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Sample records for inhibit lipid peroxidation

  1. Phytic acid inhibits lipid peroxidation in vitro.

    PubMed

    Zajdel, Alicja; Wilczok, Adam; Węglarz, Ludmiła; Dzierżewicz, Zofia

    2013-01-01

    Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation under in vitro and in vivo conditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10-20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products.

  2. Phytic Acid Inhibits Lipid Peroxidation In Vitro

    PubMed Central

    Węglarz, Ludmiła; Dzierżewicz, Zofia

    2013-01-01

    Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation under in vitro and in vivo conditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10–20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products. PMID:24260736

  3. Carvedilol inhibition of lipid peroxidation. A new antioxidative mechanism.

    PubMed

    Tadolini, B; Franconi, F

    1998-11-01

    To define the molecular mechanism(s) of carvedilol inhibition of lipid peroxidation we have utilized model systems that allow us to study the different reactions involved in this complex process. Carvedilol inhibits the peroxidation of sonicated phosphatidylcholine liposomes triggered by FeCl2 addition whereas atenolol, pindolol and labetalol are ineffective. The inhibition proved not to be ascribable (a) to an effect on Fe2+ autoxidation and thus on the generation of oxygen derived radical initiators; (b) to the scavenging of the inorganic initiators O2*- and *OH; (c) to an effect on the reductive cleavage of organic hydroperoxides by FeCl2; (d) to the scavenging of organic initiators. The observations that (a) carvedilol effectiveness is inversely proportional to the concentration of FeCl2 and lipid hydroperoxides in the assay; (b) the drug prevents the onset of lipid peroxidation stimulated by FeCl3 addition and; (c) it can form a complex with Fe3+, suggest a molecular mechanism for carvedilol action. It may inhibit lipid peroxidation by binding the Fe3+ generated during the oxidation of Fe2+ by lipid hydroperoxides in the substrate. The lag time that carvedilol introduces in the peroxidative process would correspond to the time taken for carvedilol to be titrated by Fe3+; when the drug is consumed the Fe3+ accumulates to reach the critical parameter that stimulates peroxidation. According to this molecular mechanism the antioxidant potency of carvedilol can be ascribed to its ability to bind a species, Fe3+, that is a catalyst of the process and to its lipophilic nature that concentrates it in the membranes where Fe3+ is generated by a site specific mechanism.

  4. CISD1 inhibits ferroptosis by protection against mitochondrial lipid peroxidation.

    PubMed

    Yuan, Hua; Li, Xuemei; Zhang, Xiuying; Kang, Rui; Tang, Daolin

    2016-09-16

    Ferroptosis is a form of non-apoptotic cell death originally identified in cancer cells. However, the key regulator of ferroptosis in mitochondria remains unknown. Here, we show that CDGSH iron sulfur domain 1 (CISD1, also termed mitoNEET), an iron-containing outer mitochondrial membrane protein, negatively regulates ferroptotic cancer cell death. The classical ferroptosis inducer erastin promotes CISD1 expression in an iron-dependent manner in human hepatocellular carcinoma cells (e.g., HepG2 and Hep3B). Genetic inhibition of CISD1 increased iron-mediated intramitochondrial lipid peroxidation, which contributes to erastin-induced ferroptosis. In contrast, stabilization of the iron sulfur cluster of CISD1 by pioglitazone inhibits mitochondrial iron uptake, lipid peroxidation, and subsequent ferroptosis. These findings indicate a novel role of CISD1 in protecting against mitochondrial injury in ferroptosis.

  5. The inhibition of lipid peroxidation by cinnarizine. Possible implications to its therapeutic and side-effects.

    PubMed

    Fernandes, A C; Filipe, P M; Coelho, H; Manso, C F

    1991-03-01

    Cinnarizine has antivasoconstrictor properties and improves red-cell deformability. Its major side-effects are the induction of extrapyramidal reactions. It is a calcium antagonist, but it was suggested that its effects may depend on other mechanisms, namely on antiperoxidant properties. We have studied these properties in different biological systems, intact red-cells included. The occurrence of lipid peroxidation was determined by the formation of 2-thiobarbituric acid reactive products. Cinnarizine was found to inhibit spontaneous lipid peroxidation in rat liver homogenates, copper-induced lipid peroxidation in human plasma and copper-induced and hydrogen peroxide-induced lipid peroxidation in human red-cells. In red-cells, the inhibition of lipid peroxidation is accompanied by the inhibition of hemolysis. Copper-induced red-cell lipid peroxidation is 85% inhibited by as little as 5 microM cinnarizine. The antioxidant activity of cinnarizine may contribute to explain some of the effects of this drug.

