was absent in heterozygous ROCK 2+/− KO + D mice for acetylcholine (Emax: 80 ± 5%) and attenuated for nitrergic nerve-induced relaxation. CC of ROCK 2+/− KO + D mice showed much less ROCK activity, did not exhibit p38 MAPK activation, and had reduced arginase activity and arginase II expression. These findings indicate that ROCK 2 mediates diabetes-induced elevation of arginase activity. Additionally, pretreatment of WT diabetic CC with inhibitors of arginase (ABH) or p38 MAPK (SB203580) partially prevented

Arginase activity and nitric oxide levels in patients with obstructive sleep apnea syndrome

PubMed Central

Yüksel, Meral; Okur, Hacer Kuzu; Pelin, Zerrin; Öğünç, Ayliz Velioğlu; Öztürk, Levent

2014-01-01

OBJECTIVE: Obstructive sleep apnea syndrome is characterized by repetitive obstruction of the upper airways, and it is a risk factor for cardiovascular diseases. There have been several studies demonstrating low levels of nitric oxide in patients with obstructive sleep apnea syndrome compared with healthy controls. In this study, we hypothesized that reduced nitric oxide levels would result in high arginase activity. Arginase reacts with L-arginine and produces urea and L-ornithine, whereas L-arginine is a substrate for nitric oxide synthase, which produces nitric oxide. METHODS: The study group consisted of 51 obstructive sleep apnea syndrome patients (M/F: 43/8; mean age 49±10 years of age) and 15 healthy control subjects (M/F: 13/3; mean age 46±14 years of age). Obstructive sleep apnea syndrome patients were divided into two subgroups based on the presence or absence of cardiovascular disease. Nitric oxide levels and arginase activity were measured via an enzyme-linked immunosorbent assay of serum samples. RESULTS: Serum nitric oxide levels in the control subjects were higher than in the obstructive sleep apnea patients with and without cardiovascular diseases (p<0.05). Arginase activity was significantly higher (p<0.01) in obstructive sleep apnea syndrome patients without cardiovascular diseases compared with the control group. Obstructive sleep apnea syndrome patients with cardiovascular diseases had higher arginase activity than the controls (p<0.001) and the obstructive sleep apnea syndrome patients without cardiovascular diseases (p<0.05). CONCLUSION: Low nitric oxide levels are associated with high arginase activity. The mechanism of nitric oxide depletion in sleep apnea patients suggests that increased arginase activity might reduce the substrate availability of nitric oxide synthase and thus could reduce nitric oxide levels. PMID:24714832

Oxidative esterification via photocatalytic C-H activation

EPA Science Inventory

Direct oxidative esterification of alcohol via photocatalytic C-H activation has been developed using VO@g-C3N4 catalyst; an expeditious esterification of alcohols occurs under neutral conditions using visible light as the source of energy.

Profound regulation of Na/K pump activity by transient elevations of cytoplasmic calcium in murine cardiac myocytes

PubMed Central

Lu, Fang-Min; Deisl, Christine; Hilgemann, Donald W

2016-01-01

Small changes of Na/K pump activity regulate internal Ca release in cardiac myocytes via Na/Ca exchange. We now show conversely that transient elevations of cytoplasmic Ca strongly regulate cardiac Na/K pumps. When cytoplasmic Na is submaximal, Na/K pump currents decay rapidly during extracellular K application and multiple results suggest that an inactivation mechanism is involved. Brief activation of Ca influx by reverse Na/Ca exchange enhances pump currents and attenuates current decay, while repeated Ca elevations suppress pump currents. Pump current enhancement reverses over 3 min, and results are similar in myocytes lacking the regulatory protein, phospholemman. Classical signaling mechanisms, including Ca-activated protein kinases and reactive oxygen, are evidently not involved. Electrogenic signals mediated by intramembrane movement of hydrophobic ions, such as hexyltriphenylphosphonium (C6TPP), increase and decrease in parallel with pump currents. Thus, transient Ca elevation and Na/K pump inactivation cause opposing sarcolemma changes that may affect diverse membrane processes. DOI: http://dx.doi.org/10.7554/eLife.19267.001 PMID:27627745

Elevated circulating soluble thrombomodulin activity, tissue factor activity and circulating procoagulant phospholipids: new and useful markers for pre-eclampsia?

PubMed

Rousseau, Aurélie; Favier, Rémi; Van Dreden, Patrick

2009-09-01

One of the most frequently proposed mechanisms for pre-eclampsia refers to uteroplacental thrombosis. However, the contribution of classical thrombotic risk factors remains questionable. The aims of this study were to investigate the activities of thrombomodulin, tissue factor and procoagulant phospholipids to assess endothelial cell injury in pregnant women with pre-eclampsia and to compare them with other classical markers of vascular injury and thrombotic risk. Using three new functional assays we studied the plasma levels of these new markers in 35 healthy women, 30 healthy pregnant women, and 35 women with pre-eclampsia. We found that plasma levels of thrombomodulin activity, tissue factor activity and procoagulant phospholipids were significantly elevated in women with pre-eclampsia versus normal pregnant and non-pregnant women. It is thus suggested that elevated levels of these parameters in pre-eclampsia may reflect vascular endothelium damage, and may be a more valuable biomarker than antigen for the assessment of endothelial damage in pre-eclampsia. The high increased levels of procoagulant phospholipids and tissue factor activities in pre-eclampsia could suggest that the procoagulant potential may be implicated in this complication and makes these markers very promising for the understanding, follow-up and therapeutic handling of complicated pregnancy.

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

PubMed Central

Han, Ye; Xu, Qi; Hu, Jiang-ning; Han, Xin-yue; Li, Wei; Zhao, Li-chun

2015-01-01

The purpose of this study was to evaluate the hepatoprotective effect of maltol, a food-flavoring agent, on alcohol-induced acute oxidative damage in mice. Maltol used in this study was isolated from red ginseng (Panax ginseng C.A Meyer) and analyzed by high performance liquid chromatography (HPLC) and mass spectrometry. For hepatoprotective activity in vivo, pretreatment with maltol (12.5, 25 and 50 mg/kg; 15 days) drastically prevented the elevated activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and triglyceride (TG) in serum and the levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) in liver tissue (p < 0.05). Meanwhile, the levels of hepatic antioxidant, such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were elevated by maltol pretreatment, compared to the alcohol group (p < 0.05). Histopathological examination revealed that maltol pretreatment significantly inhibited alcohol-induced hepatocyte apoptosis and fatty degeneration. Interestingly, pretreatment of maltol effectively relieved alcohol-induced oxidative damage in a dose-dependent manner. Maltol appeared to possess promising anti-oxidative and anti-inflammatory capacities. It was suggested that the hepatoprotective effect exhibited by maltol on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties. PMID:25608939

How to stabilize highly active Cu + cations in a mixed-oxide catalyst

DOE Office of Scientific and Technical Information (OSTI.GOV)

Mudiyanselage, Kumudu; Luo, Si; Kim, Hyun You

Mixed-metal oxides exhibit novel properties that are not present in their isolated constituent metal oxides and play a significant role in heterogeneous catalysis. In this study, a titanium-copper mixed-oxide (TiCuO x) film has been synthesized on Cu(111) and characterized by complementary experimental and theoretical methods. At sub-monolayer coverages of titanium, a Cu 2O-like phase coexists with TiCuO x and TiO x domains. When the mixed-oxide surface is exposed at elevated temperatures (600–650 K) to oxygen, the formation of a well-ordered TiCuO x film occurs. Stepwise oxidation of TiCuO x shows that the formation of the mixed-oxide is faster than thatmore » of pure Cu 2O. As the Ti coverage increases, Ti-rich islands (TiO x) form. The adsorption of CO has been used to probe the exposed surface sites on the TiO x–CuO x system, indicating the existence of a new Cu + adsorption site that is not present on Cu 2O/Cu(111). Adsorption of CO on Cu + sites of TiCuO x is thermally more stable than on Cu(111), Cu 2O/Cu(111) or TiO 2(110). The Cu + sites in TiCuO x domains are stable under both reducing and oxidizing conditions whereas the Cu 2O domains present on sub-monolayer loads of Ti can be reduced or oxidized under mild conditions. Furthermore, the results presented here demonstrate novel properties of TiCuO x films, which are not present on Cu(111), Cu 2O/Cu(111), or TiO 2(110), and highlight the importance of the preparation and characterization of well-defined mixed-metal oxides in order to understand fundamental processes that could guide the design of new materials.« less

How to stabilize highly active Cu + cations in a mixed-oxide catalyst

DOE PAGES

Mudiyanselage, Kumudu; Luo, Si; Kim, Hyun You; ...

2015-09-12

Mixed-metal oxides exhibit novel properties that are not present in their isolated constituent metal oxides and play a significant role in heterogeneous catalysis. In this study, a titanium-copper mixed-oxide (TiCuO x) film has been synthesized on Cu(111) and characterized by complementary experimental and theoretical methods. At sub-monolayer coverages of titanium, a Cu 2O-like phase coexists with TiCuO x and TiO x domains. When the mixed-oxide surface is exposed at elevated temperatures (600–650 K) to oxygen, the formation of a well-ordered TiCuO x film occurs. Stepwise oxidation of TiCuO x shows that the formation of the mixed-oxide is faster than thatmore » of pure Cu 2O. As the Ti coverage increases, Ti-rich islands (TiO x) form. The adsorption of CO has been used to probe the exposed surface sites on the TiO x–CuO x system, indicating the existence of a new Cu + adsorption site that is not present on Cu 2O/Cu(111). Adsorption of CO on Cu + sites of TiCuO x is thermally more stable than on Cu(111), Cu 2O/Cu(111) or TiO 2(110). The Cu + sites in TiCuO x domains are stable under both reducing and oxidizing conditions whereas the Cu 2O domains present on sub-monolayer loads of Ti can be reduced or oxidized under mild conditions. Furthermore, the results presented here demonstrate novel properties of TiCuO x films, which are not present on Cu(111), Cu 2O/Cu(111), or TiO 2(110), and highlight the importance of the preparation and characterization of well-defined mixed-metal oxides in order to understand fundamental processes that could guide the design of new materials.« less

Constitutively Elevated Salicylic Acid Levels Alter Photosynthesis and Oxidative State but Not Growth in Transgenic Populus[C][W

PubMed Central

Xue, Liang-Jiao; Guo, Wenbing; Yuan, Yinan; Anino, Edward O.; Nyamdari, Batbayar; Wilson, Mark C.; Frost, Christopher J.; Chen, Han-Yi; Babst, Benjamin A.; Harding, Scott A.; Tsai, Chung-Jui

2013-01-01

Salicylic acid (SA) has long been implicated in plant responses to oxidative stress. SA overproduction in Arabidopsis thaliana leads to dwarfism, making in planta assessment of SA effects difficult in this model system. We report that transgenic Populus tremula × alba expressing a bacterial SA synthase hyperaccumulated SA and SA conjugates without negative growth consequences. In the absence of stress, endogenously elevated SA elicited widespread metabolic and transcriptional changes that resembled those of wild-type plants exposed to oxidative stress-promoting heat treatments. Potential signaling and oxidative stress markers azelaic and gluconic acids as well as antioxidant chlorogenic acids were strongly coregulated with SA, while soluble sugars and other phenylpropanoids were inversely correlated. Photosynthetic responses to heat were attenuated in SA-overproducing plants. Network analysis identified potential drivers of SA-mediated transcriptome rewiring, including receptor-like kinases and WRKY transcription factors. Orthologs of Arabidopsis SA signaling components NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 and thioredoxins were not represented. However, all members of the expanded Populus nucleoredoxin-1 family exhibited increased expression and increased network connectivity in SA-overproducing Populus, suggesting a previously undescribed role in SA-mediated redox regulation. The SA response in Populus involved a reprogramming of carbon uptake and partitioning during stress that is compatible with constitutive chemical defense and sustained growth, contrasting with the SA response in Arabidopsis, which is transient and compromises growth if sustained. PMID:23903318

Persulfate Oxidation Regeneration of Granular Activated Carbon: Reversible Impacts on Sorption Behavior

EPA Science Inventory

Chemical oxidation regeneration of granular activated carbon (GAC) is a developing technology that can be carried out utilizing thermally-activated persulfate. During chemical regeneration of GAC, aggressive oxidative conditions lead to high acidity (pH < 2) and the accumulation ...

Effect of elevated CO2 on phosphorus nutrition of phosphate-deficient Arabidopsis thaliana (L.) Heynh under different nitrogen forms

PubMed Central

Niu, Yaofang; Chai, Rushan; Zhang, Yongsong

2013-01-01

Phosphorus (P) nutrition is always a key issue regarding plants responses to elevated CO2. Yet it is unclear of how elevated CO2 affects P uptake under different nitrogen (N) forms. This study investigated the influence of elevated CO2 (800 µl l–1) on P uptake and utilization by Arabidopsis grown in pH-buffered phosphate (P)-deficient (0.5 µM) hydroponic culture supplying with 2mM nitrate (NO3 −) or ammonium (NH4 +). After 7 d treatment, elevated CO2 enhanced the biomass production of both NO3 −- and NH4 +-fed plants but decreased the P amount absorbed per weight of roots and the P concentration in the shoots of plants supplied with NH4 +. In comparison, elevated CO2 increased the amount of P absorbed per weight of roots, as well as the P concentration in plants and alleviated P deficiency-induced symptoms of plants supplied with NO3 −. Elevated CO2 also increased the root/shoot ratio, total root surface area, and acid phosphatase activity, and enhanced the expression of genes or transcriptional factors involving in P uptake, allocation and remobilization in P deficient plants. Furthermore, elevated CO2 increased the nitric oxide (NO) level in roots of NO3 −-fed plants but decreased it in NH4 +-fed plants. NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) inhibited plant P acquisition by roots under elevated CO2. Considering all of these findings, this study concluded that a combination of elevated CO2 and NO3 − nutrition can induce a set of plant adaptive strategies to improve P status from P-deficient soluble sources and that NO may be a signalling molecule that controls these processes. PMID:23183255

Reuse performance of granular-activated carbon and activated carbon fiber in catalyzed peroxymonosulfate oxidation.

PubMed

Yang, Shiying; Li, Lei; Xiao, Tuo; Zhang, Jun; Shao, Xueting

2017-03-01

Recently, activated carbon was investigated as an efficient heterogeneous metal-free catalyst to directly activate peroxymonosulfate (PMS) for degradation of organic compounds. In this paper, the reuse performance and the possible deactivation reasons of granular-activated carbon (GAC) and activated carbon fiber (ACF) in PMS activation were investigated. As results indicated, the reusability of GAC, especially in the presence of high PMS dosage, was relatively superior to ACF in catalyzed PMS oxidation of Acid Orange 7 (AO7), which is much more easily adsorbed by ACF than by GAC. Pre-oxidation experiments were studied and it was demonstrated that PMS oxidation on ACF would retard ACF's deactivation to a big extent. After pre-adsorption with AO7, the catalytic ability of both GAC and ACF evidently diminished. However, when methanol was employed to extract the AO7-spent ACF, the catalytic ability could recover quite a bit. GAC and ACF could also effectively catalyze PMS to degrade Reactive Black 5 (RB5), which is very difficult to be adsorbed even by ACF, but both GAC and ACF have poor reuse performance for RB5 degradation. The original organic compounds or intermediate products adsorbed by GAC or ACF would be possibly responsible for the deactivation.

SHIP-1 Increases Early Oxidative Burst and Regulates Phagosome Maturation in Macrophages1

PubMed Central

Kamen, Lynn A.; Levinsohn, Jonathan; Cadwallader, Amy; Tridandapani, Susheela; Swanson, Joel A.

2010-01-01

Although the inositol phosphatase SHIP-1 is generally thought to inhibit signaling for Fc receptor-mediated phagocytosis, the product of its activity, phosphatidylinositol 3,4 bisphosphate (PI(3,4)P2) has been implicated in activation of the NADPH oxidase. This suggests that SHIP-1 positively regulates generation of reactive oxygen species after phagocytosis. To examine how SHIP-1 activity contributes to Fc receptor-mediated phagocytosis, we measured and compared phospholipid dynamics, membrane trafficking and the oxidative burst in macrophages from SHIP-1-deficient and wild-type mice. SHIP-1-deficient macrophages showed significantly elevated ratios of PI(3,4,5) P3 to PI(3,4)P2 on phagosomal membranes. Imaging reactive oxygen intermediate activities in phagosomes revealed decreased early NADPH oxidase activity in SHIP-1-deficient macrophages. SHIP-1-deficiency also altered later stages of phagosome maturation, as indicated by the persistent elevation of PI(3)P and the early localization of Rab5a to phagosomes. These direct measurements of individual organelles indicate that phagosomal SHIP-1 enhances the early oxidative burst through localized alteration of the membrane 3′ phosphoinositide composition. PMID:18490750

Molecular-level insights into intrinsic peroxidase-like activity of nanocarbon oxides.

PubMed

Zhao, Ruisheng; Zhao, Xiang; Gao, Xingfa

2015-01-12

Nanocarbon oxides have been proved to possess great peroxidase-like activity, catalyzing the oxidation of many peroxidase substrates, such as 3,3',5,5'-tetramethylbenzidine (TMB) and o-phenylenediamine dihydrochloride (OPD), accompanied by a significant color change. This chromogenic reaction is widely used to detect glucose and occult blood. The chromogenic reaction was intensively investigated with density functional theory and molecular-level insights into the nature of peroxidase-like activity were gained. A radical mechanism was unraveled and the carboxyl groups of nanocarbon oxides were identified as the reactive sites. Aromatic domains connected with the carboxyl groups were critical to the peroxidase-like activity. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Catalytic Activity and Stability of Oxides: The Role of Near-Surface Atomic Structures and Compositions.

PubMed

Feng, Zhenxing; Hong, Wesley T; Fong, Dillon D; Lee, Yueh-Lin; Yacoby, Yizhak; Morgan, Dane; Shao-Horn, Yang

2016-05-17

Electrocatalysts play an important role in catalyzing the kinetics for oxygen reduction and oxygen evolution reactions for many air-based energy storage and conversion devices, such as metal-air batteries and fuel cells. Although noble metals have been extensively used as electrocatalysts, their limited natural abundance and high costs have motivated the search for more cost-effective catalysts. Oxides are suitable candidates since they are relatively inexpensive and have shown reasonably high activity for various electrochemical reactions. However, a lack of fundamental understanding of the reaction mechanisms has been a major hurdle toward improving electrocatalytic activity. Detailed studies of the oxide surface atomic structure and chemistry (e.g., cation migration) can provide much needed insights for the design of highly efficient and stable oxide electrocatalysts. In this Account, we focus on recent advances in characterizing strontium (Sr) cation segregation and enrichment near the surface of Sr-substituted perovskite oxides under different operating conditions (e.g., high temperature, applied potential), as well as their influence on the surface oxygen exchange kinetics at elevated temperatures. We contrast Sr segregation, which is associated with Sr redistribution in the crystal lattice near the surface, with Sr enrichment, which involves Sr redistribution via the formation of secondary phases. The newly developed coherent Bragg rod analysis (COBRA) and energy-modulated differential COBRA are uniquely powerful ways of providing information about surface and interfacial cation segregation at the atomic scale for these thin film electrocatalysts. In situ ambient pressure X-ray photoelectron spectroscopy (APXPS) studies under electrochemical operating conditions give additional insights into cation migration. Direct COBRA and APXPS evidence for surface Sr segregation was found for La1-xSrxCoO3-δ and (La1-ySry)2CoO4±δ/La1-xSrxCoO3-δ oxide thin films, and

Development of Advanced ISS-WPA Catalysts for Organic Oxidation at Reduced Pressure/Temperature

NASA Technical Reports Server (NTRS)

Yu, Ping; Nalette, Tim; Kayatin, Matthew

2016-01-01

The Water Processor Assembly (WPA) at International Space Station (ISS) processes a waste stream via multi-filtration beds, where inorganic and non-volatile organic contaminants are removed, and a catalytic reactor, where low molecular weight organics not removed by the adsorption process are oxidized at elevated pressure in the presence of oxygen and elevated temperature above the normal water boiling point. Operation at an elevated pressure requires a more complex system design compared to a reactor that could operate at ambient pressure. However, catalysts currently available have insufficient activity to achieve complete oxidation of the organic load at a temperature less than the water boiling point and ambient pressure. Therefore, it is highly desirable to develop a more active and efficient catalyst at ambient pressure and a moderate temperature that is less than water boiling temperature. This paper describes our efforts in developing high efficiency water processing catalysts. Different catalyst support structures and coating metals were investigated in subscale reactors and results were compared against the flight WPA catalyst. Detailed improvements achieved on alternate metal catalysts at ambient pressure and 200 F will also be presented in the paper.

RAGE-Specific Inhibitor FPS-ZM1 Attenuates AGEs-Induced Neuroinflammation and Oxidative Stress in Rat Primary Microglia.

PubMed

Shen, Chao; Ma, Yingjuan; Zeng, Ziling; Yin, Qingqing; Hong, Yan; Hou, Xunyao; Liu, Xueping

2017-10-01

Advanced glycation end products (AGEs) enhance microglial activation and intensify the inflammatory response and oxidative stress in the brain. This process may occur due to direct cytotoxicity or interacting with AGEs receptors (RAGE), which are expressed on the surface of microglia. FPS-ZM1 is a high-affinity but nontoxic RAGE-specific inhibitor that has been recently shown to attenuate the Aβ-induced inflammatory response by blocking the ligation of Aβ to RAGE. In this study, we further investigated the effect of FPS-ZM1 on the AGEs/RAGE interaction and downstream elevation of neuroinflammation and oxidative stress in primary microglia cells. The results suggested that FPS-ZM1 significantly suppressed AGEs-induced RAGE overexpression, RAGE-dependent microglial activation, nuclear translocation of nuclear factor kappaB p65 (NF-κB p65), and the expression of downstream inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) and inducible nitric oxide synthase (iNOS)/nitric oxide (NO). Furthermore, FPS-ZM1 attenuated AGEs-stimulated NADPH oxidase (NOX) activation and reactive oxygen species (ROS) expression. Finally, FPS-ZM1 elevated the levels of transcription factors nuclear-factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1), as well as decreased antioxidant capacity and increased production of oxidative species. Our results suggest that FPS-ZM1 may be neuroprotective through attenuating microglial activation, oxidative stress and inflammation by blocking RAGE.

Antioxidant activity and protective effect of bee bread (honey and pollen) in aluminum-induced anemia, elevation of inflammatory makers and hepato-renal toxicity.

PubMed

Bakour, Meryem; Al-Waili, Noori S; El Menyiy, Nawal; Imtara, Hamada; Figuira, Anna Cristina; Al-Waili, Thia; Lyoussi, Badiaa

2017-12-01

Aluminum toxicity might be related to oxidative stress, and the antioxidant activity and protective effect of bee bread, which contains pollen, honey and bees' enzymes, on aluminum induced blood and hepato-renal toxicity was investigated in rats. Chemical analysis and antioxidant capacity of bee bread were conducted. The animal experiment in rats included; group 1: received distilled water (10 ml/kg b.wt), group 2: received aluminum chloride (662.2 mg/kg b.wt), group 3: received aluminum chloride (662.2 mg/kg b.wt) and ethanolic extract of the bee bread (500 mg/kg b.wt), and group 4: received aluminum chloride (662.2 mg/kg b.wt) and ethanolic extract of the bee bread (750 mg/kg b.wt). Doses were given once daily via a gavage. C-reactive protein, transaminases, urea, creatinine, creatinine clearance, sodium and potassium and urine sodium and potassium were determined on day 28 of the experiment. Bee bread contained protein, fat, fiber, ash, carbohydrate, phenol and flavonoids and it exhibited antioxidant activity. Aluminum caused a significant elevation of blood urea, transaminase, C-reactive protein and monocyte count and significantly decreased hemoglobin. These changes were significantly ameliorated by the use of bee bread. Bee bread has an antioxidant property, and exhibited a protective effect on aluminum induced blood and hepato-renal toxicity and elevation of inflammatory markers C-reactive protein, leukocyte and monocyte counts.