  6. Membrane lipid peroxidation: propagation and inhibition by antioxidants

    SciTech Connect

    Leung, H.W.

    1981-01-01

    Peroxidation studies in microsomes and liposomes were performed to evaluate the importance of the interaction between ascorbate and ..cap alpha..-tocopherol. The peroxidation of rat liver microsomes by FeSO/sub 4/ in the presence of ascorbate was delayed compared to when NADPH replaced ascorbate as the electron donor. To further investigate the cooperation between ascorbate and vitamin E, a liposomal system containing polyunsaturated phospholipids was used. Ascorbic acid alone (30 to 100 ..mu..M) delayed peroxidation by 20, and at higher concentrations, 60 minutes. Physiological levels of vitamin E decreased peroxidation at early times but was apparently consumed during incubation. Vitamin C and vitamin E together suppressed peroxidation at early times at approximately the sum of the individual inhibitions. At longer times, the mixture was more effective than the sum of both vitamins alone. The role of glutathione and the significance of its interaction with ascorbate were studied. Glutathione was able to reduce dehydroascorbic acid, but ascorbic acid was unable to reduce oxidized glutathione disulfide. Glutathione and ascorbic acid were oxidized by NO/sub 2/ in vitro. Pulmonary levels of glutathione and ascorbic acid in guinea pigs exposed to NO/sub 2/ were lowered. After the administration of diethyl maleate, the glutathione concentration was decreased, but the ascorbic acid concentration was unaffected. Simultaneous exposure further depressed glutathione concentration, but not the ascorbic acid concentration. (ERB)

  7. Inhibition of lipid peroxidation by S-nitrosoglutathione and copper.

    PubMed

    Rigobello, Maria Pia; Scutari, Guido; Boscolo, Rita; Bindoli, Alberto

    2002-10-01

    The antioxidant properties of S-nitrosoglutathione, a nitric oxide-derived product were studied in different experimental systems. By using the crocin bleaching test, S-nitrosoglutathione, in the presence of copper ions, shows an antioxidant capacity about six times higher than that of Trolox c and referable to the interception of peroxyl radicals by nitric oxide. Copper alone shows a modest inhibitory action, which is about seven times lower than that of Trolox c. S-nitrosoglutathione prevents lipid peroxidation induced by the well-known Fe2+/ascorbate system (IC50 = 450 microM) and the inhibitory effect is strongly reinforced by the presence of copper ions (IC50 = 6.5 microM). In addition, cumene hydroperoxide-induced lipid peroxidation is markedly decreased by S-nitrosoglutathione, provided that copper ions, maintained reduced by ascorbate, are present. Decomposition of S-nitrosoglutathione through metal catalysis and/or the presence of reducing agents and the consequent release of nitric oxide are of crucial importance for eliciting the antioxidant power. In this way, copper ions and/or reducing species with low antioxidant potency are able to promote the formation of an extremely strong antioxidant species such as nitric oxide.

  8. Identification of components of Prunus africana extract that inhibit lipid peroxidation.

    PubMed

    Hass, M A; Nowak, D M; Leonova, E; Levin, R M; Longhurst, P A

    1999-11-01

    Extractive and chromatographic separations were performed on V-1326, a chloroform extract from the bark of Prunus africana (also referred to as Pygeum africanum), which is used to treat the symptoms associated with benign prostate hyperplasia (BPH). The relative amounts of eleven identified constituents in crude V-1326 and in separated fractions were determined using gas chromatographic analysis. The ability of V-1326 and its separated fractions to inhibit ferrous ion-induced stimulation of lipid peroxidation in microsomal preparations from rabbit livers was evaluated. The extract, V-1326, and fractions containing high levels of myristic acid potently inhibited lipid peroxidation.

  9. INHIBITION OF IN VITRO LIPID PEROXIDATION (LPO) EVOKED BY CALOCYBE INDICA (MILKY MUSHROOM)

    PubMed Central

    Selvi, S; Umadevi, P.; Suja, S.; Sridhar, K.; Chinnaswamy, P.

    2006-01-01

    The present study was designed with an objective to assess the inhibition of lipid peroxidation (LPO) by the aqueous extract of Calocybe indica (milky mushroom) using an invitro model of goat liver homogenate and RBC ghosts. The invitro LPO was inhibited to a good extent by the aqueous extract of milky mushroom and the extent of inhibition being higher in the RBC membrane model when compared with liver homogenate model. PMID:22557223

  10. Inhibition of in vitro lipid peroxidation (lpo) evoked by calocybe indica (milky mushroom).

    PubMed

    Selvi, S; Umadevi, P; Suja, S; Sridhar, K; Chinnaswamy, P

    2006-07-01

    The present study was designed with an objective to assess the inhibition of lipid peroxidation (LPO) by the aqueous extract of Calocybe indica (milky mushroom) using an invitro model of goat liver homogenate and RBC ghosts. The invitro LPO was inhibited to a good extent by the aqueous extract of milky mushroom and the extent of inhibition being higher in the RBC membrane model when compared with liver homogenate model.