Elevated temperature mechanical properties and residual tensile properties of two cast superalloys and several nickel-base oxide dispersion strengthened alloys

NASA Technical Reports Server (NTRS)

Whittenberger, J. D.

1981-01-01

The elevated temperature tensile, stress-rupture and creep properties and residual tensile properties after creep straining have been determined for two cast superalloys and several wrought Ni-16Cr-4Al-yttria oxide dispersion strengthened (ODS) alloys. The creep behavior of the ODS alloys is similar to that of previously studied ODS nickel alloys. In general, the longitudinal direction is stronger than the long transverse direction, and creep is at least partially due to a diffusional creep mechanism as dispersoid-free zones were observed after creep-rupture testing. The tensile properties of the nickel-base superalloy B-1900 and cobalt-base superalloy MAR-M509 are not degraded by prior elevated temperature creep straining (at least up to 1 pct) between 1144 and 1366 K. On the other hand, the room temperature tensile properties of ODS nickel-base alloys can be reduced by prior creep strains of 0.5 pct or less between 1144 and 1477 K, with the long transverse direction being more susceptible to degradation than the longitudinal direction.

Understanding Interactions between Manganese Oxide and Gold That Lead to Enhanced Activity for Electrocatalytic Water Oxidation

PubMed Central

2015-01-01

To develop active nonprecious metal-based electrocatalysts for the oxygen evolution reaction (OER), a limiting reaction in several emerging renewable energy technologies, a deeper understanding of the activity of the first row transition metal oxides is needed. Previous studies of these catalysts have reported conflicting results on the influence of noble metal supports on the OER activity of the transition metal oxides. Our study aims to clarify the interactions between a transition metal oxide catalyst and its metal support in turning over this reaction. To achieve this goal, we examine a catalytic system comprising nanoparticulate Au, a common electrocatalytic support, and nanoparticulate MnOx, a promising OER catalyst. We conclusively demonstrate that adding Au to MnOx significantly enhances OER activity relative to MnOx in the absence of Au, producing an order of magnitude higher turnover frequency (TOF) than the TOF of the best pure MnOx catalysts reported to date. We also provide evidence that it is a local rather than bulk interaction between Au and MnOx that leads to the observed enhancement in the OER activity. Engineering improvements in nonprecious metal-based catalysts by the addition of Au or other noble metals could still represent a scalable catalyst as even trace amounts of Au are shown to lead a significant enhancement in the OER activity of MnOx. PMID:24661269

Understanding interactions between manganese oxide and gold that lead to enhanced activity for electrocatalytic water oxidation.

PubMed

Gorlin, Yelena; Chung, Chia-Jung; Benck, Jesse D; Nordlund, Dennis; Seitz, Linsey; Weng, Tsu-Chien; Sokaras, Dimosthenis; Clemens, Bruce M; Jaramillo, Thomas F

2014-04-02

To develop active nonprecious metal-based electrocatalysts for the oxygen evolution reaction (OER), a limiting reaction in several emerging renewable energy technologies, a deeper understanding of the activity of the first row transition metal oxides is needed. Previous studies of these catalysts have reported conflicting results on the influence of noble metal supports on the OER activity of the transition metal oxides. Our study aims to clarify the interactions between a transition metal oxide catalyst and its metal support in turning over this reaction. To achieve this goal, we examine a catalytic system comprising nanoparticulate Au, a common electrocatalytic support, and nanoparticulate MnO(x), a promising OER catalyst. We conclusively demonstrate that adding Au to MnO(x) significantly enhances OER activity relative to MnO(x) in the absence of Au, producing an order of magnitude higher turnover frequency (TOF) than the TOF of the best pure MnO(x) catalysts reported to date. We also provide evidence that it is a local rather than bulk interaction between Au and MnO(x) that leads to the observed enhancement in the OER activity. Engineering improvements in nonprecious metal-based catalysts by the addition of Au or other noble metals could still represent a scalable catalyst as even trace amounts of Au are shown to lead a significant enhancement in the OER activity of MnO(x).

Elevated naturally occurring arsenic in a semiarid oxidizing system, Southern High Plains aquifer, Texas, USA

USGS Publications Warehouse

Scanlon, Bridget R.; Nicot, J.-P.; Reedy, R.C.; Kurtzman, D.; Mukherjee, A.; Nordstrom, D. Kirk

2009-01-01

High groundwater As concentrations in oxidizing systems are generally associated with As adsorption onto hydrous metal (Al, Fe or Mn) oxides and mobilization with increased pH. The objective of this study was to evaluate the distribution, sources and mobilization mechanisms of As in the Southern High Plains (SHP) aquifer, Texas, relative to those in other semiarid, oxidizing systems. Elevated groundwater As levels are widespread in the southern part of the SHP (SHP-S) aquifer, with 47% of wells exceeding the current EPA maximum contaminant level (MCL) of 10 μg/L (range 0.3–164 μg/L), whereas As levels are much lower in the north (SHP-N: 9% ⩾ As MCL of 10 μg/L; range 0.2–43 μg/L). The sharp contrast in As levels between the north and south coincides with a change in total dissolved solids (TDS) from 395 mg/L (median north) to 885 mg/L (median south). Arsenic is present as arsenate (As V) in this oxidizing system and is correlated with groundwater TDS (Spearman’s ρ = 0.57). The most likely current source of As is sorbed As onto hydrous metal oxides based on correlations between As and other oxyanion-forming elements (V, ρ = 0.88; Se, ρ = 0.54; B, ρ = 0.51 and Mo, ρ = 0.46). This source is similar to that in other oxidizing systems and constitutes a secondary source; the most likely primary source being volcanic ashes in the SHP aquifer or original source rocks in the Rockies, based on co-occurrence of As and F (ρ = 0.56), oxyanion-forming elements and SiO2 (ρ = 0.41), which are found in volcanic ashes. High groundwater As concentrations in some semiarid oxidizing systems are related to high evaporation. Although correlation of As with TDS in the SHP aquifer may suggest evaporative concentration, unenriched stable isotopes (δ2H: −65 to −27; δ18O: −9.1 to −4.2) in the SHP aquifer do not support evaporation. High TDS in the SHP aquifer is most likely related to upward movement of saline water from the underlying

Reaction of CO2 with propylene oxide and styrene oxide catalyzed by a chromium(III) amine-bis(phenolate) complex.

PubMed

Dean, Rebecca K; Devaine-Pressing, Katalin; Dawe, Louise N; Kozak, Christopher M

2013-07-07

A diamine-bis(phenolate) chromium(III) complex, {CrCl[O2NN'](BuBu)}2 catalyzes the copolymerization of propylene oxide with carbon dioxide. The synthesis of this metal complex is straightforward and it can be obtained in high yields. This catalyst incorporates a tripodal amine-bis(phenolate) ligand, which differs from the salen or salan ligands typically used with Cr and Co complexes that have been employed as catalysts for the synthesis of such polycarbonates. The catalyst reported herein yields low molecular weight polymers with narrow polydispersities when the reaction is performed at room temperature. Performing the reaction at elevated temperatures causes the selective synthesis of propylene carbonate. The copolymerization activity for propylene oxide and carbon dioxide, as well as the coupling of carbon dioxide and styrene oxide to give styrene carbonate are presented.

Tension-Compression Fatigue of an Oxide/Oxide Ceramic Matrix Composite at Elevated Temperature in Air and Steam Environments

DTIC Science & Technology

2015-03-26

method has been successfully used with several materials such as silicon carbide fiber - silicon carbide matrix ( SiC / SiC ) CMCs with carbon and boron...elements [14]. These advanced ceramics include oxides, nitrides and carbides of silicon , aluminum, titanium, and zirconium [12]. One of the most...oxides over silicon carbide and other non-oxide materials. In fact, it is the inherent stability of oxides in oxidizing environments which originally

Triiodothyronine Activates Lactate Oxidation Without Impairing Fatty Acid Oxidation and Improves Weaning From Extracorporeal Membrane Oxygenation

PubMed Central

Kajimoto, Masaki; Ledee, Dolena R.; Xu, Chun; Kajimoto, Hidemi; Isern, Nancy G.; Portman, Michael A.

2017-01-01

Background Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. It has previously been shown that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. Methods and Results Nineteen immature piglets (9.1–15.3 kg) were separated into 3 groups with ECMO (6.5 h) and wean: normal circulation (Group-C); transient coronary occlusion (10 min) for ischemia-reperfusion (IR) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon (13C)-labeled lactate, medium-chain and long-chain FAs, was infused as oxidative substrates. Substrate fractional contribution (FC) to the citric acid cycle was analyzed by 13C-nuclear magnetic resonance. ECMO depressed circulating T3 levels to 40% of the baseline at 4 h and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [adenosine triphosphate]/[adenosine diphosphate] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. Conclusions T3 releases inhibition of lactate oxidation following IR injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning. PMID:25421230

Dopamine elevates intracellular zinc concentration in cultured rat embryonic cortical neurons through the cAMP-nitric oxide signaling cascade.

PubMed

Hung, Hui-Hsing; Kao, Lung-Sen; Liu, Pei-Shan; Huang, Chien-Chang; Yang, De-Ming; Pan, Chien-Yuan

2017-07-01

Zinc ion (Zn 2+ ), the second most abundant transition metal after iron in the body, is essential for neuronal activity and also induces toxicity if the concentration is abnormally high. Our previous results show that exposure of cultured cortical neurons to dopamine elevates intracellular Zn 2+ concentrations ([Zn 2+ ] i ) and induces autophagosome formation but the mechanism is not clear. In this study, we characterized the signaling pathway responsible for the dopamine-induced elevation of [Zn 2+ ] i and the effect of [Zn 2+ ] i in modulating the autophagy in cultured rat embryonic cortical neurons. N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), a membrane-permeable Zn 2+ chelator, could rescue the cell death and suppress the autophagosome puncta number induced by dopamine. Dopamine treatment increased the lipidation level of the endogenous microtubule-associated protein 1A/1B-light chain 3 (LC3 II), an autophagosome marker. TPEN added 1h before, but not after, dopamine treatment suppressed the dopamine-induced elevation of LC3 II level. Inhibitors of the dopamine D1-like receptor, protein kinase A (PKA), and NOS suppressed the dopamine-induced elevation of [Zn 2+ ] i . PKA activators and NO generators directly increased [Zn 2+ ] i in cultured neurons. Through cell fractionation, proteins with m.w. values between 5 and 10kD were found to release Zn 2+ following NO stimulation. In addition, TPEN pretreatment and an inhibitor against PKA could suppress the LC3 II level increased by NO and dopamine, respectively. Therefore, our results demonstrate that dopamine-induced elevation of [Zn 2+ ] i is mediated by the D1-like receptor-PKA-NO pathway and is important in modulating the cell death and autophagy. Copyright © 2017 Elsevier Inc. All rights reserved.

Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: A role of angiotensin AT1 receptor-NOX2 signaling axis.

PubMed

Rajtik, Tomas; Carnicka, Slavka; Szobi, Adrian; Giricz, Zoltan; O-Uchi, Jin; Hassova, Veronika; Svec, Pavel; Ferdinandy, Peter; Ravingerova, Tanya; Adameova, Adriana

2016-01-15

During ischemia/reperfusion (IR), increased activation of angiotensin AT1 receptors recruits NADPH oxidase 2 (NOX2) which contributes to oxidative stress. It is unknown whether this stimulus can induce oxidative activation of Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ) leading into the aggravation of cardiac function and whether these effects can be prevented by angiotensin AT1 receptors blockade. Losartan, a selective AT1 blocker, was used. Its effects were compared with effects of KN-93, an inhibitor of CaMKIIδ. Global IR was induced in Langendorff-perfused rat hearts. Protein expression was evaluated by immunoblotting and lipoperoxidation was measured by TBARS assay. Losartan improved LVDP recovery by 25%; however, it did not reduce reperfusion arrhythmias. Oxidized CaMKIIδ (oxCaMKIIδ) was downregulated at the end of reperfusion compared to before ischemia and losartan did not change these levels. Phosphorylation of CaMKIIδ mirrored the pattern of changes in oxCaMKIIδ levels. Losartan did not prevent the higher lipoperoxidation due to IR and did not influence NOX2 expression. Inhibition of CaMKII ameliorated cardiac IR injury; however, this was not accompanied with changes in the levels of either active form of CaMKIIδ in comparison to the angiotensin AT1 receptor blockade. In spite of no changes of oxCaMKIIδ, increased cardiac recovery of either therapy was abolished when combined together. This study showed that oxidative activation of CaMKIIδ is not elevated at the end of R phase. NOX2-oxCAMKIIδ signaling is unlikely to be involved in cardioprotective action of angiotensin AT1 receptor blockade which is partially abolished by concomitant CaMKII inhibition. Copyright © 2015 Elsevier B.V. All rights reserved.

Oxidation of limonene using activated carbon modified in dielectric barrier discharge plasma

NASA Astrophysics Data System (ADS)

Glonek, Karolina; Wróblewska, Agnieszka; Makuch, Edyta; Ulejczyk, Bogdan; Krawczyk, Krzysztof; Wróbel, Rafał. J.; Koren, Zvi C.; Michalkiewicz, Beata

2017-10-01

The waste from industrial fruits processing is utilized for the extraction of limonene, a renewable terpene biomass compound obtained from orange peels. This was followed by limonene oxidation, which produces highly useful oxygenated derivatives (carveol, and perillyl alcohol, 1,2-epoxylimonene and its diol). New catalysts were obtained by treating relatively inexpensive commercially available EuroPh and FPV activated carbons with plasma. These catalysts were characterized by the following instrumental methods XRD, sorption of N2 and CO2, SEM, EDS, TEM, XPS, and Raman spectroscopy. The activities of the plasma-treated catalysts were measured in the oxidation of limonene by means of either hydrogen peroxide or t-butyl hydroperoxide as the oxidizing agents. During the oxidation with hydrogen peroxide the new plasma-treated catalysts were more active than their untreated counterparts. This effect was noticeable in the considerable increase in the conversion of limonene. The mechanism explaining this property is proposed, and it takes into account the role of the appropriate functional groups on the surface of the catalysts. This work has shown for the first time that the commercial EuroPh and FPV activated carbons, after having been treated by plasma, are active catalysts for the selective limonene oxidation for the production of value-added industrial products.

Contribution of polyamines metabolism and GABA shunt to chilling tolerance induced by nitric oxide in cold-stored banana fruit.

PubMed

Wang, Yansheng; Luo, Zisheng; Mao, Linchun; Ying, Tiejin

2016-04-15

Effect of exogenous nitric oxide (NO) on polyamines (PAs) catabolism, γ-aminobutyric acid (GABA) shunt, proline accumulation and chilling injury of banana fruit under cold storage was investigated. Banana fruit treated with NO sustained lower chilling injury index than the control. Notably elevated nitric oxide synthetase activity and endogenous NO level were observed in NO-treated banana fruit. PAs contents in treated fruit were significantly higher than control fruit, due to the elevated activities of arginine decarboxylase and ornithine decarboxylase. NO treatment increased the activities of diamine oxidase, polyamine oxidase and glutamate decarboxylase, while reduced GABA transaminase activity to lower levels compared with control fruit, which resulted the accumulation of GABA. Besides, NO treatment upregulated proline content and significantly enhanced the ornithine aminotransferase activity. These results indicated that the chilling tolerance induced by NO treatment might be ascribed to the enhanced catabolism of PAs, GABA and proline. Copyright © 2015 Elsevier Ltd. All rights reserved.

d-Alanine 2, Leucine 5 Enkephaline (DADLE)-mediated DOR activation augments human hUCB-BFs viability subjected to oxidative stress via attenuation of the UPR.

PubMed

Mullick, Madhubanti; Venkatesh, Katari; Sen, Dwaipayan

2017-07-01

Human mesenchymal stem cells (hMSCs) although being potent in repairing injured or ischemic tissues, their success regarding tissue-regenerative approaches are hindered by the paucity in their viability. The elevated levels of reactive oxygen species (ROS) in damaged sites provoke the pernicious effects of donor MSC survival. In the present study, the effect of delta-opioid receptor (DOR) activation on human umbilical cord-blood borne fibroblasts (hUCB-BFs) survival under oxidative stress (H 2 O 2 ) was evaluated. Oxidative stress which is known to trigger pathological conditions of the unfolded protein response (UPR) leads to endoplasmic reticulum stress. Upon its activation by D-Alanine 2, Leucine 5 Enkephaline (DADLE, selective DOR agonist) in hUCB-BFs under oxidative stress, a significant down regulation (~2 folds) of key UPR genes was observed as determined by qPCR, Thioflavin-T protein aggregation assay and western blot analysis. Concomitantly, the oxidative stress-mediated cell-death was ameliorated and the viable-cells' percentage was enhanced following DOR activation. The intracellular ROS production upon H 2 O 2 treatment as determined by CM-H 2 DCFDA staining was repressed, the anti-apoptotic marker Bcl-2 was upregulated along with a significant suppression in the expression levels of pro-apoptotic proteins Bax and Bad upon DOR activation. Upon subsequent treatment with naltrindole, the effects of DADLE-induced cytoprotection were reverted significantly. These results propound the role of DADLE-mediated DOR-activation on improvement of the viability, which might succour successful hUCB-BFs transplants and greatly absolve the inefficacy of tissue-specific engineered transplants. Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.

Decreased histone deacetylase 2 impairs Nrf2 activation by oxidative stress

DOE Office of Scientific and Technical Information (OSTI.GOV)

Mercado, Nicolas; Thimmulappa, Rajesh; Thomas, Catherine M.R.

2011-03-11

Research highlights: {yields} Nrf2 anti-oxidant function is impaired when HDAC activity is inhibited. {yields} HDAC inhibition decreases Nrf2 protein stability. {yields} HDAC2 is involved in reduced Nrf2 stability and both correlate in COPD samples. {yields} HDAC inhibition increases Nrf2 acetylation. -- Abstract: Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a crucial role in cellular defence against oxidative stress by inducing the expression of multiple anti-oxidant genes. However, where high levels of oxidative stress are observed, such as chronic obstructive pulmonary disease (COPD), Nrf2 activity is reduced, although the molecular mechanism for this defect is uncertain. Here, we show thatmore » down-regulation of histone deacetylase (HDAC) 2 causes Nrf2 instability, resulting in reduced anti-oxidant gene expression and increase sensitivity to oxidative stress. Although Nrf2 protein was clearly stabilized after hydrogen peroxide (H{sub 2}O{sub 2}) stimulation in a bronchial epithelial cell line (BEAS2B), Nrf2 stability was decreased and Nrf2 acetylation increased in the presence of an HDAC inhibitor, trichostatin A (TSA). TSA also reduced Nrf2-regulated heme-oxygenase-1 (HO-1) expression in these cells, and this was confirmed in acute cigarette-smoke exposed mice in vivo. HDAC2 knock-down by RNA interference resulted in reduced H{sub 2}O{sub 2}-induced Nrf2 protein stability and activity in BEAS2B cells, whereas HDAC1 knockdown had no effect. Furthermore, monocyte-derived macrophages obtained from healthy volunteers (non-smokers and smokers) and COPD patients showed a significant correlation between HDAC2 expression and Nrf2 expression (r = 0.92, p < 0.0001). Thus, reduced HDAC2 activity in COPD may account for increased Nrf2 acetylation, reduced Nrf2 stability and impaired anti oxidant defences.« less

Oxidized trilinoleate and tridocosahexaenoate induce pica behavior and change locomotor activity.

PubMed

Kitamura, Fuki; Watanabe, Hiroyuki; Umeno, Aya; Yoshida, Yasukazu; Kurata, Kenji; Gotoh, Naohiro

2013-01-01

Pica behavior, a behavior that is characterized by eating a nonfood material such as kaolin and relates to the degree of discomfort in animals, and the variations of locomotor activity of rats after eating deteriorated fat and oil extracted from instant noodles were examined in our previous study. The result shows that oxidized fat and oil with at least 100 meq/kg in peroxide value (PV) increase pica behavior and decrease locomotor activity. In the present study, the same two behaviors were measured using autoxidized trilinoleate (tri-LA) and tridocosahexaenoate (tri-DHA) as a model of vegetable and fish oil, respectively, to compare fatty acid differences against the induction of two behaviors. The oxidized levels of tri-LA and tri-DHA were analyzed with PV and p-anisidine value (AnV), the method to analyze secondary oxidized products. The oxidation levels of respective triacylglycerol (TAG) samples were carefully adjusted to make them having almost the same PV and AnV. As the results, 600 or more meq/kg in PV of both TAGs significantly increased the consumption of kaolin pellets compared to the control group. Furthermore, 300 or more meq/kg in PV of tri-LA and 200 or more meq/kg in PV of tri-DHA demonstrated significant decrease in locomotor activity compared to control group. These results would indicate that the oxidized TAG having the same PV and/or AnV would induce the same type of pica behavior and locomotor activity. Furthermore, that the structure of oxidized products might not be important and the amount of hydroperoxide group and/or aldehyde group in deteriorated fats and oils might affect the pica behavior and locomotor activity were thought.

Mycotoxin-Containing Diet Causes Oxidative Stress in the Mouse

PubMed Central

Hou, Yan-Jun; Zhao, Yong-Yan; Xiong, Bo; Cui, Xiang-Shun; Kim, Nam-Hyung; Xu, Yin-Xue; Sun, Shao-Chen

2013-01-01

Mycotoxins which mainly consist of Aflatoxin (AF), Zearalenone (ZEN) and Deoxynivalenol (DON) are commonly found in many food commodities. Although each component has been shown to cause liver toxicity and oxidative stress in several species, there is no evidence regarding the effect of naturally contained multiple mycotoxins on tissue toxicity and oxidative stress in vivo. In the present study, mycotoxins-contaminated maize (AF 597 µg/kg, ZEN 729 µg/kg, DON 3.1 mg/kg maize) was incorporated into the diet at three different doses (0, 5 and 20%) to feed the mice, and blood and tissue samples were collected to examine the oxidative stress related indexes. The results showed that the indexes of liver, kidney and spleen were all increased and the liver and kidney morphologies changed in the mycotoxin-treated mice. Also, the treatment resulted in the elevated glutathione peroxidase (GPx) activity and malondialdehyde (MDA) level in the serum and liver, indicating the presence of the oxidative stress. Moreover, the decrease of catalase (CAT) activity in the serum, liver and kidney as well as superoxide dismutase (SOD) activity in the liver and kidney tissue further confirmed the occurrence of oxidative stress. In conclusion, our data indicate that the naturally contained mycotoxins are toxic in vivo and able to induce the oxidant stress in the mouse. PMID:23555961

Effects of melatonin on lipid peroxidation and anti-oxidant enzyme activity in rats with experimentally induced hyperthyroidism.

PubMed

Baydas, Burhanettin; Meral, Ismail

2005-07-01

1. The present study was designed to investigate the effects of high-dose melatonin on lipid peroxidation and anti-oxidant enzyme activity in rats with experimentally induced hyperthyroidism. 2. Twenty-four albino male rats, weighing 240-260 g, were randomly allotted into one of three experimental groups (control, hyperthyroid and hyperthyroid + melatonin treatment), with each group containing eight animals. Hyperthyroidism was induced by a daily with i.p. injection of 200 microg l-thyroxine for 30 days. In addition to l-thyroxin treatment, rats in the hyperthyroid + melatonin treatment group were also given daily i.p. injections of 10 mg/kg melatonin on the last 10 days of l-thyroxine treatment. Control animals received injections of an equivalent volume of saline solution. Rats received the last injection 24 h before being killed. 3. At the end of the experiment, rats in all three groups were fasted for 12 h and killed by cardiac puncture under ether anaesthesia. Blood samples were taken for the determination of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) levels and concentrations of tri-iodothyronine (T(3)) and thyroxine (T(4)). 4. It was found that MDA and SOD levels and concentrations of T(3) and T(4) were higher and the GSH level was lower in rats with hyperthyroidism compared with controls. Melatonin treatment decreased the elevated MDA and SOD levels and increased the lowered GSH level to control levels in rats with hyperthyroidism, but did not ameliorate the concentrations of T(3) and T(4). 5. It was concluded that high-dose melatonin treatment may decrease the hyperthyroidism-induced disturbances of lipid peroxidation and anti-oxidant enzyme activity and oxidative damage.

Endothelial microparticles (EMP) bind and activate monocytes: elevated EMP-monocyte conjugates in multiple sclerosis.

PubMed

Jy, Wenche; Minagar, Alireza; Jimenez, Joaquin J; Sheremata, William A; Mauro, Lucia M; Horstman, Lawrence L; Bidot, Carlos; Ahn, Yeon S

2004-09-01

Elevated plasma endothelial microparticles (EMP) have been documented in MS during exacerbation. However, the role of EMP in pathogenesis of MS remains unclear. We investigated the formation of EMP-monocyte conjugates (EMP-MoC) and their potential role in transendothelial migration of inflammatory cells in MS. EMP-MoC were assayed in 30 MS patients in exacerbation, 20 in remission and in 35 controls. EMP-leukocyte conjugation was investigated flowcytometrically by employing alpha-CD54 or alpha-CD62E for EMP, and alpha-CD45 for leukocytes. EMP-MoC were characterized by identifying adhesion molecules involved and their effect on monocyte function. In vivo (clinical): EMP-MoC were markedly elevated in exacerbation vs. remission and controls, correlating with presence of GD+ MRI lesions. Free CD54+ EMP were not elevated but free CD62E+ EMP were. In vitro: EMP bound preferentially to monocytes, less to neutrophils, but little to lymphocytes. Bound EMP activated monocytes: CD11b expression increased 50% and migration through cerebral endothelial cell layer increased 2.6-fold. Blockade of CD54 reduced binding by 80%. Most CD54+ EMP bound to monocytes, leaving little free EMP, while CD62+ EMP were found both free and bound. These results demonstrated that phenotypic subsets of EMP interacted differently with monocytes. Based on our observations, EMP may enhance inflammation and increase transendothelial migration of monocytes in MS by binding to and activating monocytes through CD54. EMP-MoC were markedly increased in MS patients in exacerbation compared to remission and may serve as a sensitive marker of MS disease activity.

A spontaneous change in the oxidation states of Pd/WO3 toward an active phase during catalytic cycles of CO oxidation

NASA Astrophysics Data System (ADS)

Jeon, Byungwook; Kim, Ansoon; Lee, Young-Ahn; Seo, Hyungtak; Kim, Yu Kwon

2017-11-01

CO oxidation over Pd/WO3 films prepared on a glass substrate has been examined at the substrate temperature of 150 - 250 °C and pressures less than 1 Torr with a stoichiometric mixture of CO and O2. Under the given reaction condition, the chemical states of the Pd/WO3 film gradually change into the most catalytically active form with the highest saturation reaction rate regardless of the initial oxidation states. The measured CO oxidation rate over the Pd/WO3 is strongly dependent on the chemical states of Pd and W. Either metallic Pd or fully oxidized PdO phase is not as catalytically active as the active form with mixed metallic Pd and thin PdO layers supported on WO3 with partially reduced W5+ state which is spontaneously obtained during the catalytic reaction cycles. Our results indicate that the facile oxygen transfer between Pd and WO3 layers not only facilitate the spontaneous changes into the active form, but also act as a promotional role in CO oxidation over the Pd layer.

Lipid oxidation induced oxidative degradation of cereal beta-glucan.

PubMed

Wang, Yu-Jie; Mäkelä, Noora; Maina, Ndegwa Henry; Lampi, Anna-Maija; Sontag-Strohm, Tuula

2016-04-15

In food systems, lipid oxidation can cause oxidation of other molecules. This research for the first time investigated oxidative degradation of β-glucan induced by lipid oxidation using an oil-in-water emulsion system which simulated a multi-phased aqueous food system containing oil and β-glucan. Lipid oxidation was monitored using peroxide value and hexanal production while β-glucan degradation was evaluated by viscosity and molecular weight measurements. The study showed that while lipid oxidation proceeded, β-glucan degradation occurred. Emulsions containing β-glucan, oil and ferrous ion showed significant viscosity and molecular weight decrease after 1 week of oxidation at room temperature. Elevated temperature (40°C) enhanced the oxidation reactions causing higher viscosity drop. In addition, the presence of β-glucan appeared to retard the hexanal production in lipid oxidation. The study revealed that lipid oxidation may induce the degradation of β-glucan in aqueous food systems where β-glucan and lipids co-exist. Copyright © 2015 Elsevier Ltd. All rights reserved.

Serum prolidase activity and oxidative status in patients with bronchial asthma.

PubMed

Cakmak, Alpay; Zeyrek, Dost; Atas, Ali; Celik, Hakim; Aksoy, Nurten; Erel, Ozcan

2009-01-01

Asthma is a disease where there is an accumulation of collagen in the reticular basal membrane of the airway leading to chronic inflammation. The enzyme prolidase plays an important role in the breakdown of collagen and the breakdown of intracellular protein especially in the final stage when peptides and dipeptides contain a high level of proline. To evaluate the relationship between prolidase activity and oxidative status in asthma patients. Comparison was made between 42 patients diagnosed with bronchial asthma and 32 healthy children of similar age and gender. Serum prolidase activity was measured spectrophotometrically. Oxidative status was determined using total antioxidant capacity (TAC) and total oxidant status (TOS) measurement. The prolidase activity of the asthma patient group was statistically significant compared with the control group (P< or =0.001). TAC and TOS levels in the asthma patient group were higher than the control group (P< or =0.001, P< or =0.002, respectively). No correlation was found between the prolidase and oxidative levels of the two groups. A positive correlation was determined between the prolidase activity and TAC in the asthma patient group (P< or =0.001, r=0.501). The prolidase enzyme activity, which plays a role in the collagen turnover, was low in the asthma patients; therefore, their collagen metabolism had undergone a change and this indicates that there may be an effect on the accumulation of collagen in the reticular basal membrane. Moreover, the high level of TOS indicates that these patients were exposed to severe oxidative stress with an increased TAC response. (c) 2009 Wiley-Liss, Inc.

Cardiovascular and metabolic activity at rest and during psychological and physical challenge in normotensives and subjects with mildly elevated blood pressure.

PubMed

Sims, J; Carroll, D

1990-03-01

Heart rate, systolic and diastolic blood pressure, and respiratory and metabolic activity were recorded prior to and during mental arithmetic and a video game task in 20 young men with mildly elevated casual systolic blood pressures. Twenty-five unambiguously normotensive young men were tested under the same protocol. For pretask baseline physiological activity, group differences emerged for all cardiovascular and metabolic variables; thus the elevated blood pressure group displayed not only higher resting cardiovascular levels than normotensive subjects, but higher levels of metabolic activity too. With regard to change in physiological activity from rest to task, the group with mildly elevated blood pressure showed reliably larger increases in heart rate to the mental arithmetic task than the normotensive subjects. These effects, however, were not paralleled by group differences in metabolic activity increase. Physiological measures were also taken prior to and during graded dynamic exercise. The subsequent calculation of individual heart rate-oxygen consumption exercise regression lines allowed the comparison of actual and predicted heart rates during psychological challenge. The subjects with mildly elevated blood pressure displayed significantly greater discrepancies between actual and predicted heart rate values than normotensives during the psychological tasks in general and mental arithmetic in particular. Group differences in physiological activity during exercise largely reflected the pattern seen at rest. A possible exception here was systolic blood pressure. Not only were systolic blood pressure levels higher throughout the exercise phase for mildly elevated blood pressure subjects, but this group evidenced more of an increase from rest to exercise than the normotensives.

Antibacterial activity of trimetal (CuZnFe) oxide nanoparticles.

PubMed

Alzahrani, Khalid E; Niazy, Abdurahman A; Alswieleh, Abdullah M; Wahab, Rizwan; El-Toni, Ahmed M; Alghamdi, Hamdan S

2018-01-01

The increasing resistance of pathogenic bacteria to antibiotics is a challenging worldwide health problem that has led to the search for new and more efficient antibacterial agents. Nanotechnology has proven to be an effective tool for the fight against bacteria. In this paper, we present the synthesis and traits of trimetal (CuZnFe) oxide nanoparticles (NPs) using X-ray diffraction, high-resolution transmission electron microscopy, and energy dispersive x-ray spectroscopy. We evaluated the antibacterial activity of these NPs against gram-negative Escherichia coli and gram-positive Enterococcus faecalis and then compared it to that of their pure single-metal oxide components CuO and ZnO. Our study showed that the antibacterial activity of the trimetal oxide NPs was greater against E . coli than against E . faecalis . Overall, the antimicrobial effect of trimetal NPs is between those of pure ZnO and CuO nanoparticles, which may mean that their cytotoxicity is also between that of pure ZnO and CuO NPs, making them potential antibiotics. However, the cytotoxicity of trimetal NPs to mammalian cells needs to be verified. The combination of three metal oxide NPs (ZnO, CuO, and Fe 2 O 3 ) in one multimetal (CuZnFe) oxide NPs will enhance the therapeutic strategy against a wide range of microbial infections. Bacteria are unlikely to develop resistance against this new NP because bacteria must go through a series of mutations to become resistant to the trimetal oxide NP. Therefore, this NP can combat existing and emerging bacterial infections.

Reduced cytochrome P4501A activity and recovery from oxidative stress during subchronic benzo[a]pyrene and benzo[e]pyrene treatment of rainbow trout

DOE Office of Scientific and Technical Information (OSTI.GOV)

Curtis, Lawrence R., E-mail: larry.curtis@oregonstate.edu; Garzon, Claudia B.; Arkoosh, Mary

2011-07-01

This study assessed the role of aryl hydrocarbon receptor (AHR) affinity, and cytochrome P4501A (CYP1A) protein and activity in polyaromatic hydrocarbon (PAH)-induced oxidative stress. In the 1-100 nM concentration range benzo[a]pyrene (BaP) but not benzo[e]pyrene (BeP) competitively displaced 2 nM [{sup 3}H]2, 3, 7, 8-tetrachloro-dibenzo-p-dioxin from rainbow trout AHR2{alpha}. Based on appearance of fluorescent aromatic compounds in bile over 3, 7, 14, 28 or 50 days of feeding 3 {mu}g of BaP or BeP/g fish/day, rainbow trout liver readily excreted these polyaromatic hydrocarbons (PAHs) and their metabolites at near steady state rates. CYP1A proteins catalyzed more than 98% of ethoxyresorufin-O-deethylasemore » (EROD) activity in rainbow trout hepatic microsomes. EROD activity of hepatic microsomes initially increased and then decreased to control activities after 50 days of feeding both PAHs. Immunohistochemistry of liver confirmed CYP1A protein increased in fish fed both PAHs after 3 days and remained elevated for up to 28 days. Neither BaP nor BeP increased hepatic DNA adduct concentrations at any time up to 50 days of feeding these PAHs. Comet assays of blood cells demonstrated marked DNA damage after 14 days of feeding both PAHs that was not significant after 50 days. There was a strong positive correlation between hepatic EROD activity and DNA damage in blood cells over time for both PAHs. Neither CYP1A protein nor 3-nitrotyrosine (a biomarker for oxidative stress) immunostaining in trunk kidney were significantly altered by BaP or BeP after 3, 7, 14, or 28 days. There was no clear association between AHR2{alpha} affinity and BaP and BeP-induced oxidative stress. - Highlights: > No direct association between aryl hydrocarbon receptor affinity and polyaromatic hydrocarbon induced oxidative stress. > There was a strong correlation between cytochrome P4501A activity and oxidative stress as measured with the comet assay. > There was no correlation between

Is moral elevation an approach-oriented emotion?

PubMed Central

Van de Vyver, Julie; Abrams, Dominic

2017-01-01

Abstract Two studies were designed to test whether moral elevation should be conceptualized as an approach-oriented emotion. The studies examined the relationship between moral elevation and the behavioral activation and inhibition systems. Study 1 (N = 80) showed that individual differences in moral elevation were associated with individual differences in behavioral activation but not inhibition. Study 2 (N = 78) showed that an elevation-inducing video promoted equally high levels of approach orientation as an anger-inducing video and significantly higher levels of approach orientation than a control video. Furthermore, the elevation-inducing stimulus (vs. the control condition) significantly promoted prosocial motivation and this effect was sequentially mediated by feelings of moral elevation followed by an approach-oriented state. Overall the results show unambiguous support for the proposal that moral elevation is an approach-oriented emotion. Applied and theoretical implications are discussed. PMID:28191027

β-Caryophyllene, a phytocannabinoid attenuates oxidative stress, neuroinflammation, glial activation, and salvages dopaminergic neurons in a rat model of Parkinson disease.

PubMed

Ojha, Shreesh; Javed, Hayate; Azimullah, Sheikh; Haque, M Emdadul

2016-07-01

Parkinson disease (PD) is a neurodegenerative disease characterized by progressive dopaminergic neurodegeneration in the substantia nigra pars compacta (SNc) area. The present study was undertaken to evaluate the neuroprotective effect of β-caryophyllene (BCP) against rotenone-induced oxidative stress and neuroinflammation in a rat model of PD. In the present study, BCP was administered once daily for 4 weeks at a dose of 50 mg/kg body weight prior to a rotenone (2.5 mg/kg body weight) challenge to mimic the progressive neurodegenerative nature of PD. Rotenone administration results in oxidative stress as evidenced by decreased activities of superoxide dismutase, catalase, and depletion of glutathione with a concomitant rise in lipid peroxidation product, malondialdehyde. Rotenone also significantly increased pro-inflammatory cytokines in the midbrain region and elevated the inflammatory mediators such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the striatum. Further, immunohistochemical analysis revealed loss of dopaminergic neurons in the SNc area and enhanced expression of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP), indicators of microglia activation, and astrocyte hypertrophy, respectively, as an index of inflammation. However, treatment with BCP rescued dopaminergic neurons and decreased microglia and astrocyte activation evidenced by reduced Iba-1 and GFAP expression. BCP in addition to attenuation of pro-inflammatory cytokines and inflammatory mediators such as COX-2 and iNOS, also restored antioxidant enzymes and inhibited lipid peroxidation as well as glutathione depletion. The findings demonstrate that BCP provides neuroprotection against rotenone-induced PD and the neuroprotective effects can be ascribed to its potent antioxidant and anti-inflammatory activities.

Effects of Potassium Permanganate Oxidation on Subsurface Microbial Activity

NASA Technical Reports Server (NTRS)

Rowland, Martin A.; Brubaker, Gaylen R.; Westray, Mark; Morris, Damon; Kohler, Keisha; McCool, Alex (Technical Monitor)

2001-01-01

In situ chemical oxidation has the potential for degrading large quantities of organic contaminants and can be more effective and timely than traditional ex situ treatment methods. However, there is a need to better characterize the potential effects of this treatment on natural processes. This study focuses on potential inhibition to anaerobic dechlorination of trichloroethene (TCE) in soils from a large manufacturing facility as a result of in situ oxidation using potassium permanganate (KMn04)Previous microcosm studies established that natural attenuation occurs on-site and that it is enhanced by the addition of ethanol to the system. A potential remediation scheme for the site involves the use of potassium permanganate to reduce levels of TCE in heavily contaminated areas, then to inject ethanol into the system to "neutralize" excess oxidant and enhance microbial degradation. However, it is currently unknown whether the exposure of indigenous microbial populations to potassium permanganate may adversely affect biological reductive dechlorination by these microorganisms. Consequently, additional microcosm studies were conducted to evaluate this remediation scheme and assess the effect of potassium permanganate addition on biological reductive dechlorination of TCE. Samples of subsurface soil and groundwater were collected from a TCE-impacted area of the site. A portion of the soil was pretreated with nutrients and ethanol to stimulate microbial activity, while the remainder of the soil was left unamended. Soil/groundwater microcosms were prepared in sealed vials using the nutrient-amended and unamended soils, and the effects of potassium permanganate addition were evaluated using two permanganate concentrations (0.8 and 2.4 percent) and two contact times (1 and 3 weeks). TCE was then re-added to each microcosm and TCE and dichloroethene (DCE) concentrations were monitored to determine the degree to which microbial dechlorination occurred following chemical

Oxidation-promoted activation of a ferrocene C-H bond by a rhodium complex.

PubMed

Labande, Agnès; Debono, Nathalie; Sournia-Saquet, Alix; Daran, Jean-Claude; Poli, Rinaldo

2013-05-14

The oxidation of a rhodium(I) complex containing a ferrocene-based heterodifunctional phosphine N-heterocyclic carbene (NHC) ligand produces a stable, planar chiral rhodium(III) complex with an unexpected C-H activation on ferrocene. The oxidation of rhodium(I) to rhodium(III) may be accomplished by initial oxidation of ferrocene to ferrocenium and subsequent electron transfer from rhodium to ferrocenium. Preliminary catalytic tests showed that the rhodium(III) complex is active for the Grignard-type arylation of 4-nitrobenzaldehyde via C-H activation of 2-phenylpyridine.

Functional Iron Oxide-Silver Hetero-Nanocomposites: Controlled Synthesis and Antibacterial Activity

NASA Astrophysics Data System (ADS)

Trang, Vu Thi; Tam, Le Thi; Van Quy, Nguyen; Huy, Tran Quang; Thuy, Nguyen Thanh; Tri, Doan Quang; Cuong, Nguyen Duy; Tuan, Pham Anh; Van Tuan, Hoang; Le, Anh-Tuan; Phan, Vu Ngoc

2017-06-01

Iron oxide-silver nanocomposites are of great interest for their antibacterial and antifungal activities. We report a two-step synthesis of functional magnetic hetero-nanocomposites of iron oxide nanoparticles and silver nanoparticles (Fe3O4-Ag). Iron oxide nanoparticles were prepared first by a co-precipitation method followed by the deposition of silver nanoparticles via a hydrothermal route. The prepared Fe3O4-Ag hetero-nanocomposites were characterized by x-ray diffraction, transmission electron microscopy, high resolution transmission electron microscopy and vibrating sample magnetometry. Their antibacterial activities were investigated by using paper-disc diffusion and direct-drop diffusion methods. The results indicate that the Fe3O4-Ag hetero-nanocomposites exhibit excellent antibacterial activities against two Gram-negative bacterial strains ( Salmonella enteritidis and Klebsiella pneumoniae).

Caloric restriction improves endothelial dysfunction during vascular aging: Effects on nitric oxide synthase isoforms and oxidative stress in rat aorta.

PubMed

Zanetti, Michela; Gortan Cappellari, Gianluca; Burekovic, Ismet; Barazzoni, Rocco; Stebel, Marco; Guarnieri, Gianfranco

2010-11-01

Aging is characterized by activation of inducible over endothelial nitric oxide synthase (iNOS and eNOS), impaired antioxidant activity and increased oxidative stress, which reduces nitric oxide bioavailability and causes endothelial dysfunction. Caloric restriction (CR) blunts oxidative stress. We investigated whether CR impacts endothelial dysfunction in aging and the underlying mechanisms. Aortas from young (YC, 6 months of age) and old (OC, 24 months of age) rats ad-libitum fed and from old rats caloric-restricted for 3-weeks (OR, 26%) were investigated. Endothelium-dependent vasorelaxation was impaired in OC, associated with reduced eNOS and increased iNOS expression (P<0.05). Aortic nitrite was similar in OC and YC, but the contribution of calcium-independent NOS to total NOS activity was increased whereas that of calcium-dependent NOS was reduced (p≤0.0003). Plasma thiobarbituric acid-reactive substances (TBARS) were elevated in OC as well as aortic nitrotyrosine (P<0.05). Expression of manganese superoxide dismutase (MnSOD) and total SOD activity were impaired in OC (P<0.05 vs. YC), whereas copper-zinc (CuZn) SOD expression was similar in OC and YC. CR restored endothelial dysfunction in old rats, reduced iNOS expression, total nitrite and calcium-independent NOS activity in aorta (P<0.05) without changes in eNOS expression and calcium-dependent NOS activity. Sirtuin-1 expression did not differ among groups. Plasma TBARS and aortic nitrotyrosine were reduced (P<0.05) in OR compared with OC. In OR CuZnSOD protein and SOD activity increased (P<0.05) without changes in MnSOD expression. Short-term CR improves age-related endothelial dysfunction. Reversal of altered iNOS/eNOS ratio, reduced oxidative stress and increased SOD enzyme activity rather than enhanced NO production appear to be involved in this effect. Copyright © 2010 Elsevier Inc. All rights reserved.

Umbelliferone prevents oxidative stress, inflammation and hematological alterations, and modulates glutamate-nitric oxide-cGMP signaling in hyperammonemic rats.

PubMed

Germoush, Mousa O; Othman, Sarah I; Al-Qaraawi, Maha A; Al-Harbi, Hanan M; Hussein, Omnia E; Al-Basher, Gadh; Alotaibi, Mohammed F; Elgebaly, Hassan A; Sandhu, Mansur A; Allam, Ahmed A; Mahmoud, Ayman M

2018-06-01

Hepatic encephalopathy (HE) is a serious neuropsychiatric complication that occurs as a result of liver failure. Umbelliferone (UMB; 7-hydroxycoumarin) is a natural product with proven hepatoprotective activity; however, nothing has yet been reported on its protective effect against hyperammonemia, the main culprit behind the symptoms of HE. Here, we evaluated the effect of UMB against ammonium chloride (NH 4 Cl)-induced hyperammonemia, oxidative stress, inflammation and hematological alterations in rats. We demonstrated the modulatory role of UMB on the glutamate-nitric oxide (NO)-cGMP pathways in the cerebrum of rats. Rats received intraperitoneal injections of NH 4 Cl (3 times/week) for 8 weeks and concomitantly received 50 mg/kg UMB. NH 4 Cl-induced rats showed significantly elevated blood ammonia and liver function markers. Lipid peroxidation and NO were increased in the liver and cerebrum of rats while the antioxidant defenses were declined. UMB significantly reduced blood ammonia, liver function markers, lipid peroxidation and NO, and enhanced the antioxidant defenses in NH 4 Cl-induced rats. UMB significantly prevented anemia, leukocytosis, thrombocytopenia and prolongation of PT and aPTT. Hyperammonemic rats showed elevated levels of cerebral TNF-α, IL-1β and glutamine as well as increased activity and expression of Na + /K + -ATPase, effects that were significantly reversed by UMB. In addition, UMB down-regulated nitric oxide synthase and soluble guanylate cyclase in the cerebrum of hyperammonemic rats. In conclusion, this study provides evidence that UMB protects against hyperammonemia via attenuation of oxidative stress and inflammation. UMB prevents hyperammonemia associated hematological alterations and therefore represents a promising protective agent against the deleterious effects of excess ammonia. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Multilineage somatic activating mutations in HRAS and NRAS cause mosaic cutaneous and skeletal lesions, elevated FGF23 and hypophosphatemia

PubMed Central

Lim, Young H.; Ovejero, Diana; Sugarman, Jeffrey S.; DeKlotz, Cynthia M.C.; Maruri, Ann; Eichenfield, Lawrence F.; Kelley, Patrick K.; Jüppner, Harald; Gottschalk, Michael; Tifft, Cynthia J.; Gafni, Rachel I.; Boyce, Alison M.; Cowen, Edward W.; Bhattacharyya, Nisan; Guthrie, Lori C.; Gahl, William A.; Golas, Gretchen; Loring, Erin C.; Overton, John D.; Mane, Shrikant M.; Lifton, Richard P.; Levy, Moise L.; Collins, Michael T.; Choate, Keith A.