  11. Antioxidant action of eugenol compounds: role of metal ion in the inhibition of lipid peroxidation.

    PubMed

    Ito, Masae; Murakami, Keiko; Yoshino, Masataka

    2005-03-01

    Antioxidant action of eugenol compounds was analyzed in relation to the role of transition metal. Iron-mediated lipid peroxidation and autooxidation of Fe2+ ion were inhibited markedly by isoeugenol, and less effectively by eugenol. Copper-dependent oxidation of low density lipoprotein (LDL) was potently inhibited by eugenol and isoeugenol to the same extent: eugenol compounds showed protective effects by prolonging lag phase and by suppressing propagation rate in the absence and presence of alpha-tocopherol. Inhibition of LDL oxidation by eugenol compounds was closely related to activities reducing copper and scavenging a stable radical, 1,1'-diphenyl-2-picrylhydrazyl (DPPH). Antioxidant properties of eugenol compounds can be explained by forming complexes with reduced metals. Potent inhibitory effect of isoeugenol on lipid peroxidation may be related to the decreased formation of perferryl ion or the iron-oxygen chelate complex as the initiating factor of lipid peroxidation by keeping iron at a reduced state. Inhibition of LDL oxidation by eugenol compounds is due to the suppression of free radical cascade of lipid peroxidation in LDL by reducing copper ion.

  12. Native and Heated Hydrolysates of Milk Proteins and Their Capacity to Inhibit Lipid Peroxidation in the Zebrafish Larvae Model.

    PubMed

    Carrillo, Wilman; Guzmán, Xavier; Vilcacundo, Edgar

    2017-09-14

    Casein and whey proteins with and without heat treatment were obtained of whole milk and four commercial milks in Ecuador, and were hydrolyzed. Then, their capacity to inhibit the lipid peroxidation using the TBARS method was evaluated at concentrations of 0.02, 0.04, 0.2, and, 0.4 mg/mL. Native and heated hydrolysates of milk proteins present high inhibitions of lipid peroxidation with a dose dependent effect both in vivo and in vitro tests. Casein and whey proteins obtained from whole milk were the ones with the highest anti-oxidant activity in vitro and in vivo test. Native casein hydrolysate at 0.4 mg/mL present a value of 55.55% of inhibition of lipid peroxidation and heated casein hydrolysate at 0.4 mg/mL presents a value of 58.00% of inhibition of lipid peroxidation. Native whey protein at 0.4 mg/mL present a value of 34.84% of inhibition of lipid peroxidation, and heated whey protein at 0.4 mg/mL presents a value of 40.86% of inhibition of lipid peroxidation. Native and heated casein hydrolysates were more active than native and heated whey protein hydrolysates. Heat treatments have an effect of increasing the in vitro inhibition of lipid peroxidation of hydrolysates of milk protein. Casein and whey hydrolysates were able to inhibiting lipid peroxidation in the zebrafish larvae model. Native casein hydrolysate obtained of whole milk presents 48.35% of inhibition TBARS in vivo, this activity was higher in heated casein hydrolysate obtained of whole milk with a value of 56.28% of inhibition TBARS in vivo. Native whey protein hydrolysate obtained of whole milk presents 35.30% of inhibition TBARS, and heated whey protein hydrolysate obtained of whole milk was higher, with a value of 43.60% of inhibition TBARS in vivo.

  13. Native and Heated Hydrolysates of Milk Proteins and Their Capacity to Inhibit Lipid Peroxidation in the Zebrafish Larvae Model