2014-01-01

Pathologically elevated serum levels of fibroblast growth factor-23 (FGF23), a bone-derived hormone that regulates phosphorus homeostasis, result in renal phosphate wasting and lead to rickets or osteomalacia. Rarely, elevated serum FGF23 levels are found in association with mosaic cutaneous disorders that affect large proportions of the skin and appear in patterns corresponding to the migration of ectodermal progenitors. The cause and source of elevated serum FGF23 is unknown. In those conditions, such as epidermal and large congenital melanocytic nevi, skin lesions are variably associated with other abnormalities in the eye, brain and vasculature. The wide distribution of involved tissues and the appearance of multiple segmental skin and bone lesions suggest that these conditions result from early embryonic somatic mutations. We report five such cases with elevated serum FGF23 and bone lesions, four with large epidermal nevi and one with a giant congenital melanocytic nevus. Exome sequencing of blood and affected skin tissue identified somatic activating mutations of HRAS or NRAS in each case without recurrent secondary mutation, and we further found that the same mutation is present in dysplastic bone. Our finding of somatic activating RAS mutation in bone, the endogenous source of FGF23, provides the first evidence that elevated serum FGF23 levels, hypophosphatemia and osteomalacia are associated with pathologic Ras activation and may provide insight in the heretofore limited understanding of the regulation of FGF23. PMID:24006476

Multilineage somatic activating mutations in HRAS and NRAS cause mosaic cutaneous and skeletal lesions, elevated FGF23 and hypophosphatemia.

PubMed

Lim, Young H; Ovejero, Diana; Sugarman, Jeffrey S; Deklotz, Cynthia M C; Maruri, Ann; Eichenfield, Lawrence F; Kelley, Patrick K; Jüppner, Harald; Gottschalk, Michael; Tifft, Cynthia J; Gafni, Rachel I; Boyce, Alison M; Cowen, Edward W; Bhattacharyya, Nisan; Guthrie, Lori C; Gahl, William A; Golas, Gretchen; Loring, Erin C; Overton, John D; Mane, Shrikant M; Lifton, Richard P; Levy, Moise L; Collins, Michael T; Choate, Keith A

2014-01-15

Pathologically elevated serum levels of fibroblast growth factor-23 (FGF23), a bone-derived hormone that regulates phosphorus homeostasis, result in renal phosphate wasting and lead to rickets or osteomalacia. Rarely, elevated serum FGF23 levels are found in association with mosaic cutaneous disorders that affect large proportions of the skin and appear in patterns corresponding to the migration of ectodermal progenitors. The cause and source of elevated serum FGF23 is unknown. In those conditions, such as epidermal and large congenital melanocytic nevi, skin lesions are variably associated with other abnormalities in the eye, brain and vasculature. The wide distribution of involved tissues and the appearance of multiple segmental skin and bone lesions suggest that these conditions result from early embryonic somatic mutations. We report five such cases with elevated serum FGF23 and bone lesions, four with large epidermal nevi and one with a giant congenital melanocytic nevus. Exome sequencing of blood and affected skin tissue identified somatic activating mutations of HRAS or NRAS in each case without recurrent secondary mutation, and we further found that the same mutation is present in dysplastic bone. Our finding of somatic activating RAS mutation in bone, the endogenous source of FGF23, provides the first evidence that elevated serum FGF23 levels, hypophosphatemia and osteomalacia are associated with pathologic Ras activation and may provide insight in the heretofore limited understanding of the regulation of FGF23.

Influence of growth conditions on subsequent submonolayer oxide decomposition on Si(111)

NASA Astrophysics Data System (ADS)

Shklyaev, A. A.; Aono, Masakazu; Suzuki, Takanori

1996-10-01

The decomposition kinetics of oxide with a coverage between 0.1 and 0.5 ML, grown by oxidation of the Si(111)-7×7 surface at temperatures between 550 and 800 °C for oxygen pressures (Pox) between 3×10-8 and 2×10-6 Torr, is investigated with optical second-harmonic generation. Through the analysis of the pressure dependence of the initial oxide-growth rate, we separate the conditions for a slow oxide growth at Pox near Ptr(T) and for a rapid oxide growth at Pox>3Ptr(T), where Ptr(T) is the transition pressure to Si-etching regime without oxide growth. For the rapidly grown oxide, the oxide decomposition rate decreases with increasing oxide coverage, whereas the activation energy of about 3 eV does not change significantly. While in the case when the oxide is desorbed at the same temperature as are used for oxide growth, the oxide decomposition is described by an apparent activation energy of 1.5 eV. For the slowly grown oxide of 0.1 ML coverage, the oxide desorption kinetics shows a rapid decomposition stage followed by a slow stage. For the slowly grown oxide of 0.3 ML coverage, the slow stage with a large activation energy of 4.1 eV becomes dominant in the latter part of decomposition. The dependence of the desorption kinetics on the oxide-growth conditions described here could be a reason for the scattering of the kinetic parameters in the literature for O2 interaction with silicon at elevated temperatures.

Increased penile expression of transforming growth factor and elevated systemic oxidative stress in rabbits with chronic partial bladder outlet obstruction.

PubMed

Lin, W-Y; Chang, P-J; Lin, Y-P; Wu, S-B; Chen, C-S; Levin, R M; Wei, Y-H

2012-02-01

There is a growing body of evidence to support the direct link between obstructive bladder dysfunction and erectile dysfunction (ED). However, there have been few pathophysiological studies to determine the relationship between lower urinary tract syndrome (LUTS) and ED. As the transforming growth factor-β1 (TGF-β1) that induces the synthesis of collagen in the penile tissues is critical for the development of ED, the first aim of this study was to investigate the expression of TGF-β1 in the penis from male rabbits with chronic partial bladder outlet obstruction (PBOO). Besides, it has been suggested that oxidative stress plays a significant role in the pathophysiological mechanism of ED. Thus, the second aim of this study was to further investigate whether the urinary or serum oxidative stress markers are involved in chronic PBOO-induced penile dysfunction. A total of 16 male New Zealand White rabbits were separated equally into four groups: a control group and PBOO groups obstructed for 2, 4 and 8 weeks respectively. Using the RT-PCR and Western blot analysis, a progressive increase of TGF-β1 in penis was found at 2, 4 and 8 weeks after obstruction. Moreover, the biomarkers for oxidative stress or oxidative damage were significantly detected in the penis of rabbits after PBOO, which include the enhancement of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in urine and plasma, plasma malondialdehyde (MDA) and total antioxidant capacity (TAC), as well as reduction of glutathione (GSH). On the basis of our results, the increase of TGF-β1 and elevated systemic oxidative stress may play key roles to contribute to penile dysfunction after chronic PBOO. © 2011 The Authors. International Journal of Andrology © 2011 European Academy of Andrology.

Shape-dependent bactericidal activity of copper oxide nanoparticle mediated by DNA and membrane damage

DOE Office of Scientific and Technical Information (OSTI.GOV)

Laha, Dipranjan; Pramanik, Arindam; Laskar, Aparna

Highlights: • Spherical and sheet shaped copper oxide nanoparticles were synthesized. • Physical characterizations of these nanoparticles were done by TEM, DLS, XRD, FTIR. • They showed shape dependent antibacterial activity on different bacterial strain. • They induced both membrane damage and ROS mediated DNA damage in bacteria. - Abstract: In this work, we synthesized spherical and sheet shaped copper oxide nanoparticles and their physical characterizations were done by the X-ray diffraction, fourier transform infrared spectroscopy, transmission electron microscopy and dynamic light scattering. The antibacterial activity of these nanoparticles was determined on both gram positive and gram negative bacterial. Sphericalmore » shaped copper oxide nanoparticles showed more antibacterial property on gram positive bacteria where as sheet shaped copper oxide nanoparticles are more active on gram negative bacteria. We also demonstrated that copper oxide nanoparticles produced reactive oxygen species in both gram negative and gram positive bacteria. Furthermore, they induced membrane damage as determined by atomic force microscopy and scanning electron microscopy. Thus production of and membrane damage are major mechanisms of the bactericidal activity of these copper oxide nanoparticles. Finally it was concluded that antibacterial activity of nanoparticles depend on physicochemical properties of copper oxide nanoparticles and bacterial strain.« less

Plasma membrane calcium ATPase 4 (PMCA4) co-ordinates calcium and nitric oxide signaling in regulating murine sperm functional activity.

PubMed

Olli, Kristine E; Li, Kun; Galileo, Deni S; Martin-DeLeon, Patricia A

2018-01-01

Reduced sperm motility (asthenospermia) and resulting infertility arise from deletion of the Plasma Membrane Ca 2+ -ATPase 4 (Pmca4) gene which encodes the highly conserved Ca 2+ efflux pump, PMCA4. This is the major Ca 2+ clearance protein in murine sperm. Since the mechanism underlying asthenospermia in PMCA4's absence or reduced activity is unknown, we investigated if sperm PMCA4 negatively regulates nitric oxide synthases (NOSs) and when absent NO, peroxynitrite, and oxidative stress levels are increased. Using co-immunoprecipitation (Co-IP) and Fluorescence Resonance Energy Transfer (FRET), we show an association of PMCA4 with the NOSs in elevated cytosolic [Ca 2+ ] in capacitated and Ca 2+ ionophore-treated sperm and with neuronal (nNOS) at basal [Ca 2+ ] (ucapacitated sperm). FRET efficiencies for PMCA4-eNOS were 35% and 23% in capacitated and uncapacitated sperm, significantly (p < 0.01) different, with the molecules being <10 nm apart. For PMCA4-nNOS, this interaction was seen only for capacitated sperm where FRET efficiency was 24%, significantly (p < 0.05) higher than in uncapacitated sperm (6%). PMCA4 and the NOSs were identified as interacting partners in a quaternary complex that includes Caveolin1, which co-immunoprecipitated with eNOS in a Ca 2+ -dependent manner. In Pmca4 -/- sperm NOS activity was elevated twofold in capacitated/uncapacitated sperm (vs. wild-type), accompanied by a twofold increase in peroxynitrite levels and significantly (p < 0.001) increased numbers of apoptotic germ cells. The data support a quaternary complex model in which PMCA4 co-ordinates Ca 2+ and NO signaling to maintain motility, with increased NO levels resulting in asthenospermia in Pmca4 -/- males. They suggest the involvement of PMCA4 mutations in human asthenospermia, with diagnostic relevance. © 2017 Wiley Periodicals, Inc.

Waiting to win: elevated striatal and orbitofrontal cortical activity during reward anticipation in euthymic bipolar disorder adults

PubMed Central

Nusslock, Robin; Almeida, Jorge RC; Forbes, Erika E; Versace, Amelia; Frank, Ellen; LaBarbara, Edmund J; Klein, Crystal R; Phillips, Mary L

2012-01-01

Objective Bipolar disorder may be characterized by a hypersensitivity to reward-relevant stimuli, potentially underlying the emotional lability and dysregulation that characterizes the illness. In parallel, research highlights the predominant role of striatal and orbitofrontal cortical (OFC) regions in reward-processing and approach-related affect. We aimed to examine whether bipolar disorder, relative to healthy, participants displayed elevated activity in these regions during reward processing. Methods Twenty-one euthymic bipolar I disorder and 20 healthy control participants with no lifetime history of psychiatric disorder underwent functional magnetic resonance imaging (fMRI) scanning during a card-guessing paradigm designed to examine reward-related brain function to anticipation and receipt of monetary reward and loss. Data were collected using a 3T Siemens Trio scanner. Results Region-of-interest analyses revealed that bipolar disorder participants displayed greater ventral striatal and right-sided orbitofrontal [Brodmann area (BA) 11] activity during anticipation, but not outcome, of monetary reward, relative to healthy controls (p < 0.05, corrected). Wholebrain analyses indicated that bipolar disorder, relative to healthy, participants also displayed elevated left-lateral OFC activity (BA 47) activity during reward anticipation (p < 0.05, corrected). Conclusions Elevated ventral striatal and OFC activity during reward anticipation may represent a neural mechanism for predisposition to expansive mood and hypo/mania in response to reward-relevant cues that characterizes bipolar disorder. Our findings contrast with research reporting blunted activity in the ventral striatum during reward processing in unipolar depressed individuals, relative to healthy controls. Examination of reward-related neural activity in bipolar disorder is a promising research focus to facilitate identification of biological markers of the illness. PMID:22548898

Does oxidative stress affect the activity of the sodium-proton exchanger?

PubMed

Bober, Joanna; Kedzierska, Karolina; Kwiatkowska, Ewa; Stachowska, Ewa; Gołembiewska, Edyta; Mazur, Olech; Staniewicz, Zdzisław; Ciechanowski, Kazimierz; Chlubek, Dariusz

2010-01-01

Accumulation of reactive oxygen species (ROS) takes place in patients with chronic renal failure (CRF). Oxidative stress causes disorders in the activity of the sodium-proton exchanger (NHE). Studies on NHE in CRF produced results that are discrepant and difficult to interpret. The aim of this study was to demonstrate that oxidative stress had an effect on the activity of NHE. We enrolled 87 subjects divided into 4 groups: patients with CRF treated conservatively; patients with CRF hemodialyzed without glucose--HD-g(-); patients with CRF hemodialyzed with glucose--HD-g(+); controls (C). The activity of NHE, the rate of proton efflux V(max), Michaelis constant (Km), and the concentration of thiobarbituric acid-reactive substances (TBARS, an indicator of oxidative stress) in plasma, as well as the concentration of reduced glutathione in blood were determined. The concentration of TBARS was significantly higher in hemodialyzed patients before and after dialysis and in patients with CRF on conservative treatment in comparison with group C. TBARS in plasma correlated negatively with VpH(i)6.4 in group C and with V(max) and VpH(i)6.4 after HD in group HD-g(-). We found that the concentration of creatinine correlated with TBARS (p < 0.0001; r = +0.51) in the conservatively treated group. We observed a marked oxidative stress and decreased NHE activity when dialysis was done without glucose, whereas patients dialyzed with glucose demonstrated a relatively low intensity of oxidative stress.

Cloud droplet activation through oxidation of organic aerosol influenced by temperature and particle phase state: CLOUD ACTIVATION BY AGED ORGANIC AEROSOL

DOE PAGES

Slade, Jonathan H.; Shiraiwa, Manabu; Arangio, Andrea; ...

2017-02-04

Chemical aging of organic aerosol (OA) through multiphase oxidation reactions can alter their cloud condensation nuclei (CCN) activity and hygroscopicity. However, the oxidation kinetics and OA reactivity depend strongly on the particle phase state, potentially influencing the hydrophobic-to-hydrophilic conversion rate of carbonaceous aerosol. Here, amorphous Suwannee River fulvic acid (SRFA) aerosol particles, a surrogate humic-like substance (HULIS) that contributes substantially to global OA mass, are oxidized by OH radicals at different temperatures and phase states. When oxidized at low temperature in a glassy solid state, the hygroscopicity of SRFA particles increased by almost a factor of two, whereas oxidation ofmore » liquid-like SRFA particles at higher temperatures did not affect CCN activity. Low-temperature oxidation appears to promote the formation of highly-oxygenated particle-bound fragmentation products with lower molar mass and greater CCN activity, underscoring the importance of chemical aging in the free troposphere and its influence on the CCN activity of OA.« less

Neonatal iron supplementation potentiates oxidative stress, energetic dysfunction and neurodegeneration in the R6/2 mouse model of Huntington's disease

PubMed Central

Berggren, Kiersten L.; Chen, Jianfang; Fox, Julia; Miller, Jonathan; Dodds, Lindsay; Dugas, Bryan; Vargas, Liset; Lothian, Amber; McAllum, Erin; Volitakis, Irene; Roberts, Blaine; Bush, Ashley I.; Fox, Jonathan H.

2015-01-01

Huntington’s disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion that encodes a polyglutamine tract in huntingtin (htt) protein. Dysregulation of brain iron homeostasis, oxidative stress and neurodegeneration are consistent features of the HD phenotype. Therefore, environmental factors that exacerbate oxidative stress and iron dysregulation may potentiate HD. Iron supplementation in the human population is common during infant and adult-life stages. In this study, iron supplementation in neonatal HD mice resulted in deterioration of spontaneous motor running activity, elevated levels of brain lactate and oxidized glutathione consistent with increased energetic dysfunction and oxidative stress, and increased striatal and motor cortical neuronal atrophy, collectively demonstrating potentiation of the disease phenotype. Oxidative stress, energetic, and anatomic markers of degeneration were not affected in wild-type littermate iron-supplemented mice. Further, there was no effect of elevated iron intake on disease outcomes in adult HD mice. We have demonstrated an interaction between the mutant huntingtin gene and iron supplementation in neonatal HD mice. Findings indicate that elevated neonatal iron intake potentiates mouse HD and promotes oxidative stress and energetic dysfunction in brain. Neonatal-infant dietary iron intake level may be an environmental modifier of human HD. PMID:25703232

Experimental increase in baseline corticosterone level reduces oxidative damage and enhances innate immune response

PubMed Central

Pătraș, Laura; Pap, Péter L.; Vincze, Orsolya; Mureșan, Cosmin; Németh, József; Lendvai, Ádám Z.

2018-01-01

Glucocorticoid (GC) hormones are significant regulators of homeostasis. The physiological effects of GCs critically depend on the time of exposure (short vs. long) as well as on their circulating levels (baseline vs. stress-induced). Previous experiments, in which chronic and high elevation of GC levels was induced, indicate that GCs impair both the activity of the immune system and the oxidative balance. Nonetheless, our knowledge on how mildly elevated GC levels, a situation much more common in nature, might influence homeostasis is limited. Therefore, we studied whether an increase in GC level within the baseline range suppresses or enhances condition (body mass, hematocrit and coccidian infestation) and physiological state (humoral innate immune system activity and oxidative balance). We implanted captive house sparrows Passer domesticus with either 60 days release corticosterone (CORT) or control pellets. CORT-treated birds had elevated baseline CORT levels one week after the implantation, but following this CORT returned to its pre-treatment level and the experimental groups had similar CORT levels one and two months following the implantation. The mass of tail feathers grown during the initial phase of treatment was smaller in treated than in control birds. CORT implantation had a transient negative effect on body mass and hematocrit, but both of these traits resumed the pre-treatment values by one month post-treatment. CORT treatment lowered oxidative damage to lipids (malondialdehyde) and enhanced constitutive innate immunity at one week and one month post-implantation. Our findings suggest that a relatively short-term (i.e. few days) elevation of baseline CORT might have a positive and stimulatory effect on animal physiology. PMID:29432437

Neutral sphingomyelinase-3 mediates TNF-stimulated oxidant activity in skeletal muscle.

PubMed

Moylan, Jennifer S; Smith, Jeffrey D; Wolf Horrell, Erin M; McLean, Julie B; Deevska, Gergana M; Bonnell, Mark R; Nikolova-Karakashian, Mariana N; Reid, Michael B

2014-01-01

Sphingolipid and oxidant signaling affect glucose uptake, atrophy, and force production of skeletal muscle similarly and both are stimulated by tumor necrosis factor (TNF), suggesting a connection between systems. Sphingolipid signaling is initiated by neutral sphingomyelinase (nSMase), a family of agonist-activated effector enzymes. Northern blot analyses suggest that nSMase3 may be a striated muscle-specific nSMase. The present study tested the hypothesis that nSMase3 protein is expressed in skeletal muscle and functions to regulate TNF-stimulated oxidant production. We demonstrate constitutive nSMase activity in skeletal muscles of healthy mice and humans and in differentiated C2C12 myotubes. nSMase3 (Smpd4 gene) mRNA is highly expressed in muscle. An nSMase3 protein doublet (88 and 85 kD) is derived from alternative mRNA splicing of exon 11. The proteins partition differently. The full-length 88 kD isoform (nSMase3a) fractionates with membrane proteins that are resistant to detergent extraction; the 85 kD isoform lacking exon 11 (nSMase3b) is more readily extracted and fractionates with detergent soluble membrane proteins; neither variant is detected in the cytosol. By immunofluorescence microscopy, nSMase3 resides in both internal and sarcolemmal membranes. Finally, myotube nSMase activity and cytosolic oxidant activity are stimulated by TNF. Both if these responses are inhibited by nSMase3 knockdown. These findings identify nSMase3 as an intermediate that links TNF receptor activation, sphingolipid signaling, and skeletal muscle oxidant production. Our data show that nSMase3 acts as a signaling nSMase in skeletal muscle that is essential for TNF-stimulated oxidant activity.

Facial muscle activity, Response Entropy, and State Entropy indices during noxious stimuli in propofol-nitrous oxide or propofol-nitrous oxide-remifentanil anaesthesia without neuromuscular block.

PubMed

Aho, A J; Yli-Hankala, A; Lyytikäinen, L-P; Jäntti, V

2009-02-01

Entropy is an anaesthetic EEG monitoring method, calculating two numerical parameters: State Entropy (SE, range 0-91) and Response Entropy (RE, range 0-100). Low Entropy numbers indicate unconsciousness. SE uses the frequency range 0.8-32 Hz, representing predominantly the EEG activity. RE is calculated at 0.8-47 Hz, consisting of both EEG and facial EMG. RE-SE difference (RE-SE) can indicate EMG, reflecting nociception. We studied RE-SE and EMG in patients anaesthetized without neuromuscular blockers. Thirty-one women were studied in propofol-nitrous oxide (P) or propofol-nitrous oxide-remifentanil (PR) anaesthesia. Target SE value was 40-60. RE-SE was measured before and after endotracheal intubation, and before and after the commencement of surgery. The spectral content of the signal was analysed off-line. Appearance of EMG on EEG was verified visually. RE, SE, and RE-SE increased during intubation in both groups. Elevated RE was followed by increased SE values in most cases. In these patients, spectral analysis of the signal revealed increased activity starting from low (<20 Hz) frequency area up to the highest measured frequencies. This was associated with appearance of EMG in raw signal. No spectral alterations or EMG were seen in patients with stable Entropy values. Increased RE is followed by increased SE at nociceptive stimuli in patients not receiving neuromuscular blockers. Owing to their overlapping power spectra, the contribution of EMG and EEG cannot be accurately separated with frequency analysis in the range of 10-40 Hz.

7-Nitroindazole, a neuronal nitric oxide synthase inhibitor, impairs passive-avoidance and elevated plus-maze memory performance in rats.

PubMed

Yildiz Akar, Furuzan; Ulak, Guner; Tanyeri, Pelin; Erden, Faruk; Utkan, Tijen; Gacar, Nejat

2007-10-01

The role of nitric oxide (NO) on cognitive performance in a modified elevated plus-maze (mEPM) and passive-avoidance (PA) task was investigated by using the NO synthase (NOS) inhibitor 7-nitroindazole (7-NI) and an NO precursor l-arginine. The interaction between the activation of N-methyl-d-aspartate (NMDA) receptors and NO synthesis on memory retention was also studied. 7-NI, l-arginine or MK-801, a non-competitive NMDA receptor antagonist were injected intraperitoneally (i.p) to male Wistar rats 30 min before the first training session of the PA test or 30 min before on the first day testing (acquisition session) of mEPM task. Transfer latency, the time rat took to move from the open arm to the enclosed arm, was used as an index of learning and memory in a mEPM test. The retention session was performed 24 h after the acquisition one. In the PA task, the retention test was carried out 24 h after training and reduction of retention latency was used to evaluate the acquisition of learning and memory. Blood glucose level and locomotor activity of the rats was also evaluated. 7-NI (10, 20, 25, 50 mg/kg) and MK-801 (0.15 mg/kg) significantly prolonged the transfer latency on retention session in a mEPM test and shortened step-through latency in PA test. 7-NI-induced impairment in memory and learning was partly reversed by l-arginine (200 mg/kg), a competitive substrate for NOS. However subeffective doses of 7-NI (5 mg/kg) and MK-801 (0.075 mg/kg) given in combination significantly impaired plus-maze and PA performances in rats. Thus NMDA receptor mediated NO pathways may be implicated in the PA and mEPM behaviours in rats. Since 7-NI does not affect blood pressure and did not alter blood glucose level and locomotor activity in conscious rats, 7-NI-induced impairment of memory is not due to either hypertension, changes in blood glucose level or effects on locomotor activity.

Exercise training attenuates sympathetic activation and oxidative stress in diet-induced obesity.

PubMed

Li, G; Liu, J-Y; Zhang, H-X; Li, Q; Zhang, S-W

2015-01-01

It is known that excessive sympathetic activity and oxidative stress are enhanced in obesity. This study aimed to clarify whether exercise training (ET) attenuates sympathetic activation and oxidative stress in obesity. The obesity was induced by high-fat diet (HFD) for 12 weeks. Male Sprague-Dawley rats were assigned to four groups: regular diet (RD) plus sedentary (RD-S), RD plus ET (RD-ET), HFD plus sedentary (HFD-S), and HFD plus ET (HFD-ET). The rats in RD-ET and HFD-ET groups were trained on a motorized treadmill for 60 min/day, five days/week for 8 weeks. The sympathetic activity was evaluated by the plasma norepinephrine (NE) level. The superoxide anion, malondialdehyde and F2-isoprostanes levels in serum and muscles were measured to evaluate oxidative stress. The ET prevented the increases in the body weight, arterial pressure and white adipose tissue mass in HFD rats. The NE level in plasma and oxidative stress related parameters got lower in HFD-ET group compared with HFD-S group. We have found decreased mRNA and protein levels of toll-like receptor (TLR)-2 and TLR-4 by ET in HFD rats. These findings suggest that ET may be effective for attenuating sympathetic activation and oxidative stress in diet-induced obesity.

The β1 Subunit Enhances Oxidative Regulation of Large-Conductance Calcium-activated K+ Channels

PubMed Central

Santarelli, Lindsey Ciali; Chen, Jianguo; Heinemann, Stefan H.; Hoshi, Toshinori

2004-01-01

Oxidative stress may alter the functions of many proteins including the Slo1 large conductance calcium-activated potassium channel (BKCa). Previous results demonstrated that in the virtual absence of Ca2+, the oxidant chloramine-T (Ch-T), without the involvement of cysteine oxidation, increases the open probability and slows the deactivation of BKCa channels formed by human Slo1 (hSlo1) α subunits alone. Because native BKCa channel complexes may include the auxiliary subunit β1, we investigated whether β1 influences the oxidative regulation of hSlo1. Oxidation by Ch-T with β1 present shifted the half-activation voltage much further in the hyperpolarizing direction (−75 mV) as compared with that with α alone (−30 mV). This shift was eliminated in the presence of high [Ca2+]i, but the increase in open probability in the virtual absence of Ca2+ remained significant at physiologically relevant voltages. Furthermore, the slowing of channel deactivation after oxidation was even more dramatic in the presence of β1. Oxidation of cysteine and methionine residues within β1 was not involved in these potentiated effects because expression of mutant β1 subunits lacking cysteine or methionine residues produced results similar to those with wild-type β1. Unlike the results with α alone, oxidation by Ch-T caused a significant acceleration of channel activation only when β1 was present. The β1 M177 mutation disrupted normal channel activation and prevented the Ch-T–induced acceleration of activation. Overall, the functional effects of oxidation of the hSlo1 pore-forming α subunit are greatly amplified by the presence of β1, which leads to the additional increase in channel open probability and the slowing of deactivation. Furthermore, M177 within β1 is a critical structural determinant of channel activation and oxidative sensitivity. Together, the oxidized BKCa channel complex with β1 has a considerable chance of being open within the physiological voltage

Novel antioxidants' synthesis and their anti-oxidative activity through activating Nrf2 signaling pathway.

PubMed

Wu, Jianzhang; Ren, Jiye; Yao, Song; Wang, Jiabing; Huang, Lili; Zhou, Peng; Yun, Di; Xu, Qing; Wu, Shoubiao; Wang, Zhankun; Qiu, Peihong

2017-04-01

Novel structure compounds (WS) containing 3,4,5-trimethoxyphenyl and acyl pyrazole were designed and synthesized based combination principles. Among them, WS13 was screened out to possess desirable anti-oxidative activity in vitro. Cell survival assay and apoptosis experiment in H 2 O 2 induced PC12 cells injury model all showed that its cytoprotection exhibited a concentration-effect manner. WS13 at 10μM could remove ROS with equal effiency to edaravone. Further, it clearly activated Nrf2 nuclear translocation and upregulated GCLC mRNA transcription and protein expression in dose-dependent manner, and its cytoprotection was reversed by GCLC protein inhibitor. In total, WS13 with further promotion can serve as Nrf2-GCLC activator in anti-oxidative therapy. Copyright © 2017 Elsevier Ltd. All rights reserved.

Protective role of integrin-linked kinase against oxidative stress and in maintenance of genomic integrity

PubMed Central

Im, Michelle; Dagnino, Lina

2018-01-01

The balance between the production of reactive oxygen species and activation of antioxidant pathways is essential to maintain a normal redox state in all tissues. Oxidative stress caused by excessive oxidant species generation can cause damage to DNA and other macromolecules, affecting cell function and viability. Here we show that integrin-linked kinase (ILK) plays a key role in eliciting a protective response to oxidative damage in epidermal cells. Inactivation of the Ilk gene causes elevated levels of intracellular oxidant species (IOS) and DNA damage in the absence of exogenous oxidative insults. In ILK-deficient cells, excessive IOS production can be prevented through inhibition of NADPH oxidase activity, with a concomitant reduction in DNA damage. Additionally, ILK is necessary for DNA repair processes following UVB-induced damage, as ILK-deficient cells show a significantly impaired ability to remove cyclobutane pyrimidine dimers following irradiation. Thus, ILK is essential to maintain cellular redox balance and, in its absence, epidermal cells become more susceptible to oxidative damage through mechanisms that involve IOS production by NADPH oxidase activity. PMID:29568383

Protective role of integrin-linked kinase against oxidative stress and in maintenance of genomic integrity.

PubMed

Im, Michelle; Dagnino, Lina

2018-03-02

The balance between the production of reactive oxygen species and activation of antioxidant pathways is essential to maintain a normal redox state in all tissues. Oxidative stress caused by excessive oxidant species generation can cause damage to DNA and other macromolecules, affecting cell function and viability. Here we show that integrin-linked kinase (ILK) plays a key role in eliciting a protective response to oxidative damage in epidermal cells. Inactivation of the Ilk gene causes elevated levels of intracellular oxidant species (IOS) and DNA damage in the absence of exogenous oxidative insults. In ILK-deficient cells, excessive IOS production can be prevented through inhibition of NADPH oxidase activity, with a concomitant reduction in DNA damage. Additionally, ILK is necessary for DNA repair processes following UVB-induced damage, as ILK-deficient cells show a significantly impaired ability to remove cyclobutane pyrimidine dimers following irradiation. Thus, ILK is essential to maintain cellular redox balance and, in its absence, epidermal cells become more susceptible to oxidative damage through mechanisms that involve IOS production by NADPH oxidase activity.

Bicarbonate-induced activation of H₂O₂ for metal-free oxidative desulfurization.

PubMed

Bokare, Alok D; Choi, Wonyong

2016-03-05

Efficient oxidative desulfurization (ODS) of model oil containing dibenzothiophene (DBT) and aromatic thiophenic derivatives has been achieved at room temperature using hydrogen peroxide activation by inorganic bicarbonate (HCO3(-)). Using in-situ formation of peroxymonocarbonate as oxidant, the transformation of main model substrate DBT to corresponding DBT-sulfone was easily accomplished in biphasic reaction conditions. In the presence of water-acetonitrile polar phase, increasing the water content upto 50% decreased the extraction capacity more than 3 times, but ∼ 90% DBT oxidation was still achieved. The oxidizing capacity of bicarbonate catalyst was maintained during repeated ODS cycles, but DBT removal efficiency was critically dependent on the extraction capacity of the polar phase. Under heterogeneous reaction conditions, bicarbonate-modified ion-exchange resin achieved similar ODS activity compared to the homogeneous catalytic system. Additionally, the efficient formation of peroxymonocarbonate using gaseous CO2 precursor in alkaline conditions was also utilized for DBT oxidation. The present study proposes the NaHCO3/H2O2 catalytic system as an efficient and cheap metal-free alternative for the oxidative removal of aromatic sulfur compounds from fuel oil. Copyright © 2015 Elsevier B.V. All rights reserved.

Removal of a putative inhibitory element reduces the calcium-dependent calmodulin activation of neuronal nitric-oxide synthase.

PubMed

Montgomery, H J; Romanov, V; Guillemette, J G

2000-02-18

Neuronal nitric-oxide synthase (NOS) and endothelial NOS are constitutive NOS isoforms that are activated by binding calmodulin in response to elevated intracellular calcium. In contrast, the inducible NOS isoform binds calmodulin at low basal levels of calcium in resting cells. Primary sequence comparisons show that each constitutive NOS isozyme contains a polypeptide segment within its reductase domain, which is absent in the inducible NOS enzyme. To study a possible link between the presence of these additional polypeptide segments in constitutive NOS enzymes and their calcium-dependent calmodulin activation, three deletion mutants were created. The putative inhibitory insert was removed from the FMN binding regions of the neuronal NOS holoenzyme and from two truncated neuronal NOS reductase enzymes in which the calmodulin binding region was either included or deleted. All three mutant enzymes showed reduced incorporation of FMN and required reconstitution with exogenous FMN for activity. The combined removal of both the calmodulin binding domain and the putative inhibitory insert did not result in a calmodulin-independent neuronal NOS reductase. Thus, although the putative inhibitory element has an effect on the calcium-dependent calmodulin activation of neuronal NOS, it does not have the properties of the typical autoinhibitory domain found in calmodulin-activated enzymes.

Characterization of hsp27 kinases activated by elevated aortic pressure in heart

PubMed Central

Boivin, Benoit; Khairallah, Maya; Cartier, Raymond; Allen, Bruce G.

2013-01-01

Chronic hemodynamic overload results in left ventricular hypertrophy, fibroblast proliferation, and interstitial fibrosis. The small heat shock protein hsp27 has been shown to be cardioprotective and this requires a phosphorylatable form of this protein. To further understand the regulation of hsp27 in heart in response to stress, we investigated the ability of elevated aortic pressure to activate hsp27-kinase activities. Isolated hearts were subjected to retrograde perfusion and then snap-frozen. Hsp27-kinase activity was measured in vitro as hsp27 phosphorylation. Immune complex assays revealed that MK2 activity was low in non-perfused hearts and increased following crystalline perfusion at 60 or 120 mmHg. Hsp27-kinase activities were further studied following ion-exchange chromatography. Anion exchange chromatography on Mono Q revealed 2 peaks (‘b’ and ‘c’) of hsp27-kinase activity. A third peak ‘a’ was detected upon chromatography of the Mono Q flow-through fractions on the cation exchange resin, Mono S. The hsp27-kinase activity underlying peaks ‘a’ and ‘c’ increased as perfusion pressure was increased from 40 to 120 mmHg. In contrast, peak ‘b’ increased over pressures 60–100 mmHg but was decreased at 120 mmHg. Peaks ‘a’, ‘b’, and ‘c’ contained MK2 immunoreactivity, whereas MK3 and MK5 immunoreactivity was detected in peak ‘a’. p38 MAPK and phospho-p38 MAPK were also detected in peaks ‘b’ and ‘c’ but absent from peak ‘a’. Hsp27-kinase activity in peaks ‘b’ and ‘c’ (120 mmHg) eluted from a Superose 12 gel filtration column with an apparent molecular mass of 50-kDa. Hence, peaks ‘b’ and ‘c’ were not a result of MK2 forming complexes. In-gel hsp27-kinase assays revealed a single 49-kDa renaturable hsp27-kinase activity in peaks ‘b’ and ‘c’ at 60 mmHg, whereas several hsp27-kinases (p43, p49, p54, p66) were detected in peaks ‘b’ and ‘c’ from hearts perfused at 120 mmHg. Thus

Lipoic acid synthetase deficiency causes neonatal-onset epilepsy, defective mitochondrial energy metabolism, and glycine elevation.

PubMed

Mayr, Johannes A; Zimmermann, Franz A; Fauth, Christine; Bergheim, Christa; Meierhofer, David; Radmayr, Doris; Zschocke, Johannes; Koch, Johannes; Sperl, Wolfgang

2011-12-09

Lipoic acid is an essential prosthetic group of four mitochondrial enzymes involved in the oxidative decarboxylation of pyruvate, α-ketoglutarate, and branched chain amino acids and in the glycine cleavage. Lipoic acid is synthesized stepwise within mitochondria through a process that includes lipoic acid synthetase. We identified the homozygous mutation c.746G>A (p.Arg249His) in LIAS in an individual with neonatal-onset epilepsy, muscular hypotonia, lactic acidosis, and elevated glycine concentration in plasma and urine. Investigation of the mitochondrial energy metabolism showed reduced oxidation of pyruvate and decreased pyruvate dehydrogenase complex activity. A pronounced reduction of the prosthetic group lipoamide was found in lipoylated proteins. Copyright © 2011 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.

Transcriptome and biomineralization responses of the pearl oyster Pinctada fucata to elevated CO2 and temperature.

PubMed

Li, Shiguo; Liu, Chuang; Huang, Jingliang; Liu, Yangjia; Zhang, Shuwen; Zheng, Guilan; Xie, Liping; Zhang, Rongqing

2016-01-06

Ocean acidification and global warming have been shown to significantly affect the physiological performances of marine calcifiers; however, the underlying mechanisms remain poorly understood. In this study, the transcriptome and biomineralization responses of Pinctada fucata to elevated CO2 (pH 7.8 and pH 7.5) and temperature (25 °C and 31 °C) are investigated. Increases in CO2 and temperature induced significant changes in gene expression, alkaline phosphatase activity, net calcification rates and relative calcium content, whereas no changes are observed in the shell ultrastructure. "Ion and acid-base regulation" related genes and "amino acid metabolism" pathway respond to the elevated CO2 (pH 7.8), suggesting that P. fucata implements a compensatory acid-base mechanism to mitigate the effects of low pH. Additionally, "anti-oxidation"-related genes and "Toll-like receptor signaling", "arachidonic acid metabolism", "lysosome" and "other glycan degradation" pathways exhibited responses to elevated temperature (25 °C and 31 °C), suggesting that P. fucata utilizes anti-oxidative and lysosome strategies to alleviate the effects of temperature stress. These responses are energy-consuming processes, which can lead to a decrease in biomineralization capacity. This study therefore is important for understanding the mechanisms by which pearl oysters respond to changing environments and predicting the effects of global climate change on pearl aquaculture.

Effect of simvastatin on the antihypertensive activity of losartan in hypertensive hypercholesterolemic animals and patients: role of nitric oxide, oxidative stress, and high-sensitivity C-reactive protein.

PubMed

Abdel-Zaher, Ahmed O; Elkoussi, Alaa Eldin A; Abudahab, Lotfy H; Elbakry, Mohammed H; Elsayed, Elsayed Abu-Elwafa

2014-06-01

This study investigated whether simvastatin has antihypertensive activity and can enhance the antihypertensive effect of losartan in hypertensive hypercholesterolemic animals and patients. Hypertension and hypercholesterolemia were induced in rats by L-NAME and cholesterol-enriched diet, respectively. In these animals, repeated administration of simvastatin decreased the systolic blood pressure, enhanced its progressive reductions induced by repeated administration of losartan, and corrected the compromised lipid profile. Concomitantly, repeated administration of simvastatin, losartan, or simvastatin in combination with losartan to these animals increased nitric oxide (NO) production and decreased the elevated serum malondialdehyde (MDA) and high-sensitivity C-reactive protein (hs-CRP) levels. Effects of combined treatment were greater than those of simvastatin or losartan alone. In hypertensive hypercholesterolemic patients, repeated administration of losartan decreased systolic and diastolic blood pressure, increased NO production, and decreased the elevated serum MDA and hs-CRP levels. Addition of simvastatin to losartan therapy enhanced these effects and corrected the compromised lipid profile. Simvastatin inhibited the contractile responses of isolated aortic rings induced by angiotensin II and enhanced the inhibitory effect of losartan on this preparation. l-arginine and acetylcholine enhanced, while L-NAME inhibited the effects of simvastatin, losartan, and their combination on these contractile responses. Thus, simvastatin exerts antihypertensive effect in hypertensive hypercholesterolemic animals and enhances the antihypertensive effect of losartan in hypertensive hypercholesterolemic animals and patients. Besides, its cholesterol-lowering effect, the ability of simvastatin to ameliorate endothelial dysfunction through increasing NO bioavailability and through suppression of oxidative stress and vascular inflammation may play an important role in these

Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice.

PubMed

Abdel-Salam, Omar M E; Youness, Eman R; Mohammed, Nadia A; Morsy, Safaa M Youssef; Omara, Enayat A; Sleem, Amany A

2014-05-01

Citric acid is a weak organic acid found in the greatest amounts in citrus fruits. This study examined the effect of citric acid on endotoxin-induced oxidative stress of the brain and liver. Mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 200 μg/kg). Citric acid was given orally at 1, 2, or 4 g/kg at time of endotoxin injection and mice were euthanized 4 h later. LPS induced oxidative stress in the brain and liver tissue, resulting in marked increase in lipid peroxidation (malondialdehyde [MDA]) and nitrite, while significantly decreasing reduced glutathione, glutathione peroxidase (GPx), and paraoxonase 1 (PON1) activity. Tumor necrosis factor-alpha (TNF-α) showed a pronounced increase in brain tissue after endotoxin injection. The administration of citric acid (1-2 g/kg) attenuated LPS-induced elevations in brain MDA, nitrite, TNF-α, GPx, and PON1 activity. In the liver, nitrite was decreased by 1 g/kg citric acid. GPx activity was increased, while PON1 activity was decreased by citric acid. The LPS-induced liver injury, DNA fragmentation, serum transaminase elevations, caspase-3, and inducible nitric oxide synthase expression were attenuated by 1-2 g/kg citric acid. DNA fragmentation, however, increased after 4 g/kg citric acid. Thus in this model of systemic inflammation, citric acid (1-2 g/kg) decreased brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation.

Citric Acid Effects on Brain and Liver Oxidative Stress in Lipopolysaccharide-Treated Mice

PubMed Central

Youness, Eman R.; Mohammed, Nadia A.; Morsy, Safaa M. Youssef; Omara, Enayat A.; Sleem, Amany A.

2014-01-01

Abstract Citric acid is a weak organic acid found in the greatest amounts in citrus fruits. This study examined the effect of citric acid on endotoxin-induced oxidative stress of the brain and liver. Mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 200 μg/kg). Citric acid was given orally at 1, 2, or 4 g/kg at time of endotoxin injection and mice were euthanized 4 h later. LPS induced oxidative stress in the brain and liver tissue, resulting in marked increase in lipid peroxidation (malondialdehyde [MDA]) and nitrite, while significantly decreasing reduced glutathione, glutathione peroxidase (GPx), and paraoxonase 1 (PON1) activity. Tumor necrosis factor-alpha (TNF-α) showed a pronounced increase in brain tissue after endotoxin injection. The administration of citric acid (1–2 g/kg) attenuated LPS-induced elevations in brain MDA, nitrite, TNF-α, GPx, and PON1 activity. In the liver, nitrite was decreased by 1 g/kg citric acid. GPx activity was increased, while PON1 activity was decreased by citric acid. The LPS-induced liver injury, DNA fragmentation, serum transaminase elevations, caspase-3, and inducible nitric oxide synthase expression were attenuated by 1–2 g/kg citric acid. DNA fragmentation, however, increased after 4 g/kg citric acid. Thus in this model of systemic inflammation, citric acid (1–2 g/kg) decreased brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation. PMID:24433072

In vitro antimicrobial activity of Medilox® super-oxidized water.

PubMed

Gunaydin, Murat; Esen, Saban; Karadag, Adil; Unal, Nevzat; Yanik, Keramettin; Odabasi, Hakan; Birinci, Asuman

2014-07-14

Super-oxidized water is one of the broad spectrum disinfectants, which was introduced recently. There are many researches to find reliable chemicals which are effective, inexpensive, easy to obtain and use, and effective for disinfection of microorganisms leading hospital infections. Antimicrobial activity of super-oxidized water is promising. The aim of this study was to investigate the in-vitro antimicrobial activity of different concentrations of Medilox® super-oxidized water that is approved by the Food and Drug Administration (FDA) as high level disinfectant. In this study, super-oxidized water obtained from Medilox® [Soosan E & C, Korea] device, which had been already installed in our hospital, was used. Antimicrobial activities of different concentrations of super-oxidized water (1/1, 1/2, 1/5, 1/10, 1/20, 1/50, 1/100) at different exposure times (1, 2, 5, 10, 30 min) against six ATCC strains, eight antibiotic resistant bacteria, yeasts and molds were evaluated using qualitative suspension test. Dey-Engley Neutralizing Broth [Sigma-Aldrich, USA] was used as neutralizing agent. Medilox® was found to be effective against all standard strains (Acinetobacter baumannii 19606, Escherichia coli 25922, Enterococcus faecalis 29212, Klebsiella pneumoniae 254988, Pseudomonas aeruginosa 27853, Staphylococcus aureus 29213), all clinical isolates (Acinetobacter baumannii, Escherichia coli, vancomycin-resistant Enterococcus faecium, Klebsiella pneumoniae, Pseudomonas aeruginosa, methicillin-resistant Staphylococcus aureus, Bacillus subtilis, Myroides spp.), and all yeastsat 1/1 dilution in ≥1 minute. It was found to be effective on Aspergillus flavus at 1/1 dilution in ≥2 minutes and on certain molds in ≥5 minutes. Medilox® super-oxidized water is a broad spectrum, on-site producible disinfectant, which is effective on bacteria and fungi and can be used for the control of nosocomial infection.

Enhancement of Catalytic Activity of Reduced Graphene Oxide Via Transition Metal Doping Strategy

NASA Astrophysics Data System (ADS)

Lee, Hangil; Hong, Jung A.

2017-06-01

To compare the catalytic oxidation activities of reduced graphene oxide (rGO) and rGO samples doped with five different transition metals (TM-rGO), we determine their effects on the oxidation of L-cysteine (Cys) in aqueous solution by performing electrochemistry (EC) measurements and on the photocatalytic oxidation of Cys by using high-resolution photoemission spectroscopy (HRPES) under UV illumination. Our results show that Cr-, Fe-, and Co-doped rGO with 3+ charge states (stable oxide forms: Cr3+, Fe3+, and Co3+) exhibit enhanced catalytic activities that are due to the charge states of the doped metal ions as we compare them with Cr-, Fe-, and Co-doped rGO with 2+ charge states.

Delta-aminolevulinate dehydratase activity and oxidative stress markers in preeclampsia.

PubMed

de Lucca, Leidiane; Rodrigues, Fabiane; Jantsch, Letícia B; Kober, Helena; Neme, Walter S; Gallarreta, Francisco M P; Gonçalves, Thissiane L

2016-12-01

Preeclampsia is an important pregnancy-specific multisystem disorder characterized by the onset of hypertension and proteinuria. It is of unknown etiology and involves serious risks for the pregnant women and fetus. One of the main factors involved in the pathophysiology of preeclampsia is oxidative stress, where excess free radicals produce harmful effects, including damage to macromolecules such as lipids, proteins and DNA. In addition, the sulfhydryl delta-aminolevulinate dehydratase enzyme (δ-ALA-D) that is part of the heme biosynthetic pathway in pro-oxidant conditions can be inhibited, which may result in the accumulation of 5-aminolevulinic acid (ALA), associated with the overproduction of free radicals, suggesting it to be an indirect marker of oxidative stress. As hypertensive pregnancy complications are a major cause of morbidity and mortality maternal and fetal where oxidative stress appears to be an important factor involved in preeclampsia, the aim of this study was to evaluate the activity of δ-ALA-D and classic oxidative stress markers in the blood of pregnant women with mild and severe preeclampsia. The analysis and quantification of the following oxidative stress markers were performed: thiobarbituric acid-reactive species (TBARS); presence of protein and non-protein thiol group; quantification of vitamin C; Catalase and δ-ALA--D activities in samples of blood of pregnant women with mild preeclampsia (n=25), with severe preeclampsia (n=30) and in a control group of healthy pregnant women (n=30). TBARS was significantly higher in women with preeclampsia, while the presence of thiol groups, levels of vitamin C, catalase and δ-ALA-D activity were significantly lower in groups of pregnant women with preeclampsia compared with healthy women. In addition, the results showed no significant difference between groups of pregnant women with mild and severe preeclampsia. The data suggest a state of increased oxidative stress in pregnant women with

Elevated phospholipase D activity in androgen-insensitive prostate cancer cells promotes both survival and metastatic phenotypes.