    PubMed Central

    Carrillo, Wilman; Guzmán, Xavier; Vilcacundo, Edgar

    2017-01-01

    Casein and whey proteins with and without heat treatment were obtained of whole milk and four commercial milks in Ecuador, and were hydrolyzed. Then, their capacity to inhibit the lipid peroxidation using the TBARS method was evaluated at concentrations of 0.02, 0.04, 0.2, and, 0.4 mg/mL. Native and heated hydrolysates of milk proteins present high inhibitions of lipid peroxidation with a dose dependent effect both in vivo and in vitro tests. Casein and whey proteins obtained from whole milk were the ones with the highest anti-oxidant activity in vitro and in vivo test. Native casein hydrolysate at 0.4 mg/mL present a value of 55.55% of inhibition of lipid peroxidation and heated casein hydrolysate at 0.4 mg/mL presents a value of 58.00% of inhibition of lipid peroxidation. Native whey protein at 0.4 mg/mL present a value of 34.84% of inhibition of lipid peroxidation, and heated whey protein at 0.4 mg/mL presents a value of 40.86% of inhibition of lipid peroxidation. Native and heated casein hydrolysates were more active than native and heated whey protein hydrolysates. Heat treatments have an effect of increasing the in vitro inhibition of lipid peroxidation of hydrolysates of milk protein. Casein and whey hydrolysates were able to inhibiting lipid peroxidation in the zebrafish larvae model. Native casein hydrolysate obtained of whole milk presents 48.35% of inhibition TBARS in vivo, this activity was higher in heated casein hydrolysate obtained of whole milk with a value of 56.28% of inhibition TBARS in vivo. Native whey protein hydrolysate obtained of whole milk presents 35.30% of inhibition TBARS, and heated whey protein hydrolysate obtained of whole milk was higher, with a value of 43.60% of inhibition TBARS in vivo. PMID:28906440

  14. Inhibition of lipid peroxidation in rat brain by nifedipine and clorazepate after electrically induced seizures.

    PubMed

    Kułak, W; Sobaniec, W; Sobaniec-Lotowska, M

    1993-01-01

    The effect of nifedipine and clorazepate on the concentration of lipid peroxides (LP) in rat brain, and the characteristics of electrically induced seizures were assessed. A significant increase in the concentration of brain LP after electroshock was found. Both nifedipine (1.00 mg/kg per os) and clorazepate (20 mg/kg intraperitoneally) decreased the levels of LP in the rat brain after electroshock. Nifedipine combined with clorazepate brought an inhibition of LP formation and an additive anticonvulsant activity.

  15. Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis.

    PubMed

    Giardino, I; Fard, A K; Hatchell, D L; Brownlee, M

    1998-07-01

    Aminoguanidine (AG) treatment, like nerve growth factor (NGF) treatment, prevents diabetes-induced apoptosis of retinal Müller cells in the rat eye, but the mechanism involved is unknown. In this study, the effects of preincubation with AG on oxidant-induced apoptosis, oxidant-induced intracellular reactive oxygen species (ROS) production, and lipid peroxidation were determined in rat retinal Müller cells and compared with the effects of NGF, a protein that protects neuronal cells from oxidative stress. The effect of AG on rabbit vitreous lipid peroxide levels was also determined. After exposure to increasing concentrations of H2O2, there was a corresponding increase in the percentage of apoptotic Müller cells. Preincubation with AG for 48 h completely inhibited oxidant-induced apoptosis in response to 10 micromol/l H2O2 (+AG 0 vs. 10 micromol/l, NS), and reduced the percentage of apoptotic cells in response to 50 micromol/l H2O2 by 50% (+AG vs. -AG, P < 0.01). Longer preincubation did not increase the antiapoptotic effect of AG. The effect of AG was dose-dependent. Similar results were obtained after preincubation with NGF. Both AG and NGF preincubation prevented the twofold increase in oxidant-induced lipid peroxides. The fivefold increase in oxidant-induced ROS production was decreased 100% by NGF, but only 61% by AG preincubation. The twofold increase in vitreous lipid peroxide level in diabetic rabbits was completely prevented by AG treatment. AG reduced H2O2-induced benzoate hydroxylation in a dose-dependent manner. Intracellular glutathione content was unchanged. These data demonstrate that AG can act as an antioxidant in vivo, quenching hydroxyl radicals and lipid peroxidation in cells and tissues and preventing oxidant-induced apoptosis.

  16. Acetaminophen inhibits hemoprotein-catalyzed lipid peroxidation and attenuates rhabdomyolysis-induced renal failure

    PubMed Central

    Boutaud, Olivier; Moore, Kevin P.; Reeder, Brandon J.; Harry, David; Howie, Alexander J.; Wang, Shuhe; Carney, Clare K.; Masterson, Tina S.; Amin, Taneem; Wright, David W.; Wilson, Michael T.; Oates, John A.; Roberts, L. Jackson

    2010-01-01

    Hemoproteins, hemoglobin and myoglobin, once released from cells can cause severe oxidative damage as a consequence of heme redox cycling between ferric and ferryl states that generates radical species that induce lipid peroxidation. We demonstrate in vitro that acetaminophen inhibits hemoprotein-induced lipid peroxidation by reducing ferryl heme to its ferric state and quenching globin radicals. Severe muscle injury (rhabdomyolysis) is accompanied by the release of myoglobin that becomes deposited in the kidney, causing renal injury. We previously showed in a rat model of rhabdomyolysis that redox cycling between ferric and ferryl myoglobin yields radical species that cause severe oxidative damage to the kidney. In this model, acetaminophen at therapeutic plasma concentrations significantly decreased oxidant injury in the kidney, improved renal function, and reduced renal damage. These findings also provide a hypothesis for potential therapeutic applications for acetaminophen in diseases involving hemoprotein-mediated oxidative injury. PMID:20133658

  17. Inhibition of lipid peroxidation by extracts/subfractions of Chickrassy ( Chukrasia tabularis A. Juss.)

    NASA Astrophysics Data System (ADS)

    Kaur, Rajbir; Thind, Tarunpreet Singh; Singh, Bikram; Arora, Saroj

    2009-01-01

    Polyphenols and polyphenol-rich fractions of plants have been reported to have protective effects against lipid peroxidation, most probably by serving as scavengers of free radicals and/or by chelating metal ions. In the present study, the effect of different extracts/subfractions of Chickrassy ( Chukrasia tabularis) on peroxyl radical mediated damage to the polyunsaturated fatty acids was investigated. Liver homogenate was used as experimental material. The production of malondialdehyde served as a marker of lipid peroxidation and oxidative stress. It was observed that polyphenol-rich fractions, particularly the ethyl acetate fractions of bark and leaves, showed the highest protective activity of 83.02% and 88.62% inhibition, respectively. This study will help in knowing the scientific validation of this plant, for its use in ayurvedic formulations.

  18. Lipid peroxidation inhibition and antiradical activities of some leaf fractions of Mangifera indica.

    PubMed

    Badmus, Jelili A; Adedosu, Temitope O; Fatoki, John O; Adegbite, Victor A; Adaramoye, Oluwatosin A; Odunola, Oyeronke A

    2011-01-01

    This study was undertaken to assess in vitro lipid peroxidation inhibitions and anti-radical activities of methanolic, chloroform, ethyl acetate and water fractions of Mangifera indica leaf. Inhibition of Fe(2+)-induced lipid peroxidation (LPO) in egg, brain, and liver homogenates, 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl (OH-) radical scavenging activities were evaluated. Total phenol was assessed in all fractions, and the reducing power of methanolic fraction was compared to gallic acid and ascorbic acid. The results showed that Fe2+ induced significant lipid peroxidation (LPO) in all the homogenates. Ethyl acetate fraction showed the highest percentage inhibition of LPO in both egg yolk (68.3%) and brain (66.3%), while the aqueous fraction exerted the highest inhibition in liver homogenate (89.1%) at a concentration of 10 microg/mL. These observed inhibitions of LPO by these fractions were higher than that of ascorbic acid used as a standard. The DPPH radical scavenging ability exhibited by ethyl acetate fraction was found to be the highest with IC50 value of 1.5 microg/mL. The ethyl acetate and methanolic fractions had the highest OH- radical scavenging ability with the same IC50 value of 5 microg/mL. The total phenol content of ethyl acetate fraction was the highest with 0.127 microg/mg gallic acid equivalent (GAE). The reductive potential of methanolic fraction showed a concentration-dependent increase. This study showed that inhibition of LPO and the DPPH and OH- radicals scavenging abilities of Mangifera indica leaf could be related to the presence of phenolic compounds. Therefore, the ethyl acetate fraction of the leaf may be a good source of natural antioxidative agent.

  19. Potential antioxidant and lipid peroxidation inhibition of Phyllanthus acidus leaf extract in minced pork.

    PubMed

    Nguyen, Tuyen Thi Kim; Laosinwattana, Chamroon; Teerarak, Montinee; Pilasombut, Komkhae