PubMed

Utter, Matthew; Chakraborty, Sohag; Goren, Limor; Feuser, Lucas; Zhu, Yuan-Shan; Foster, David A

2018-06-01

Prostate cells are hormonally driven to grow and divide. Typical treatments for prostate cancer involve blocking activation of the androgen receptor by androgens. Androgen deprivation therapy can lead to the selection of cancer cells that grow and divide independently of androgen receptor activation. Prostate cancer cells that are insensitive to androgens commonly display metastatic phenotypes and reduced long-term survival of patients. In this study we provide evidence that androgen-insensitive prostate cancer cells have elevated PLD activity relative to the androgen-sensitive prostate cancer cells. PLD activity has been linked with promoting survival in many human cancer cell lines; and consistent with the previous studies, suppression of PLD activity in the prostate cancer cells resulted in apoptotic cell death. Of significance, suppressing the elevated PLD activity in androgen resistant prostate cancer lines also blocked the ability of these cells to migrate and invade Matrigel™. Since survival signals are generally an early event in tumorigenesis, the apparent coupling of survival and metastatic phenotypes implies that metastasis is an earlier event in malignant prostate cancer than generally thought. This finding has implications for screening strategies designed to identify prostate cancers before dissemination. Copyright © 2018 Elsevier B.V. All rights reserved.

Synthesis and photocatalytic activity of electrospun niobium oxide nanofibers

DOE Office of Scientific and Technical Information (OSTI.GOV)

Qi, Shishun; Zuo, Ruzhong, E-mail: piezolab@hfut.edu.cn; Liu, Yi

2013-03-15

Graphical abstract: Different morphologies are obtained for the electrospun niobium oxide nanofibers with different phase structures. The nanofibers of the two phase structures present different band gap value and the light absorption. Hexagonal phase nanofibers show better photocatalytic activity compared with the orthorhombic nanofibers. Highlights: ► Niobium oxide nanofibers of two phase structures were fabricated by electrospinning. ► Photocatalytic properties of the niobium oxide nanofibers were first explored. ► Nanofibers of different phase structures showed different photocatalytic activities. ► Reasons for the differences in the photocatalysis were carefully discussed. - Abstract: Niobium oxide (Nb{sub 2}O{sub 5}) nanofibers have been synthesizedmore » by sol–gel based electrospinning technique. Pure hexagonal phase (H-Nb{sub 2}O{sub 5}) and orthorhombic phase (O-Nb{sub 2}O{sub 5}) nanofibers were obtained by thermally annealing the electrospun Nb{sub 2}O{sub 5}/polyvinylpyrrolidone composite fibers in air at 500 °C and 700 °C, respectively. The fibers were characterized using the X-ray diffraction, scanning electron microscopy, specific surface area analyzer and UV–vis diffuse reflectance spectroscopy. Photocatalytic activities of the obtained nanofibers were evaluated depending on the degradation of methyl orange. The results indicate that the heat-treatment temperature, the crystalline structure and the morphology affected the physical and chemical properties of the as-prepared Nb{sub 2}O{sub 5} nanofibers. The H-Nb{sub 2}O{sub 5} nanofibers obtained at lower temperature showed better potential for the application as a promising photocatalyst.« less

In situ-generated metal oxide catalyst during CO oxidation reaction transformed from redox-active metal-organic framework-supported palladium nanoparticles

PubMed Central

2012-01-01

The preparation of redox-active metal-organic framework (ra-MOF)-supported Pd nanoparticles (NPs) via the redox couple-driven method is reported, which can yield unprotected metallic NPs at room temperature within 10 min without the use of reducing agents. The Pd@ra-MOF has been exploited as a precursor of an active catalyst for CO oxidation. Under the CO oxidation reaction condition, Pd@ra-MOF is transformed into a PdOx-NiOy/C nanocomposite to generate catalytically active species in situ, and the resultant nanocatalyst shows sustainable activity through synergistic stabilization. PMID:22898143

NOpiates: Novel Dual Action Neuronal Nitric Oxide Synthase Inhibitors with μ-Opioid Agonist Activity.

PubMed

Renton, Paul; Green, Brenda; Maddaford, Shawn; Rakhit, Suman; Andrews, John S

2012-03-08

A novel series of benzimidazole designed multiple ligands (DMLs) with activity at the neuronal nitric oxide synthase (nNOS) enzyme and the μ-opioid receptor was developed. Targeting of the structurally dissimilar heme-containing enzyme and the μ-opioid GPCR was predicated on the modulatory role of nitric oxide on μ-opioid receptor function. Structure-activity relationship studies yielded lead compound 24 with excellent nNOS inhibitory activity (IC50 = 0.44 μM), selectivity over both endothelial nitric oxide synthase (10-fold) and inducible nitric oxide synthase (125-fold), and potent μ-opioid binding affinity, K i = 5.4 nM. The functional activity as measured in the cyclic adenosine monosphospate secondary messenger assay resulted in full agonist activity (EC50 = 0.34 μM). This work represents a novel approach in the development of new analgesics for the treatment of pain.

Effects of acute cigarette smoking on total blood count and markers of oxidative stress in active and passive smokers.

PubMed

Lymperaki, E; Makedou, K; Iliadis, S; Vagdatli, E

2015-01-01

Free radicals, as a product of cigarette smoke, are considered to have deleterious effects causing oxidative stress. Acute active smoking seems to be followed by transient leukocytosis and delayed increase in neutrophil activation. The aim of the present study was to investigate the oxidative status of smokers and passive non-smokers, as well as the impact that acute cigarette smoking has on hematological parameters. Thirty-two healthy volunteers, 16 active smokers (Group A) aged 20-23 years and 16 age-matched, non-smokers (Group B), 18 women and 14 men in total, participated voluntarily in the study. All subjects did not have any food, drink, or cigarette smoking for eight hours before the study. Each time, two active smokers and two non-smokers were exposed simultaneously for half an hour to the smoke of two cigarettes smoked consecutively by the smokers. Blood was drawn before and after the exposure to cigarette smoke. Whole blood was analyzed immediately for total blood count parameters and serum was stored in -70(◦)C until serum levels of malondialdehyde (MDA) and vitamin E (VitE), and total antioxidant capacity (TAC) were determined. No statistical significant difference was observed in the values of white blood cells and their subpopulations between the two groups and within the same group before and after exposure to cigarette smoke. In the group of smokers, granulocyte/lymphocyte ratio increased significantly, MDA levels showed significant elevation and protective VitE serum levels decreased significantly, whereas TAC was reduced, but not significantly, after the exposure. In the group of passive, non-smokers the results of the blood count parameters, MDA and VitE were similar to Group A, and there was a significant decrease in TAC, as well. Between the two groups, only hematocrit values and MDA levels differed significantly before the exposure to smoke, and no other significant difference was detected before or after the exposure, between active and

Iron active electrode and method of making same

DOEpatents

Jackovitz, John F.; Seidel, Joseph; Pantier, Earl A.

1982-10-26

An iron active electrode and method of preparing same in which iron sulfate is calcined in an oxidizing atmosphere at a temperature in the range of from about 600.degree. C. to about 850.degree. C. for a time sufficient to produce an iron oxide with a trace amount of sulfate. The calcined material is loaded into an electrically conductive support and then heated in a reducing atmosphere at an elevated temperature to produce activated iron having a trace amount of sulfide which is formed into an electrode plate.

Transgenic Mouse Model for Reducing Oxidative Damage in Bone

NASA Technical Reports Server (NTRS)

Schreurs, Ann-Sofie; Torres, S.; Truong, T.; Moyer, E. L.; Kumar, A.; Tahimic, Candice C. G.; Alwood, J. S.; Limoli, C. L.; Globus, R. K.

2016-01-01

Bone loss can occur due to many challenges such age, radiation, microgravity, and Reactive Oxygen Species (ROS) play a critical role in bone resorption by osteoclasts (Bartell et al. 2014). We hypothesize that suppression of excess ROS in skeletal cells, both osteoblasts and osteoclasts, regulates skeletal growth and remodeling. To test our hypothesis, we used transgenic mCAT mice which overexpress the human anti-oxidant catalase gene targeted to the mitochondria, the main site for endogenous ROS production. mCAT mice have a longer life-span than wildtype controls and have been used to study various age-related disorders. To stimulate remodeling, 16 week old mCAT mice or wildtype mice were exposed to treatment (hindlimb-unloading and total body-irradiation) or sham treatment conditions (control). Tissues were harvested 2 weeks later for skeletal analysis (microcomputed tomography), biochemical analysis (gene expression and oxidative damage measurements), and ex vivo bone marrow derived cell culture (osteoblastogenesis and osteoclastogenesis). mCAT mice expressed the transgene and displayed elevated catalase activity in skeletal tissue and marrow-derived osteoblasts and osteoclasts grown ex vivo. In addition, when challenged with treatment, bone tissues from wildtype mice showed elevated levels of malondialdehyde (MDA), indicating oxidative damage) whereas mCAT mice did not. Correlation analysis revealed that increased catalase activity significantly correlated with decreased MDA levels and that increased oxidative damage correlated with decreased percent bone volume (BVTV). In addition, ex-vivo cultured osteoblast colony growth correlated with catalase activity in the osteoblasts. Thus, we showed that these transgenic mice can be used as a model to study the relationship between markers of oxidative damage and skeletal properties. mCAT mice displayed reduced BVTV and trabecular number relative to wildtype mice, as well as increased structural model index in the

Cocaine promotes oxidative stress and microglial-macrophage activation in rat cerebellum

PubMed Central

López-Pedrajas, Rosa; Ramírez-Lamelas, Dolores T.; Muriach, Borja; Sánchez-Villarejo, María V.; Almansa, Inmaculada; Vidal-Gil, Lorena; Romero, Francisco J.; Barcia, Jorge M.; Muriach, María

2015-01-01

Different mechanisms have been suggested for cocaine neurotoxicity, including oxidative stress alterations. Nuclear factor kappa B (NF-κB), considered a sensor of oxidative stress and inflammation, is involved in drug toxicity and addiction. NF-κB is a key mediator for immune responses that induces microglial/macrophage activation under inflammatory processes and neuronal injury/degeneration. Although cerebellum is commonly associated to motor control, muscular tone, and balance. Its relation with addiction is getting relevance, being associated to compulsive and perseverative behaviors. Some reports indicate that cerebellar microglial activation induced by cannabis or ethanol, promote cerebellar alterations and these alterations could be associated to addictive-related behaviors. After considering the effects of some drugs on cerebellum, the aim of the present work analyzes pro-inflammatory changes after cocaine exposure. Rats received daily 15 mg/kg cocaine i.p., for 18 days. Reduced and oxidized forms of glutathione (GSH) and oxidized glutathione (GSSG), glutathione peroxidase (GPx) activity and glutamate were determined in cerebellar homogenates. NF-κB activity, CD68, and GFAP expression were determined. Cerebellar GPx activity and GSH/GSSG ratio are significantly decreased after cocaine exposure. A significant increase of glutamate concentration is also observed. Interestingly, increased NF-κB activity is also accompanied by an increased expression of the lysosomal mononuclear phagocytic marker ED1 without GFAP alterations. Current trends in addiction biology are focusing on the role of cerebellum on addictive behaviors. Cocaine-induced cerebellar changes described herein fit with previosus data showing cerebellar alterations on addict subjects and support the proposed role of cerebelum in addiction. PMID:26283916

Cocaine promotes oxidative stress and microglial-macrophage activation in rat cerebellum.

PubMed

López-Pedrajas, Rosa; Ramírez-Lamelas, Dolores T; Muriach, Borja; Sánchez-Villarejo, María V; Almansa, Inmaculada; Vidal-Gil, Lorena; Romero, Francisco J; Barcia, Jorge M; Muriach, María

2015-01-01

Different mechanisms have been suggested for cocaine neurotoxicity, including oxidative stress alterations. Nuclear factor kappa B (NF-κB), considered a sensor of oxidative stress and inflammation, is involved in drug toxicity and addiction. NF-κB is a key mediator for immune responses that induces microglial/macrophage activation under inflammatory processes and neuronal injury/degeneration. Although cerebellum is commonly associated to motor control, muscular tone, and balance. Its relation with addiction is getting relevance, being associated to compulsive and perseverative behaviors. Some reports indicate that cerebellar microglial activation induced by cannabis or ethanol, promote cerebellar alterations and these alterations could be associated to addictive-related behaviors. After considering the effects of some drugs on cerebellum, the aim of the present work analyzes pro-inflammatory changes after cocaine exposure. Rats received daily 15 mg/kg cocaine i.p., for 18 days. Reduced and oxidized forms of glutathione (GSH) and oxidized glutathione (GSSG), glutathione peroxidase (GPx) activity and glutamate were determined in cerebellar homogenates. NF-κB activity, CD68, and GFAP expression were determined. Cerebellar GPx activity and GSH/GSSG ratio are significantly decreased after cocaine exposure. A significant increase of glutamate concentration is also observed. Interestingly, increased NF-κB activity is also accompanied by an increased expression of the lysosomal mononuclear phagocytic marker ED1 without GFAP alterations. Current trends in addiction biology are focusing on the role of cerebellum on addictive behaviors. Cocaine-induced cerebellar changes described herein fit with previosus data showing cerebellar alterations on addict subjects and support the proposed role of cerebelum in addiction.

Feedback inhibition of nitric oxide synthase activity by nitric oxide.

PubMed Central

Assreuy, J.; Cunha, F. Q.; Liew, F. Y.; Moncada, S.

1993-01-01

1. A murine macrophage cell line, J774, expressed nitric oxide (NO) synthase activity in response to interferon-gamma (IFN-gamma, 10 u ml-1) plus lipopolysaccharide (LPS, 10 ng ml-1). The enzyme activity was first detectable 6 h after incubation, peaked at 12 h and became undetectable after 48 h. 2. The decline in the NO synthase activity was not due to inhibition by stable substances secreted by the cells into the culture supernatant. 3. The decline in the NO synthase activity was significantly slowed down in cells cultured in a low L-arginine medium or with added haemoglobin, suggesting that NO may be involved in a feedback inhibitory mechanism. 4. The addition of NO generators, S-nitroso-acetyl-penicillamine (SNAP) or S-nitroso-glutathione (GSNO) markedly inhibited the NO synthase activity in a dose-dependent manner. The effect of NO on the enzyme was not due to the inhibition of de novo protein synthesis. 5. SNAP directly inhibited the inducible NO synthase extracted from activated J774 cells, as well as the constitutive NO synthase extracted from the rat brain. 6. The enzyme activity of J774 cells was not restored after the removal of SNAP by gel filtration, suggesting that NO inhibits NO synthase irreversibly. PMID:7682140

Architectural design and physical activity: an observational study of staircase and elevator use in different buildings.

PubMed

Bassett, David R; Browning, Ray; Conger, Scott A; Wolff, Dana L; Flynn, Jennifer I

2013-05-01

The indoor built environment has the potential to influence levels of physical activity. However, the extent to which architectural design in commercial buildings can influence the percentage of people choosing to use the stairs versus elevators is unknown. The purpose of this study was to determine if buildings with centrally located, accessible, and aesthetically pleasing staircases result in a greater percentage of people taking the stairs. Direct observations of stair and elevator use were conducted in 3 buildings on a university campus. One of the buildings had a bank of 4 centrally located elevators and a fire escape stairwell behind a steel door. The other 2 buildings had centrally located staircases and out-of-the-way elevators. The percentage of people who ascended the stairs was 8.1% in the elevator-centric building, compared with 72.8% and 81.1% in the 2 stair-centric buildings (P < .001). In addition, the percentage of people who descended the stairs was 10.8% in the first building, compared with 89.5% and 93.7% in the stair-centric buildings (P < .001). The results of the current study suggest that if buildings are constructed with centrally located, accessible, and aesthetically pleasing staircases, a greater percentage of people will choose to take the stairs.

Controlling lipid oxidation via a biomimetic iron chelating active packaging material.

PubMed

Tian, Fang; Decker, Eric A; Goddard, Julie M

2013-12-18

Previously, a siderophore-mimetic metal chelating active packaging film was developed by grafting poly(hydroxamic acid) (PHA) from the surface of polypropylene (PP) films. The objective of the current work was to demonstrate the potential applicability of this PP-g-PHA film to control iron-promoted lipid oxidation in food emulsions. The iron chelating activity of this film was investigated, and the surface chemistry and color intensity of films were also analyzed after iron chelation. In comparison to the iron chelating activity in the free Fe(3+) solution, the PP-g-PHA film retained approximately 50 and 30% of its activity in nitrilotriacetic acid (NTA)/Fe(3+) and citric acid/Fe(3+) solutions, respectively (pH 5.0), indicating a strong chelating strength for iron. The ability of PP-g-PHA films to control lipid oxidation was demonstrated in a model emulsion system (pH 3.0). PP-g-PHA films performed even better than ethylenediaminetetraacetic acid (EDTA) in preventing the formation of volatile oxidation products. The particle size and ζ potential results of emulsions indicated that PP-g-PHA films had no adverse effects on the stability of the emulsion system. Attenuated total reflectance Fourier transform infrared spectroscopy (ATR-FTIR) analysis suggested a non-migratory nature of the PP-g-PHA film surface. These results suggest that such biomimetic, non-migratory metal chelating active packaging films have commercial potential in protecting foods against iron-promoted lipid oxidation.

Single Silver Adatoms on Nanostructured Manganese Oxide Surfaces: Boosting Oxygen Activation for Benzene Abatement.

PubMed

Chen, Yaxin; Huang, Zhiwei; Zhou, Meijuan; Ma, Zhen; Chen, Jianmin; Tang, Xingfu

2017-02-21

The involvement of a great amount of active oxygen species is a crucial requirement for catalytic oxidation of benzene, because complete mineralization of one benzene molecule needs 15 oxygen atoms. Here, we disperse single silver adatoms on nanostructured hollandite manganese oxide (HMO) surfaces by using a thermal diffusion method. The single-atom silver catalyst (Ag 1 /HMO) shows high catalytic activity in benzene oxidation, and 100% conversion is achieved at 220 °C at a high space velocity of 23 000 h -1 . The Mars-van Krevelen mechanism is valid in our case as the reaction orders for both benzene and O 2 approach one, according to reaction kinetics data. Data from H 2 temperature-programmed reduction and O core-level X-ray photoelectron spectra (XPS) reveal that Ag 1 /HMO possesses a great amount of active surface lattice oxygen available for benzene oxidation. Valence-band XPS and density functional theoretical calculations demonstrate that the single Ag adatoms have the upshifted 4d orbitals, thus facilitating the activation of gaseous oxygen. Therefore, the excellent activation abilities of Ag 1 /HMO toward both surface lattice oxygen and gaseous oxygen account for its high catalytic activity in benzene oxidation. This work may assist with the rational design of efficient metal-oxide catalysts for the abatement of volatile organic compounds such as benzene.

Hindlimb unloading increases oxidative stress and disrupts antioxidant capacity in skeletal muscle

NASA Technical Reports Server (NTRS)

Lawler, John M.; Song, Wook; Demaree, Scott R.; Bloomfield, S. A. (Principal Investigator)

2003-01-01

Skeletal muscle disuse with space-flight and ground-based models (e.g., hindlimb unloading) results in dramatic skeletal muscle atrophy and weakness. Pathological conditions that cause muscle wasting (i.e., heart failure, muscular dystrophy, sepsis, COPD, cancer) are characterized by elevated "oxidative stress," where antioxidant defenses are overwhelmed by oxidant production. However, the existence, cellular mechanisms, and ramifications of oxidative stress in skeletal muscle subjected to hindlimb unloading are poorly understood. Thus we examined the effects of hindlimb unloading on hindlimb muscle antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase), nonenzymatic antioxidant scavenging capacity (ASC), total hydroperoxides, and dichlorohydrofluorescein diacetate (DCFH-DA) oxidation, a direct indicator of oxidative stress. Twelve 6 month old Sprague Dawley rats were divided into two groups: 28 d of hindlimb unloading (n = 6) and controls (n = 6). Hindlimb unloading resulted in a small decrease in Mn-superoxide dismutase activity (10.1%) in the soleus muscle, while Cu,Zn-superoxide dismutase increased 71.2%. In contrast, catalase and glutathione peroxidase, antioxidant enzymes that remove hydroperoxides, were significantly reduced in the soleus with hindlimb unloading by 54.5 and 16.1%, respectively. Hindlimb unloading also significantly reduced ASC. Hindlimb unloading increased soleus lipid hydroperoxide levels by 21.6% and hindlimb muscle DCFH-DA oxidation by 162.1%. These results indicate that hindlimb unloading results in a disruption of antioxidant status, elevation of hydroperoxides, and an increase in oxidative stress.

Elevated hepatic fatty acid elongase-5 activity corrects dietary fat-induced hyperglycemia in obese BL/6J mice[S

PubMed Central

Tripathy, Sasmita; Torres-Gonzalez, Moises; Jump, Donald B.

2010-01-01

Elevated hepatic fatty acid elongase-5 (Elovl5) activity lowers blood glucose in fasted chow-fed C57BL/6J mice. As high-fat diets induce hyperglycemia and suppress hepatic Elovl5 activity, we tested the hypothesis that elevated hepatic Elovl5 expression attenuates hyperglycemia in high-fat-diet-induced obese mice. Increasing hepatic Elovl5 activity by a recombinant adenoviral approach restored blood glucose and insulin, HOMA-IR, and glucose tolerance to normal values in obese mice. Elevated Elovl5 activity increased hepatic content of Elovl5 products (20:3,n-6, 22:4,n-6) and suppressed levels of enzymes (Pck1, G6Pc) and transcription factors (FoxO1 and PGC1α, but not CRTC2) involved in gluconeogenesis. Effects of Elovl5 on FoxO1 nuclear abundance correlated with increased phosphorylation of FoxO1, Akt, and the catalytic unit of PP2A, as well as a decline in cellular abundance of TRB3. Such changes are mechanistically linked to the regulation of FoxO1 nuclear abundance and gluconeogenesis. These results show that Elovl5 activity impacts the hepatic abundance and phosphorylation status of multiple proteins involved in gluconeogenesis. Our findings establish a link between fatty acid elongation and hepatic glucose metabolism and suggest a role for regulators of Elovl5 activity in the treatment of diet-induced hyperglycemia. PMID:20488798

Sarcopenia is a risk factor for elevated aminotransferase in men independently of body mass index, dietary habits, and physical activity.

PubMed

Yoo, Ki Deok; Jun, Dae Won; Lee, Kang Nyeong; Lee, Hang Lak; Lee, Oh Young; Yoon, Byung Chul; Choi, Ho Soon

2015-04-01

Aminotransferase activity is a surrogate marker of liver injury showing strong correlations with obesity and metabolic syndrome. However, elevated aminotransferase activity is not uncommon in non-obese and non-alcoholic patients in clinical practice. To examine the relationship between sarcopenia and aminotransferase activity in a large population-based cohort. Data from the Korean National Health and Nutrition Examinations were used. A total of 13,431 subjects were included. A whole-body dual X-ray absorptiometry scan was performed on each patient to measure total and regional muscle mass. Appendicular skeletal muscle mass indices were also obtained. The prevalence of sarcopenia was significantly higher in the group with elevated aminotransferase levels than in the normal liver enzyme group (males: 26.5% vs. 16.9%; females: 38.3% vs. 22.1%, p<0.05). The skeletal muscle index was negatively correlated with most cardiometabolic risk factors, including fasting glucose and cholesterol levels. The frequency of elevated aminotransferase increased in male patients with sarcopenia after adjusting for potential confounding factors including age, body mass index, fasting glucose level, dietary, and exercise habits. However, the correlation was no longer observed in women after adjusting for body mass index. Sarcopenia is a risk factor for elevated aminotransferase in men, independently of body mass index, dietary habits, and physical activity. Copyright © 2015 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

Oxidative stress is associated with decreased heart rate variability in patients with chronic kidney disease.