    2017-09-01

    This study investigated the effect of extraction solvents on antioxidant bio-active compounds as well as potential antioxidant and lipid peroxidation inhibition of Phyllanthus acidus (P. acidus) leaf extract in minced pork. The effect of various solvent systems of water, 25%, 50%, 75% (v/v) ethanol in water and absolute ethanol on the extraction crude yield, total phenolic content, total flavonoid content and in vitro antioxidant activities of P. acidus leaves was determined. In addition, antioxidant activities of the addition of crude extract from P. aciuds leaves at 2.5 and 5 g/kg in minced pork on 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, 2,2'-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical cation decolorization, reducing power and inhibition of lipid peroxidation (thiobarbituric acid reactive substances; TBARS) were determined. Moreover, sensory evaluation of the samples was undertaken by using a 7-point hedonic scale. The results showed that the highest crude yield (2.8 g/100 g dry weight) was obtained from water which also had the highest recovery yield for total phenolic content, total flavonoid content and the strongest antioxidant activity. The addition of crude water extract from P. acidus leaves was more effective in retarding lipid peroxidation and higher antioxidant activity than control and butylated hydroxytoluene in minced pork. In particular, the samples containing P. acidus extract had no significant effect on the sensory scores of overall appearance, color, odor, texture, flavor, and overall acceptability compared to the control. Water solvent was an optimally appropriate solvent for P. acidus leaf extraction because of its ability to yield the highest amount of bio-active compounds and in vitro antioxidant property. Particularly, P. acidus crude water extract also strongly expressed the capacity to retard lipid oxidation, radical scavenging, radical cation decolorization and reducing power in

  20. Inhibition of photosystem II precedes thylakoid membrane lipid peroxidation in bisulfite-treated leaves of Phaseolus vulgaris

    SciTech Connect

    Covello, P.S.; Dumbroff, E.B.; Thompson, J.E. Univ. of Guelph, Ontario ); Chang, A. )

    1989-08-01

    Exposure of leaves to SO{sub 2} bisulfite is known to induce peroxidation of thylakoid lipids and to inhibit photosynthetic electron transport. In the present study, we have examined the temporal relationship between bisulfite-induced thylakoid lipid peroxidation and inhibition of electron transport in an attempt to clarify the primary mechanism of SO{sub 2} phytotoxicity. Primary leaves of bean (Phaseolus vulgaris L. cv Kinghorn) were floated on a solution of NaHSO{sub 3}, and the effects of this treatment on photosynthetic electron transport were determined in vivo by measurements of chlorophyll a fluorescence induction and in vitro by biochemical measurements of the light reactions using isolated thylakoids. Lipid peroxidation in treated leaves was followed by monitoring ethane emission from leaf segments and by measuring changes in fatty acid composition and lipid fluidity in isolated thylakoids. A 1 hour treatment with bisulfite inhibited photosystem II (PSII) activity by 70% without modifying Photosystem I, and this inhibitory effect was not light-dependent. By contrast, lipid peroxidation was not detectable until after the inhibition of PSII and was strongly light dependent. This temporal separation of events together with the differential effect of light suggests that bisulfite-induced inhibition of PSII is not a secondary effect of lipid peroxidation, and that bisulfite acts directly on one or more components of PSII.

  1. Resveratrol ameliorates methotrexate-induced hepatotoxicity in rats via inhibition of lipid peroxidation.

    PubMed

    Dalaklioglu, S; Genc, G E; Aksoy, N H; Akcit, F; Gumuslu, S

    2013-06-01

    Hepatotoxicity is one of the major complications of methotrexate (MTX) therapy. This study was carried out to evaluate the possible protective effect of resveratrol (trans-3,5,4'-trihydroxystilbene, RVT) against MTX-induced hepatotoxicity. Rats were randomly divided into four groups as control, MTX treated (7 mg/kg/day, intraperitoneally (i.p.), once daily for 3 consecutive days), MTX + RVT treated (20 mg/kg/day, i.p.), and RVT treated. First dose of RVT was administrated 3 days before the MTX injection and continued for 3 days. Histopathology of liver was evaluated by light microscopy. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were used as biochemical markers of MTX-induced hepatic injury. The levels of thiobarbituric acid reactive substances (TBARS, a marker of lipid peroxidation) and activities of hepatic antioxidant enzymes such as catalase (CAT) and glutathione-S-transferase (GST) were used to analyze the oxidative stress-mediated lipid peroxidation in liver sections. Our results showed that MTX administration significantly increased ALT, ASP, and ALP levels. TBARS, CAT, and GST levels were also markedly increased in liver after MTX administration. RVT treatment significantly prevented MTX-induced hepatotoxicity, as indicated by AST, ALT, and ALP levels and liver histopathology. Moreover, administration of RVT significantly decreased the elevated levels of TBARS and activities of CAT and GST in the liver compared to MTX-treated group. These results revealed that RVT may have a protective effect against MTX-induced hepatotoxicity by inhibiting oxidative stress-mediated lipid peroxidation. Consequently, RVT treatment might be a promising strategy against MTX-induced hepatotoxicity.