PubMed

Fadaee, Shannon B; Beetham, Kassia S; Howden, Erin J; Stanton, Tony; Isbel, Nicole M; Coombes, Jeff S

2017-09-01

Elevated oxidative stress and reduced heart rate variability (HRV) is prevalent in patients with chronic kidney disease (CKD) and is associated with increased morbidity and mortality. Previous studies have identified a positive association between elevated oxidative stress and autonomic dysfunction, however this relationship has not yet been investigated in the CKD population. Plasma was collected from 78 patients with stage 3-4 CKD (estimated glomerular filtration rate 25-60 ml/min/1.73 m 2 ) for the assessment of oxidative stress, including plasma total F2-isoprostanes, glutathione peroxidase activity and total antioxidant capacity. Time and frequency HRV parameters were measured from a three lead electrocardiogram. Participants with elevated F2-isoprostanes had reduced HRV compared to patients with normal levels of F2-isoprostanes. A number of HRV parameters were found to be inversely correlated with F2-isoprostanes in all CKD patients, including SDNN (r = -0.337; P < 0.01), VLF (r = -0.281, P = 0.01), LF (r = -0.315, P < 0.01) and total power (r = -0.288, P = 0.01). Multiple linear regression found F2-isoprostanes to be an independent predictor of SDNN (r 2  = 0.287, β = -0.272, P = 0.01). Oxidative stress is significantly and independently associated with HRV in patients with CKD. Identifying oxidative stress in the pathogenesis of autonomic dysfunction may help target therapeutic strategies.

Nitric oxide-induced calcium release: activation of type 1 ryanodine receptor by endogenous nitric oxide.

PubMed

Kakizawa, Sho; Yamazawa, Toshiko; Iino, Masamitsu

2013-01-01

Ryanodine receptors (RyRs), located in the sarcoplasmic/endoplasmic reticulum (SR/ER) membrane, are required for intracellular Ca2+ release that is involved in a wide range of cellular functions. In addition to Ca2+-induced Ca2+ release in cardiac cells and voltage-induced Ca2+ release in skeletal muscle cells, we recently identified another mode of intracellular Ca2+ mobilization mediated by RyR, i.e., nitric oxide-induced Ca2+ release (NICR), in cerebellar Purkinje cells. NICR is evoked by neuronal activity, is dependent on S-nitrosylation of type 1 RyR (RyR1) and is involved in the induction of long-term potentiation (LTP) of cerebellar synapses. In this addendum, we examined whether peroxynitrite, which is produced by the reaction of nitric oxide with superoxide, may also have an effect on the Ca2+ release via RyR1 and the cerebellar LTP. We found that scavengers of peroxynitrite have no significant effect either on the Ca2+ release via RyR1 or on the cerebellar LTP. We also found that an application of a high concentration of peroxynitrite does not reproduce neuronal activity-dependent Ca2+ release in Purkinje cells. These results support that NICR is induced by endogenous nitric oxide produced by neuronal activity through S-nitrosylation of RyR1.

Detection of HOCl-mediated protein oxidation products in the extracellular matrix of human atherosclerotic plaques.

PubMed Central

Woods, Alan A; Linton, Stuart M; Davies, Michael J

2003-01-01

Oxidation is believed to play a role in atherosclerosis. Oxidized lipids, sterols and proteins have been detected in early, intermediate and advanced human lesions at elevated levels. The spectrum of oxidized side-chain products detected on proteins from homogenates of advanced human lesions has been interpreted in terms of the occurrence of two oxidative mechanisms, one involving oxygen-derived radicals catalysed by trace transition metal ions, and a second involving chlorinating species (HOCl or Cl2), generated by the haem enzyme myeloperoxidase (MPO). As MPO is released extracellularly by activated monocytes (and possibly macrophages) and is a highly basic protein, it would be expected to associate with polyanions such as the glycosaminoglycans of the extracellular matrix, and might result in damage being localized at such sites. In this study proteins extracted from extracellular matrix material obtained from advanced human atherosclerotic lesions are shown to contain elevated levels of oxidized amino acids [3,4-dihydroxyphenylalanine (DOPA), di-tyrosine, 2-hydroxyphenylalanine ( o-Tyr)] when compared with healthy (human and pig) arterial tissue. These matrix-derived materials account for 83-96% of the total oxidized protein side-chain products detected in these plaques. Oxidation of matrix components extracted from healthy artery tissue, and model proteins, with reagent HOCl is shown to give rise to a similar pattern of products to those detected in advanced human lesions. The detection of elevated levels of DOPA and o-Tyr, which have been previously attributed to the occurrence of oxygen-radical-mediated reactions, by HOCl treatment, suggests an alternative route to the formation of these materials in plaques. This is believed to involve the formation and subsequent decomposition of protein chloramines. PMID:12456264

Elucidating anionic oxygen activity in lithium-rich layered oxides

DOE Office of Scientific and Technical Information (OSTI.GOV)

Xu, Jing; Sun, Meiling; Qiao, Ruimin

Recent research has explored combining conventional transition metal redox with anionic lattice oxygen redox as a new and exciting direction to search for high-capacity lithium-ion cathodes. For this study, we probe the poorly understood electrochemical activity of anionic oxygen from a material perspective by elucidating the effect of the transition metal on oxygen redox activity. We study two lithium-rich layered oxides, specifically lithium nickel metal oxides where metal is either manganese or ruthenium, which possess similar structure and discharge characteristics, but exhibit distinctly different charge profiles. By combining X-ray spectroscopy with operando differential electrochemical mass spectrometry, we reveal completely differentmore » oxygen redox activity in each material, likely resulting from the different interaction between the lattice oxygen and transition metals. This work provides additional insights into the complex mechanism of oxygen redox and development of advanced high-capacity lithium-ion cathodes.« less

Elucidating anionic oxygen activity in lithium-rich layered oxides

DOE PAGES

Xu, Jing; Sun, Meiling; Qiao, Ruimin; ...

2018-03-05

Recent research has explored combining conventional transition metal redox with anionic lattice oxygen redox as a new and exciting direction to search for high-capacity lithium-ion cathodes. For this study, we probe the poorly understood electrochemical activity of anionic oxygen from a material perspective by elucidating the effect of the transition metal on oxygen redox activity. We study two lithium-rich layered oxides, specifically lithium nickel metal oxides where metal is either manganese or ruthenium, which possess similar structure and discharge characteristics, but exhibit distinctly different charge profiles. By combining X-ray spectroscopy with operando differential electrochemical mass spectrometry, we reveal completely differentmore » oxygen redox activity in each material, likely resulting from the different interaction between the lattice oxygen and transition metals. This work provides additional insights into the complex mechanism of oxygen redox and development of advanced high-capacity lithium-ion cathodes.« less

Mitochondrial oxidative stress is the achille's heel of melanoma cells resistant to Braf-mutant inhibitor

PubMed Central

André, Fanny; Jonneaux, Aurélie; Scalbert, Camille; Garçon, Guillaume; Malet-Martino, Myriam; Balayssac, Stéphane; Rocchi, Stephane; Savina, Ariel; Formstecher, Pierre; Mortier, Laurent; Kluza, Jérome; Marchetti, Philippe

2013-01-01

Vemurafenib/PLX4032, a selective inhibitor of mutant BRAFV600E, constitutes a paradigm shift in melanoma therapy. Unfortunately, acquired resistance, which unavoidably occurs, represents one major limitation to clinical responses. Recent studies have highlighted that vemurafenib activated oxidative metabolism in BRAFV600E melanomas expressing PGC1α. However, the oxidative state of melanoma resistant to BRAF inhibitors is unknown. We established representative in vitro and in vivo models of human melanoma resistant to vemurafenib including primary specimens derived from melanoma patients. Firstly, our study reveals that vemurafenib increased mitochondrial respiration and ROS production in BRAFV600E melanoma cell lines regardless the expression of PGC1α. Secondly, melanoma cells that have acquired resistance to vemurafenib displayed intrinsically high rates of mitochondrial respiration associated with elevated mitochondrial oxidative stress irrespective of the presence of vemurafenib. Thirdly, the elevated ROS level rendered vemurafenib-resistant melanoma cells prone to cell death induced by pro-oxidants including the clinical trial drug, elesclomol. Based on these observations, we propose that the mitochondrial oxidative signature of resistant melanoma constitutes a novel opportunity to overcome resistance to BRAF inhibition. PMID:24161908

NOpiates: Novel Dual Action Neuronal Nitric Oxide Synthase Inhibitors with μ-Opioid Agonist Activity

PubMed Central

2012-01-01

A novel series of benzimidazole designed multiple ligands (DMLs) with activity at the neuronal nitric oxide synthase (nNOS) enzyme and the μ-opioid receptor was developed. Targeting of the structurally dissimilar heme-containing enzyme and the μ-opioid GPCR was predicated on the modulatory role of nitric oxide on μ-opioid receptor function. Structure–activity relationship studies yielded lead compound 24 with excellent nNOS inhibitory activity (IC50 = 0.44 μM), selectivity over both endothelial nitric oxide synthase (10-fold) and inducible nitric oxide synthase (125-fold), and potent μ-opioid binding affinity, Ki = 5.4 nM. The functional activity as measured in the cyclic adenosine monosphospate secondary messenger assay resulted in full agonist activity (EC50 = 0.34 μM). This work represents a novel approach in the development of new analgesics for the treatment of pain. PMID:24900459

Active CMV and EBV infections in renal transplant recipients with unexplained fever and elevated serum creatinine.

PubMed

Hasannia, Tahereh; Moosavi Movahed, Seyed Majid; Vakili, Rosita; Rafatpanah, Houshang; Hekmat, Reza; Valizadeh, Narges; Rezaee, Seyed Abdolrahim

2016-10-01

Proper identification of active cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections are helpful for monitoring antiviral treatment in transplant recipients. Qualitative and quantitative CMV, EBV DNA PCR techniques in the context of serological tests are performed for early detection and differentiation of active and latent CMV and EBV infections in renal transplantation. Basically, 129 renal transplanted recipients monitored carefully and hospitalized for unexplained elevated creatinine levels or high fever and 21 of their donors were studied. CMV DNA was detected in 63.5% of the febrile episodes following transplantation and in 46.42% of readmitted patients using qualitative PCR method. In the first group, 15% of the patients and in the second group 42.85% of the patients had copy numbers more than cutoff point (900 copies/mL). Cutoff point had 100% sensitivity and 82.5% specificity for active and symptomatic CMV infection. Only 15.5% of the subjects were positive for EBV infection by qualitative PCR method. Among them 5% had >2000 copies/mL and were symptomatic. One subject with a history of three times hospitalization had higher EBV viral load and developed post-transplant lymphoproliferative disorder. CMV load was significantly correlated with elevated creatinine levels (OR = 3.1, p = 0.006), abnormal heart sounds (OR = 4.7; p = 0.02) and hypertension (OR = 3.6; p = 0.03). Only qRT-PCR could differentiate between latent and active infections and might be clinically useful for monitoring symptomatic CMV and EBV infections and initiation of the antiviral therapy. Elevated creatinine levels, hypertension, and abnormal heart sounds could be considered as main manifestations of HCMV infection in kidney recipients.

High-intensity interval training prevents oxidant-mediated diaphragm muscle weakness in hypertensive mice.

PubMed

Bowen, T Scott; Eisenkolb, Sophia; Drobner, Juliane; Fischer, Tina; Werner, Sarah; Linke, Axel; Mangner, Norman; Schuler, Gerhard; Adams, Volker

2017-01-01

Hypertension is a key risk factor for heart failure, with the latter characterized by diaphragm muscle weakness that is mediated in part by increased oxidative stress. In the present study, we used a deoxycorticosterone acetate (DOCA)-salt mouse model to determine whether hypertension could independently induce diaphragm dysfunction and further investigated the effects of high-intensity interval training (HIIT). Sham-treated (n = 11), DOCA-salt-treated (n = 11), and DOCA-salt+HIIT-treated (n = 15) mice were studied over 4 wk. Diaphragm contractile function, protein expression, enzyme activity, and fiber cross-sectional area and type were subsequently determined. Elevated blood pressure confirmed hypertension in DOCA-salt mice independent of HIIT (P < 0.05). Diaphragm forces were impaired by ∼15-20% in DOCA-salt vs. sham-treated mice (P < 0.05), but this effect was prevented after HIIT. Myosin heavy chain (MyHC) protein expression tended to decrease (∼30%; P = 0.06) in DOCA-salt vs. sham- and DOCA-salt+HIIT mice, whereas oxidative stress increased (P < 0.05). Enzyme activity of NADPH oxidase was higher, but superoxide dismutase was lower, with MyHC oxidation elevated by ∼50%. HIIT further prevented direct oxidant-mediated diaphragm contractile dysfunction (P < 0.05) after a 30 min exposure to H 2 O- 2 (1 mM). Our data suggest that hypertension induces diaphragm contractile dysfunction via an oxidant-mediated mechanism that is prevented by HIIT.-Bowen, T. S., Eisenkolb, S., Drobner, J., Fischer, T., Werner, S., Linke, A., Mangner, N., Schuler, G., Adams, V. High-intensity interval training prevents oxidant-mediated diaphragm muscle weakness in hypertensive mice. © FASEB.

Mitigation of acrylamide-induced behavioral deficits, oxidative impairments and neurotoxicity by oral supplements of geraniol (a monoterpene) in a rat model.

PubMed

Prasad, Sathya N; Muralidhara

2014-11-05

In the recent past, several phytoconstituents are being explored for their potential neuromodulatory effects in neurological diseases. Repeated exposure of acrylamide (ACR) leads to varying degree of neuronal damage in experimental animals and humans. In view of this, the present study investigated the efficacy of geraniol (GE, a natural monoterpene) to mitigate acrylamide (ACR)-induced oxidative stress, mitochondrial dysfunction and neurotoxicity in a rat model and compared its efficacy to that of curcumin (CU, a spice active principle with multiple biological activities). ACR administration (50mg/kg bw, i.p. 3times/week) for 4weeks to growing rats caused typical symptoms of neuropathy. ACR rats provided with daily oral supplements of phytoconstituents (GE: 100mg/kg bw/d; CU: 50mg/kg bw/d, 4weeks) exhibited marked improvement in behavioral tests. Both phytoconstituents markedly attenuated ACR-induced oxidative stress as evidenced by the diminished levels of reactive oxygen species, malondialdehyde and nitric oxide and restored the reduced glutathione levels in sciatic nerve (SN) and brain regions (cortex - Ct, cerebellum - Cb). Further, both phytoconstituents effectively diminished ACR-induced elevation in cytosolic calcium levels in SN and Cb. Furthermore, diminution in the levels of oxidative markers in the mitochondria was associated with elevation in the activities of antioxidant enzymes. While ACR mediated elevation in the acetylcholinesterase activity was reduced by both actives, the depletion in dopamine levels was restored only by CU in brain regions. Taken together our findings for the first time demonstrate that the neuromodulatory propensity of GE is indeed comparable to that of CU and may be exploited as a therapeutic adjuvant in the management of varied human neuropathy conditions. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Elevated small GTPase activation influences the cell proliferation signaling control in Niemann-Pick type C fibroblasts.

PubMed

Corey, Deborah A; Kelley, Thomas J

2007-07-01

Niemann-Pick type C (NPC) disease is characterized at the cellular level by the intracellular accumulation of free cholesterol. We have previously identified a similar phenotype in cystic fibrosis (CF) cell models that results in the activation of the small GTPase RhoA. The hypothesis of this study was that NPC cells would also exhibit an increase in small GTPase activation. An examination of the active, GTP-bound form of GTPases revealed a basal increase in the content of the active-form Ras and RhoA small GTPases in NPC fibroblasts compared to wt controls. To assess whether this increase in GTP-bound Ras and RhoA manifests a functional outcome, the expression of the proliferation control proteins p21/waf1 and cyclin D were examined. Consistent with increased GTPase signaling, p21/waf1 expression is reduced and cyclin D expression is elevated in NPC fibroblasts. Interestingly, cell growth rate is not altered in NPC fibroblasts compared to wt cells. However, NPC sensitivity to statin treatment is reversed by addition of the isoprenoid geranylgeranyl pyrophosphate (GGPP), a modifier of RhoA. It is concluded that Ras and RhoA basal activation is elevated in NPC fibroblasts and has an impact on cell survival pathways.

Expression and Activity of Nitric Oxide Synthase Isoforms in Methamphetamine-Induced Striatal Dopamine Toxicity

PubMed Central

Friend, Danielle M.; Son, Jong H.; Keefe, Kristen A.

2013-01-01

Nitric oxide is implicated in methamphetamine (METH)-induced neurotoxicity; however, the source of the nitric oxide has not been identified. Previous work has also revealed that animals with partial dopamine loss induced by a neurotoxic regimen of methamphetamine fail to exhibit further decreases in striatal dopamine when re-exposed to methamphetamine 7–30 days later. The current study examined nitric oxide synthase expression and activity and protein nitration in striata of animals administered saline or neurotoxic regimens of methamphetamine at postnatal days 60 and/or 90, resulting in four treatment groups: Saline:Saline, METH:Saline, Saline:METH, and METH:METH. Acute administration of methamphetamine on postnatal day 90 (Saline:METH and METH:METH) increased nitric oxide production, as evidenced by increased protein nitration. Methamphetamine did not, however, change the expression of endothelial or inducible isoforms of nitric oxide synthase, nor did it change the number of cells positive for neuronal nitric oxide synthase mRNA expression or the amount of neuronal nitric oxide synthase mRNA per cell. However, nitric oxide synthase activity in striatal interneurons was increased in the Saline:METH and METH:METH animals. These data suggest that increased nitric oxide production after a neurotoxic regimen of methamphetamine results from increased nitric oxide synthase activity, rather than an induction of mRNA, and that constitutively expressed neuronal nitric oxide synthase is the most likely source of nitric oxide after methamphetamine administration. Of interest, animals rendered resistant to further methamphetamine-induced dopamine depletions still show equivalent degrees of methamphetamine-induced nitric oxide production, suggesting that nitric oxide production alone in response to methamphetamine is not sufficient to induce acute neurotoxic injury. PMID:23230214

Reduction and Oxidation of the Active Site Iron in Tyrosine Hydroxylase: Kinetics and Specificity†

PubMed Central

Frantom, Patrick A.; Seravalli, Javier; Ragsdale, Stephen W.; Fitzpatrick, Paul F.

2006-01-01

Tyrosine hydroxylase (TyrH) is a pterin-dependent enzyme that catalyzes the hydroxylation of tyrosine to form dihydroxyphenylalanine. The oxidation state of the active site iron atom plays a central role in the regulation of the enzyme. The kinetics of reduction of ferric TyrH by several reductants were determined by anaerobic stopped-flow spectroscopy. Anaerobic rapid freeze–quench EPR confirmed that the change in the near-UV absorbance of TyrH upon adding reductant corresponded to iron reduction. Tetrahydrobiopterin reduces wild-type TyrH following a simple second-order mechanism with a rate constant of 2.8 ± 0.1 mM−1 s−1. 6-Methyltetrahydropterin reduces the ferric enzyme with a second-order rate constant of 6.1 ± 0.1 mM−1 s−1 and exhibits saturation kinetics. No EPR signal for a radical intermediate was detected. Ascorbate, glutathione, and 1,4-benzoquinone all reduce ferric TyrH, but much more slowly than tetrahydrobiopterin, suggesting that the pterin is a physiological reductant. E332A TyrH, which has an elevated Km for tetrahydropterin in the catalytic reaction, is reduced by tetrahydropterins with the same kinetic parameters as those of the wild-type enzyme, suggesting that BH4 does not bind in the catalytic conformation during the reduction. Oxidation of ferrous TyrH by molecular oxygen can be described as a single-step second-order reaction, with a rate constant of 210 mM−1 s−1. S40E TyrH, which mimics the phosphorylated state of the enzyme, has oxidation and reduction kinetics similar to those of the wild-type enzyme, suggesting that phosphorylation does not directly regulate the interconversion of the ferric and ferrous forms. PMID:16475826

Human plasma paraoxonase 1 (PON1) arylesterase activity during aging: correlation with susceptibility of LDL oxidation.

PubMed

Mehdi, Mohammad Murtaza; Rizvi, Syed Ibrahim

2012-08-01

The role of free radicals has long been proposed as a cause for the aging process. Oxidative stress is considered a major factor for altering many physiological processes and enzymatic activities during aging and is also known to play a major role in the development of several age-dependent diseases. Paraoxonase 1 (PON1) is an anti-atherosclerotic enzyme that mainly prevents accumulation of lipoperoxides and inhibits the lipid oxidation in low-density lipoproteins (LDL). This study was undertaken to investigate the antioxidant behavior of PON1 by measuring its arylesterase activity. The susceptibility of LDL for oxidation and the radical scavenging activity of plasma were also measured during aging in humans. Arylesterase activity of PON1 was measured in plasma of human subjects between 20 and 81 years of age of both genders. The susceptibility of LDL for oxidation and radical scavenging activity were measured in plasma. Decrease in plasma arylesterase activity of PON1, increase in susceptibility of LDL for oxidation and decrease in plasma radical scavenging activity were observed as a function of human age. The study provides evidence of a relationship between PON1 activity, LDL oxidation and free radical scavenging activity of plasma. The present results emphasize the dependency of PON1 activity to prevailing oxidative stress during human aging. Our findings assume significance in view of the possible categorization of PON1 as a longevity gene. Copyright © 2012 IMSS. Published by Elsevier Inc. All rights reserved.

Elevated Prostate Health Index (phi) and Biopsy Reclassification During Active Surveillance of Prostate Cancer.

PubMed

Andreas, Darian; Tosoian, Jeffrey J; Landis, Patricia; Wolf, Sacha; Glavaris, Stephanie; Lotan, Tamara L; Schaeffer, Edward M; Sokoll, Lori J; Ross, Ashley E

2016-07-01

The Prostate Health Index (phi) has been FDA approved for decision-making regarding prostate biopsy. Phi has additionally been shown to positively correlate with tumor volume, extraprostatic disease and higher Gleason grade tumors. Here we describe a case in which an elevated phi encouraged biopsy of a gentleman undergoing active surveillance leading to reclassification of his disease as high risk prostate cancer.

Gene expression responses of paper birch to elevated O3 and CO2 during leaf maturation and senescence

NASA Astrophysics Data System (ADS)

Kontunen-Soppela, S.; Parviainen, J.; Ruhanen, H.; Brosché, M.; Keinanen, M.; Thakur, R. C.; Kolehmainen, M.; Kangasjarvi, J.; Oksanen, E.; Karnosky, D. F.; Vapaavuori, E.