  2. Free radical scavenging, DNA protection, and inhibition of lipid peroxidation mediated by uric acid.

    PubMed

    Stinefelt, Beth; Leonard, Stephen S; Blemings, Kenneth P; Shi, Xianglin; Klandorf, Hillar

    2005-01-01

    Uric acid (UA) has been proposed to be the dominant antioxidant in birds. The objective of this study was to investigate the quenching effect of varying concentrations of UA, including those found in avian plasma, on specific reactive oxygen species (ROS) and to determine the ability of UA to protect DNA and cellular membranes from ROS-mediated damage. Hydroxyl (OH) and superoxide (O2-) radicals were detected by electron spin resonance (ESR) and their presence was reduced following addition of UA (p <0.05) in a concentration-dependent manner. UA inhibited hydroxyl-mediated DNA damage, indicated by the presence of more precise, dense bands of lambda Hind III DNA after agarose gel electrophoresis and ethidium bromide staining (p <0.05). Lipid peroxidation of silica-exposed RAW 264.7 cell membranes was diminished (p <0.02) after addition of UA to the cell incubation mixture. These studies demonstrate that UA scavenges hydroxyl and superoxide radicals and protects against DNA damage and lipid peroxidation. These results indicate specific antioxidant protection that UA may afford birds against ROS-mediated damage.

  3. Withania somnifera (Ashwagandha) attenuates antioxidant defense in aged spinal cord and inhibits copper induced lipid peroxidation and protein oxidative modifications.

    PubMed

    Gupta, Sanjeev K; Dua, Anita; Vohra, Bhupinder P S

    2003-01-01

    Withania somnifera is classified in Ayurveda, the ancient Indian system of medicine, as a rasayana, a group of plant-derived drugs which promote physical and mental health, augment resistance of the body against disease and diverse adverse environmental factors, revitalize the body in debilitated conditions and increase longevity. We investigated the effects of Withania somnifera on copper-induced lipid peroxidation and antioxidant enzymes in aging spinal cord of Wistar rats. The activity of glutathione peroxidase (GPx) decreased significantly in the spinal cord from adult to aged mice. Treatment with Withania somnifera successfully attenuated GPx activity and inhibited lipid peroxidation in a dose dependent manner. Withania somnifera inhibited both the lipid peroxidation and protein oxidative modification induced by copper. These effects were similar to those of superoxide dismutase and mannitol. The results indicate the therapeutic potential of Withania somnifera in aging and copper-induced pathophysiological conditions.

  4. Inhibition of iron induced lipid peroxidation and antioxidant activity of Indian spices and Acacia in vitro.

    PubMed

    Yadav, Amit Singh; Bhatnagar, Deepak

    2010-03-01

    The spices used in the Indian foods such as Star anise (Illicium verum), Bay leaves (Cinnamomum zeylanicum) and Cobra's saffron (Mesua ferrea), and Acacia (Acacia catechu), which have medicinal value, were used as test samples, to find their effect on in vitro lipid peroxidation (LPO). Rat liver post mitochondrial supernatant (PMS) in Tris HCl buffer, pH 7.4 was incubated for 0 and 1 h, with various test extracts in three different oxidant systems. The results show that addition of test samples to FeCl(3) medium at 0 h significantly stop the initiation of the LPO. However, the propagation phase of LPO was inhibited by Cobra's saffron and Acacia and not by Star anise and Bay leaves. The test samples also showed strong reducing power and superoxide radical scavenging activity. Cobra's saffron and Acacia showed the highest antioxidant activity, probably due to the higher polyphenol content as compared to other test samples.

  5. Inhibition of lipid peroxidation, cyclooxygenase enzyme and human tumor cell proliferation by compounds in herbal water.

    PubMed

    Liu, Yunbao; Mulabagal, Vanisree; Bowen-Forbes, Camille S; Aviayan, Rejanish; Nair, Muraleedharan G

    2009-09-01

    A powdered mixture of dried herbs, "Panamrutham", is sold in India for the preparation of "herbal drinking water". The hot water extract of this herbal mixture gave lipid peroxidation (LPO), cyclo-oxygenase (COX-1 and -2) enzyme and human tumor cell proliferation inhibitory activities between 25 and 250 microg/mL. The bioassay-guided purification of the water extract afforded a novel compound (1), along with phenolics (2, 4, 6, and 7) and sesquiterpenoids (3 and 5). The isolates were evaluated for LPO, COX-1 and -2 enzyme and human tumor cell proliferation inhibitory activities. At 25 microg/mL, compounds 1-7 inhibited LPO by 22-73% and COX-1 and -2 enzymes by 3-14% and 14-74%, respectively. Compounds 5 and 6 at 25 microg/mL showed growth inhibition of colon, gastric, lung, breast and central nervous system human tumor cell lines by 60 and 67, 43 and 60, 24 and 64, 34 and 65, 6 and 27%, respectively. Compounds 2, 4 and 7 displayed weak or moderate growth inhibition of colon, gastric and breast human tumor cell lines. This is the first report on the LPO inhibitory activities of compounds 1 and 3-7 and the COX and tumor cell proliferation inhibitory activities of compounds 1, 3-5 and 7.