2009-12-01

Forest trees are exposed to increasing concentrations of O3 and CO2 simultaneously. The rise of concentration in these gases causes changes in the gene expression of trees, which can be small in acclimated trees, but yet pivotal for the metabolism of the trees. We have studied the response of paper birch (Betula papyrifera) leaf gene expression to elevated O3 and CO2 concentrations during leaf maturation and senescence. The hypotheses were:(1) Elevated O3 induces oxidative stress in leaves. During long O3-exposure repair mechanisms are activated. Because chemical defense requires energy and carbon uptake is reduced, leaf senescence is activated earlier. Alternatively, the senescence-associated processes, remobilization and storage of carbohydrates and nutrients, may not be completed. (2) In the combination of elevated CO2+O3, the O3-caused damages are not seen or they are smaller, due to closure of the stomata under elevated CO2 and decreased O3 uptake by the leaves. On the other hand, elevated CO2 may provide energy and increase defense chemicals, enabling leaves to repair the O3-caused damages. Gene expression responses of paper birch leaves to elevated O3 and CO2 were studied with microarray analyses. Samples were collected from the long-term O3 and CO2 fumigation experiment Aspen FACE in Rhinelander, WI, USA (http://aspenface.mtu.edu/). The site contains 12 FACE rings receiving CO2, O3, CO2+O3, and ambient air (controls). Birches have been exposed to elevated CO2 (550ppm) and O3 (1.5X ambient) since 1998. Leaf samples were collected in July, August and September 2004. The cDNA-microarrays used for hybridizations consisted of Populus euphratica ESTs representing ca 6500 different genes. In order to detect similar gene expression patterns within samplings and treatments, the microarray data was analyzed with multivariate methods; clustering with Self-Organizing Map, finding optimal cluster grouping by K-means clustering and visualizing the results with Sammon

Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

El-Mas, Mahmoud M., E-mail: mahelm@hotmail.com; Abdel-Rahman, Abdel A., E-mail: abdelrahmana@ecu.edu

Evidence suggests that male rats are protected against the hypotensive and myocardial depressant effects of ethanol compared with females. We investigated whether E{sub 2} modifies the myocardial and oxidative effects of ethanol in male rats. Conscious male rats received ethanol (0.5, 1 or 1.5 g/kg i.v.) 30-min after E{sub 2} (1 μg/kg i.v.) or its vehicle (saline), and hearts were collected at the conclusion of hemodynamic measurements for ex vivo molecular studies. Ethanol had no effect in vehicle-treated rats, but it caused dose-related reductions in LV developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of rise in LV pressure (dP/dt{sub max})more » and systolic (SBP) and diastolic (DBP) blood pressures in E{sub 2}-pretreated rats. These effects were associated with elevated (i) indices of reactive oxygen species (ROS), (ii) malondialdehyde (MDA) protein adducts, and (iii) phosphorylated death-associated protein kinase-3 (DAPK3), Akt, and extracellular signal-regulated kinases (ERK1/2). Enhanced myocardial anti-oxidant enzymes (heme oxygenase-1, catalase and aldehyde dehydrogenase 2) activities were also demonstrated. In conclusion, E{sub 2} promotes ethanol-evoked myocardial oxidative stress and dysfunction in male rats. The present findings highlight the risk of developing myocardial dysfunction in men who consume alcohol while receiving E{sub 2} for specific medical conditions. - Highlights: • Ethanol lowers blood pressure and causes LV dysfunction in E{sub 2}-treated rats. • E{sub 2}/ethanol aggravates cardiac oxidative state via of DAPK3/Akt/ERK activation. • E{sub 2}/ethanol causes a feedback increase in cardiac HO-1, catalase and ALDH2. • Alcohol might increase risk of myocardial dysfunction in men treated with E{sub 2}.« less

Rapid estimation of the oxidative activities of individual phenolics in crude plant extracts.

PubMed

Vihakas, Matti; Pälijärvi, Maija; Karonen, Maarit; Roininen, Heikki; Salminen, Juha-Pekka

2014-07-01

Previous studies of purified phenolic compounds have revealed that some phenolics, especially ellagitannins, can autoxidise under alkaline conditions, which predominate in the midgut of lepidopteran larvae. To facilitate screening for the pro-oxidant activities of all types of phenolic compounds from crude plant extracts, we developed a method that combined our recent spectrophotometric bioactivity method with an additional chromatographic step via UPLC-DAD-MS. This method allowed us to estimate the total pro-oxidant capacities of crude extracts from 12 plant species and to identify the individual phenolic compounds that were responsible for the detected activities. It was found that the pro-oxidant capacities of the plant species (i.e., the concentrations of the easily-oxidised phenolics) varied from 0 to 57 mg/g dry wt, representing from 0% to 46% of the total phenolics from different species. UPLC-DAD-MS analysis revealed that most flavonol and flavone glycosides were only slightly affected by alkaline conditions, thus indicating their low pro-oxidant activity. Interestingly, myricetin-type compounds differed from the other flavonoids, as their concentrations decreased strongly due to alkaline incubation. The same effect was detected for hydrolysable tannins and prodelphinidins, suggesting that a pyrogallol sub-structure could be a key structural component that partially explains their easy oxidation at high pH. Other types of phenolic compounds, such as hydroxycinnamic acids, were relatively active, as well. These findings demonstrate that this method displays the potential to identify most of the active and inactive pro-oxidant phenolic compounds in various plant species. Copyright © 2014 Elsevier Ltd. All rights reserved.

Activity of Cu-activated carbon fiber catalyst in wet oxidation of ammonia solution.

PubMed

Hung, Chang-Mao

2009-07-30

Aqueous solutions of 200-1000 mg/L of ammonia were oxidized in a trickle-bed reactor using Cu-activated carbon fiber (ACF) catalysts, which were prepared by incipient wet impregnation with aqueous solutions of copper nitrate that was deposited on ACF substrates. The results reveal that the conversion of ammonia by wet oxidation in the presence of Cu-ACF catalysts was a function of the metal loading weight ratio of the catalyst. The total conversion efficiency of ammonia was 95% during wet oxidation over the catalyst at 463 K at an oxygen partial pressure of 3.0 MPa. Moreover, the effect of the initial concentration of ammonia and the reaction temperature on the removal of ammonia from the effluent streams was also studied at a liquid space velocity of less than 3.0 h(-1).

Oxidative stress tolerance in intertidal red seaweed Hypnea musciformis (Wulfen) in relation to environmental components.

PubMed

Maharana, Dusmant; Das, Priya Brata; Verlecar, Xivanand N; Pise, Navnath M; Gauns, Manguesh

2015-12-01

Oxidative stress parameters in relation to temperature and other factors have been analysed in Hypnea musciformis, the red seaweed from Anjuna beach, Goa, with an aim to understand its susceptibility to the changing seasons. The results indicate that elevated temperature, sunshine and dessication during peak summer in May enhanced the activity of lipid peroxide, hydrogen peroxide and antioxidants such as catalase, glutathione and ascorbic acid. Statistical tests using multivariate analysis of variance and correlation analysis showed that oxidative stress and antioxidants maintain significant relation with temperature, salinity, sunshine and pH at an individual or interactive level. The dissolved nitrates, phosphates and biological oxygen demand in ambient waters and the trace metals in seaweeds maintained sufficiently low values to provide any indication that could exert contaminant oxidative stress responses. The present field studies suggest that elevated antioxidant content in H. musciformis offer sufficient relief to sustain against harsh environmental stresses for its colonization in the rocky intertidal zone.

Serum prolidase enzyme activity in obese subjects and its relationship with oxidative stress markers.

PubMed

Aslan, Mehmet; Duzenli, Ufuk; Esen, Ramazan; Soyoral, Yasemin Usul

2017-10-01

The relationship between increased serum enzyme activity of prolidase and increased rate of collagen turnover in the arterial wall has been asserted in previous studies. Collagen reflects much of the strength to the connective tissue involved in the arterial wall. Atherosclerosis is very common vessel disease and oxidative stress plays a pivotal role in the etiopathogenesis. Our objective was to examine the serum enzyme activity of prolidase and its possible relationships with oxidative stress parameters in obese subjects. Our present study was conducted 27 obese subjects and 26 age-matched healthy control subjects. The serum enzyme activity of prolidase in all study population was evaluated spectrophotometrically. Oxidative stress levels in obese subjects were analyzed with total antioxidant capacity (TAC) and total oxidant status (TOS) as well as oxidative stress index (OSI). Obese subjects have higher serum TOS and OSI indicators as well as prolidase activity than those in control subjects (for all; p<0.001). Moreover, obese subjects have lower levels of TAC than in those in healthy subjects (p<0.001). In the Pearson's correlation analysis, enzyme activity of prolidase was positively related with TOS (p<0.001, r=0.529) and OSI (p<0.001, r=0.519) as well as BMI (p<0.001, r=0.692) and inversely related with TAC (p<0.05, r=-0.405) in obese subjects. Increased serum prolidase activity and decreased antioxidant levels are likely to be a results of increased of oxidative stress levels in obese subjects. The significantly correlation between increased oxidative stress and increased prolidase activity may play a pivotal role in etiopathogenesis of atherosclerotic cardiovascular diseases in obese subjects. Copyright © 2017 Elsevier B.V. All rights reserved.

Effects of physical activity on systemic oxidative/DNA status in breast cancer survivors

PubMed Central

Tomasello, Barbara; Malfa, Giuseppe Antonio; Strazzanti, Angela; Gangi, Santi; Di Giacomo, Claudia; Basile, Francesco; Renis, Marcella

2017-01-01

Physical activity offers a paradoxical hormetic effect and a health benefit to cancer survivors; however, the biochemical mechanisms have not been entirely elucidated. Despite the well-documented evidence implicating oxidative stress in breast cancer, the association between health benefits and redox status has not been investigated in survivors who participate in dragon boating. The present study investigated the plasmatic systemic oxidative status (SOS) in breast cancer survivors involved in two distinct physical training exercises. A total of 75 breast cancer survivors were allocated to one of three groups: Control (resting), dragon boat racing and walking group; the latter is a type of aerobic conditioning exercise often advised to cancer patients. Various biochemical oxidative stress markers were examined, including oxidant status (hydroperoxide levels, lipid oxidation) and antioxidant status (enzymatic activities of superoxide dismutase and glutathione peroxidase, reduced glutathione levels and antioxidant capability). In addition, the individual DNA fragmentation and DNA repair capability of nucleotide excision repair (NER) systems were examined by comet assays. According to the results, all patients exhibited high levels of oxidative stress. Physical activity maintained this oxidative stress condition but simultaneously had a positive influence on the antioxidant component of the SOS, particularly in the dragon boat racing group. DNA fragmentation, according to the levels of single- and double-strand breaks, were within the normal range in the two survivor groups that were involved in training activities. Radiation-induced damage was not completely recognised or repaired by NER systems in any of the patients, probably leading to radiosensitivity and/or susceptibility of patients to cancer. These findings suggest that physical activity, particularly dragon boat racing, that modulates SOS and DNA repair capability could represent a strategy for enhancing the

Effects of physical activity on systemic oxidative/DNA status in breast cancer survivors.

PubMed

Tomasello, Barbara; Malfa, Giuseppe Antonio; Strazzanti, Angela; Gangi, Santi; Di Giacomo, Claudia; Basile, Francesco; Renis, Marcella

2017-01-01

Physical activity offers a paradoxical hormetic effect and a health benefit to cancer survivors; however, the biochemical mechanisms have not been entirely elucidated. Despite the well-documented evidence implicating oxidative stress in breast cancer, the association between health benefits and redox status has not been investigated in survivors who participate in dragon boating. The present study investigated the plasmatic systemic oxidative status (SOS) in breast cancer survivors involved in two distinct physical training exercises. A total of 75 breast cancer survivors were allocated to one of three groups: Control (resting), dragon boat racing and walking group; the latter is a type of aerobic conditioning exercise often advised to cancer patients. Various biochemical oxidative stress markers were examined, including oxidant status (hydroperoxide levels, lipid oxidation) and antioxidant status (enzymatic activities of superoxide dismutase and glutathione peroxidase, reduced glutathione levels and antioxidant capability). In addition, the individual DNA fragmentation and DNA repair capability of nucleotide excision repair (NER) systems were examined by comet assays. According to the results, all patients exhibited high levels of oxidative stress. Physical activity maintained this oxidative stress condition but simultaneously had a positive influence on the antioxidant component of the SOS, particularly in the dragon boat racing group. DNA fragmentation, according to the levels of single- and double-strand breaks, were within the normal range in the two survivor groups that were involved in training activities. Radiation-induced damage was not completely recognised or repaired by NER systems in any of the patients, probably leading to radiosensitivity and/or susceptibility of patients to cancer. These findings suggest that physical activity, particularly dragon boat racing, that modulates SOS and DNA repair capability could represent a strategy for enhancing the

SPM local oxidation nanolithography with active control of cantilever dynamics

NASA Astrophysics Data System (ADS)

Nishimura, S.; Takemura, Y.; Shirakashi, J.

2007-04-01

Local oxidation nanolithography using scanning probe microscope (SPM) has enabled us to fabricate nanometer-scale oxide wires on material surfaces. Here, we study tapping mode SPM local oxidation experiments for silicon by controlling the dynamic properties of the cantilever. Dependence of feature size of fabricated oxide wires on the amplitude of the cantilever was precisely investigated. The quality factor (Q) was fixed at a natural value of ~500. By enhancing the amplitude of the cantilever, both width and height of fabricated Si oxide wires were decreased. With the variation of the amplitude of the cantilever from 0.5 V to 3.0 V (DC voltage = 22.5 V, scanning speed = 20 nm/s), the feature size of Si oxide wires was well controlled, ranging from 40 nm to 18 nm in width and 2.3 nm to 0.6 nm in height. Standard deviation of width on Si oxide wires formed by tapping mode SPM is around 2.0 nm, which is smaller than that of contact mode Si oxide wires. Furthermore, the variation of the oscillation amplitude of the cantilever does not affect the size uniformity of the wires. These results imply that the SPM local oxidation nanolithography with active control of cantilever dynamics is a useful technique for producing higher controllability on the nanometer-scale fabrication of Si oxide wires.

PML is a ROS sensor activating p53 upon oxidative stress

PubMed Central

Soilihi, Hassane

2017-01-01

Promyelocytic leukemia (PML) nuclear bodies (NBs) recruit partner proteins, including p53 and its regulators, thereby controlling their abundance or function. Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation promotes NB biogenesis. However, physiological links between PML and oxidative stress response in vivo remain unexplored. Here, we identify PML as a reactive oxygen species (ROS) sensor. Pml−/− cells accumulate ROS, whereas PML expression decreases ROS levels. Unexpectedly, Pml−/− embryos survive acute glutathione depletion. Moreover, Pml−/− animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosis. Molecularly, Pml−/− animals fail to properly activate oxidative stress–responsive p53 targets, whereas the NRF2 response is amplified and accelerated. Finally, in an oxidative stress–prone background, Pml−/− animals display a longevity phenotype, likely reflecting decreased basal p53 activation. Thus, similar to p53, PML exerts basal antioxidant properties but also drives oxidative stress–induced changes in cell survival/proliferation or metabolism in vivo. Through NB biogenesis, PML therefore couples ROS sensing to p53 responses, shedding a new light on the role of PML in senescence or stem cell biology. PMID:28931625

PML is a ROS sensor activating p53 upon oxidative stress.

PubMed

Niwa-Kawakita, Michiko; Ferhi, Omar; Soilihi, Hassane; Le Bras, Morgane; Lallemand-Breitenbach, Valérie; de Thé, Hugues

2017-11-06

Promyelocytic leukemia (PML) nuclear bodies (NBs) recruit partner proteins, including p53 and its regulators, thereby controlling their abundance or function. Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation promotes NB biogenesis. However, physiological links between PML and oxidative stress response in vivo remain unexplored. Here, we identify PML as a reactive oxygen species (ROS) sensor. Pml -/- cells accumulate ROS, whereas PML expression decreases ROS levels. Unexpectedly, Pml -/- embryos survive acute glutathione depletion. Moreover, Pml -/- animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosis. Molecularly, Pml -/- animals fail to properly activate oxidative stress-responsive p53 targets, whereas the NRF2 response is amplified and accelerated. Finally, in an oxidative stress-prone background, Pml -/- animals display a longevity phenotype, likely reflecting decreased basal p53 activation. Thus, similar to p53, PML exerts basal antioxidant properties but also drives oxidative stress-induced changes in cell survival/proliferation or metabolism in vivo. Through NB biogenesis, PML therefore couples ROS sensing to p53 responses, shedding a new light on the role of PML in senescence or stem cell biology. © 2017 Niwa-Kawakita et al.

C—H Oxidation of Ingenanes Enables Potent and Selective Protein Kinase C Isoform Activation

PubMed Central

Jin, Yehua; Yeh, Chien‐Hung; Kuttruff, Christian A.; Jørgensen, Lars; Dünstl, Georg; Felding, Jakob; Natarajan, Swaminathan R.

2015-01-01

Abstract Ingenol derivatives with varying degrees of oxidation were prepared by two‐phase terpene synthesis. This strategy has allowed access to analogues that cannot be prepared by semisynthesis from natural ingenol. Complex ingenanes resulting from divergent C—H oxidation of a common intermediate were found to interact with protein kinase C in a manner that correlates well with the oxidation state of the ingenane core. Even though previous work on ingenanes has suggested a strong correlation between potential to activate PKCδ and induction of neutrophil oxidative burst, the current study shows that the potential to activate PKCβII is of key importance while interaction with PKCδ is dispensable. Thus, key modifications of the ingenane core allowed PKC isoform selectivity wherein PKCδ‐driven activation of keratinocytes is strongly reduced or even absent while PKCβII‐driven activation of neutrophils is retained. PMID:26418078

Dual-functional Pt-on-Pd supported on reduced graphene oxide hybrids: peroxidase-mimic activity and an enhanced electrocatalytic oxidation characteristic.

PubMed

Zhang, Xiahong; Wu, Genghuang; Cai, Zhixiong; Chen, Xi

2015-03-01

In this study, a facile hydrothermal method was developed to synthesize Pt-on-Pd supported on reduced graphene oxide (Pt-on-Pd/RGO) hybrids. Because of the synergistic effect between Pt-on-Pd and RGO, the obtained Pt-on-Pd/RGO had superior peroxidase-mimic activities in H2O2 reduction and TMB oxidation. The reaction medium was optimized and a sensing approach for H2O2 was developed with a linear range from 0.98 to 130.7 μM of H2O2. In addition, the characteristic of electrocatalytic oxidation of methanol was investigated. The peak current density value, j(f), for the Pt-on-Pd/RGO hybrid (328 mA mg(Pt)(-1)) was about 1.85 fold higher than that of commercial Pt black (177 mA mg(Pt)(-1)) and, also, more durable electrocatalytic activity could be obtained. For the first time, the dual-functional Pt-on-Pd/RGO with peroxidase-mimic activity and an enhanced electrocatalytic oxidation characteristic was reported. Copyright © 2014 Elsevier B.V. All rights reserved.

Elevated Concentrations of Serum Immunoglobulin Free Light Chains in Systemic Lupus Erythematosus Patients in Relation to Disease Activity, Inflammatory Status, B Cell Activity and Epstein-Barr Virus Antibodies

PubMed Central

Draborg, Anette H.; Lydolph, Magnus C.; Westergaard, Marie; Olesen Larsen, Severin; Nielsen, Christoffer T.; Duus, Karen; Jacobsen, Søren; Houen, Gunnar

2015-01-01

Objective In this study, we examined the concentration of serum immunoglobulin free light chains (FLCs) in systemic lupus erythematosus (SLE) patients and investigated its association with various disease parameters in order to evaluate the role of FLCs as a potential biomarker in SLE. Furthermore, FLCs’ association with Epstein-Barr virus (EBV) antibodies was examined. Methods Using a nephelometric assay, κFLC and λFLC concentrations were quantified in sera from 45 SLE patients and 40 healthy controls. SLE patients with renal insufficiency were excluded in order to preclude high concentrations of serum FLCs due to decreased clearance. Results Serum FLC concentrations were significantly elevated in SLE patients compared to healthy controls (p<0.0001) also after adjusting for Ig levels (p<0.0001). The concentration of serum FLCs correlated with a global disease activity (SLE disease activity index (SLEDAI)) score of the SLE patients (r = 0.399, p = 0.007). Furthermore, concentrations of FLCs correlated with titers of dsDNA antibodies (r = 0.383, p = 0.009), and FLC levels and SLEDAI scores correlated in the anti-dsDNA-positive SLE patients, but not in anti-dsDNA-negative SLE patients. Total immunoglobulin (IgG and IgA) concentrations correlated with FLC concentrations and elevated FLC levels were additionally shown to associate with the inflammatory marker C-reactive protein and also with complement consumption determined by low C4 in SLE patients. Collectively, results indicated that elevated serum FLCs reflects increased B cell activity in relation to inflammation. SLE patients had an increased seropositivity of EBV-directed antibodies that did not associate with elevated FLC concentrations. An explanation for this could be that serum FLC concentrations reflect the current EBV activity (reactivation) whereas EBV-directed antibodies reflect the extent of previous infection/reactivations. Conclusion SLE patients have elevated concentrations of serum FLCs that

Hepatic and renal oxidative stress in acute toxicity of N-nitrosodiethylamine in rats.

PubMed

Bansal, A K; Trivedi, R; Soni, G L; Bhatnagar, D

2000-09-01

Nitrosoamines such as N-nitrosodiethylamine (NDEA) produce oxidative stress due to generation of reactive oxygen species and may alter antioxidant defence system in the tissues. NDEA was administered ip as a single dose to rats in LD50 or in lower amounts and the animals were sacrificed after 0-48 hr of treatment. The results showed that lipid peroxidation in liver increased, however no significant increase in kidney LPO was observed after NDEA administration. Superoxide dismutase (SOD) and glutathione reductase (GSH-R) activity increased in liver, however, catalase (CAT) activity in liver was inhibited in NDEA treated rats. Kidney showed an increase in SOD activity after an initial decrease along with increase in GSH-R activity in NDEA treated rats. However, kidney CAT activity was not significantly altered in NDEA intoxicated rats. Serum transaminases, serum alkaline phosphatase blood urea nitrogen, serum creatinine and scrum proteins were elevated in NDEA treated rats. The results indicate NDEA-induced oxidative stress and alteration in antioxidant enzymes in liver and kidney to neutralise oxidative stress.

THE CAFETERIA DIET INCREASES FAT MASS AND CHRONICALLY ELEVATES LUMBAR SYMPATHETIC NERVE ACTIVITY IN RATS

PubMed Central

Muntzel, Martin S.; Al-Naimi, Omar Ali S.; Barclay, Alicia; Ajasin, David

2012-01-01

Obesity causes sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Because high-fat induced weight gain in rats elevates plasma leptin at 1–3 days following onset of calorie dense diets, we hypothesized that diet-induced overfeeding will increase sympathetic activity within one week following onset of the regimen. To test this, we continuously measured sympathetic activity and blood pressure before and during the onset of diet-induced obesity using a high calorie cafeteria-style diet. Female Wistar rats, in which radiotelemeters had been implanted for continuous monitoring of lumbar sympathetic activity, mean arterial pressure, and heart rate, were randomly assigned to groups that received regular chow (control) or a cafeteria diet for a period of 15 days. This short-term cafeteria-feeding regimen caused modest but non-significant increases in body weight (P = 0.07) and a doubling of brown and white adipose tissue (P < 0.01). The increases in fat mass were accompanied by elevations in plasma leptin (P < 0.001) but no change in glucose. Overall heart rates and blood pressure were higher in cafeteria rats compared with controls (P < 0.05). Cafeteria diet-induced weight gain caused increases in lumbar sympathetic nerve activity that became significant by the 12th day of the diet (p < 0.001). These data show, for the first time, that the high-fat cafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats. PMID:23090774

Yomogin, an inhibitor of nitric oxide production in LPS-activated macrophages.

PubMed

Ryu, J H; Lee, H J; Jeong, Y S; Ryu, S Y; Han, Y N

1998-08-01

In activated macrophages the inducible form of nitric oxide synthase (i-NOS) generates high amounts of toxic mediator, nitric oxide (NO) which contributes to the circulatory failure associated with septic shock. A sesquiterpene lactone compound (yomogin) isolated from medicinal plant Artemisia princeps Pampan inhibited the production of NO in LPS-activated RAW 264.7 cells by suppressing i-NOS enzyme expression. Thus, yomogin may be a useful candidate for the development of new drugs to treat endotoxemia and inflammation accompanied by the overproduction of NO.

Bactericidal activity of partially oxidized nanodiamonds.

PubMed

Wehling, Julia; Dringen, Ralf; Zare, Richard N; Maas, Michael; Rezwan, Kurosch

2014-06-24

Nanodiamonds are a class of carbon-based nanoparticles that are rapidly gaining attention, particularly for biomedical applications, i.e., as drug carriers, for bioimaging, or as implant coatings. Nanodiamonds have generally been considered biocompatible with a broad variety of eukaryotic cells. We show that, depending on their surface composition, nanodiamonds kill Gram-positive and -negative bacteria rapidly and efficiently. We investigated six different types of nanodiamonds exhibiting diverse oxygen-containing surface groups that were created using standard pretreatment methods for forming nanodiamond dispersions. Our experiments suggest that the antibacterial activity of nanodiamond is linked to the presence of partially oxidized and negatively charged surfaces, specifically those containing acid anhydride groups. Furthermore, proteins were found to control the bactericidal properties of nanodiamonds by covering these surface groups, which explains the previously reported biocompatibility of nanodiamonds. Our findings describe the discovery of an exciting property of partially oxidized nanodiamonds as a potent antibacterial agent.

Effects of tillage on the Fe oxides activation in soil

NASA Astrophysics Data System (ADS)