  6. Inhibition of microsomal lipid peroxidation by cytosolic protein in presence of ADP and high concentration of Fe2+.

    PubMed

    Ramasarma, T; Muakkassah-Kelly, S; Hochstein, P

    1984-12-06

    Microsomal lipid peroxidation induced by NADPH, but not by ascorbate, was found to be inhibited by liver cytosol. This inhibition was not dependent on glutathione and was enhanced by ADP in presence of Fe2+ at a concentration of 50 microM or higher. ATP was also effective, but not AMP or cyclic AMP. The cytosolic factor appeared to be a protein as it was heat-labile (greater than 70 degrees C), was non-dialyzable and was precipitated by ammonium sulfate and acetone. It was stable for several months in frozen state and also when heated at 50 degrees C for 10 min. The inhibition by the cytosolic protein was obtained by producing a lag in the activity of lipid peroxidation and was reversed by ceruloplasmin but not by catalase, cytochrome c, hemoglobin or superoxide dismutase. This inhibitory effect by cytosol was limited to formation of lipid peroxides whereas oxygen uptake and NADPH oxidation remained unaffected. Regulation of lipid peroxidation by nucleotide-Fe complexes and cytosolic proteins is indicated by these studies.

  7. Inhibition of cumene hydroperoxide-induced lipid peroxidation by a novel pyridoindole antioxidant in rat liver microsomes.

    PubMed

    Stefek, M; Masarykova, M; Benes, L

    1992-06-01

    The ability of stobadine, a novel pyridoindole antioxidant, to inhibit lipid peroxidation induced by cumene hydroperoxide was investigated in rat liver microsomes. In the micromolar range stobadine effectively inhibited lipid peroxidation as measured by the formation of thiobarbituric acid reactive products. The peroxidation-related degradation of microsomal cytochrome P-450 was prevented by stobadine in the same pattern. Another line of evidence in support of the antioxidant action of stobadine was given by its inhibition of cumene hydroperoxide-induced oxygen consumption in microsomal incubations. Inhibition of lipid peroxidation was not a function of decreased bioactivation of cumene hydroperoxide, as stobadine did not affect the rate of cytochrome P-450 dependent cleavage of cumene hydroperoxide. Neither had stobadine any effect on cytochrome P-450 peroxidase function characterized by the rate of cumene hydroperoxide-dependent oxidation of TMPD, and no direct spectral interaction with microsomal cytochrome P-450 was observed in the micromolar region. We suggest that it is the ability of stobadine to scavenge alkoxyl and peroxyl radicals that is predominantly responsible for the observed antioxidant effect.

  8. Inhibition of lipid peroxidation promoted by iron(III) and ascorbate.

    PubMed

    Beach, D C; Giroux, E

    1992-09-01

    Peroxidation of rat liver microsomes and of phospholipid isolated from them was studied using iron(III) and ascorbate initiation. One-half equivalent of citrate per iron equivalent maintained solubility of the metal ion at neutral pH. Several metal chelators, including additional citrate, blocked peroxidation, but catalase did not. These characteristics are consistent with those reported by others (D. M. Miller and S. D. Aust (1989) Arch. Biochem. Biophys. 271, 113-119). Several antioxidants, principally tocopherol analogues and nitroxides, and, as well, a nonenzymatic component of "thymol-free" catalase, potently blocked lipid peroxidation, or, equivalently, dioxygen depletion from suspensions of peroxidizing microsomes. Chromanols were the most active antioxidants. No thiol studied had significant antioxidant activity in the test system.

  9. Lipid peroxidation and coupled vitamin oxidation in simulated and human gastric fluid inhibited by dietary polyphenols: health implications.

    PubMed

    Gorelik, Shlomit; Lapidot, Tair; Shaham, Inbal; Granit, Rina; Ligumsky, Moshe; Kohen, Ron; Kanner, Joseph

    2005-05-04

    The Western diet contains large quantities of oxidized lipids, because a large proportion of the food in the diet is consumed in a fried, heated, processed, or stored form. We investigated the reaction that could occur in the acidic pH of the stomach and accelerate the generation of lipid hydroperoxides and cooxidation of dietary vitamins. To estimate the oxygen content in the stomach after food consumption, oxygen released from masticated bread (20 g) into deoxygenated water (100 mL) was measured. Under these conditions, the oxygen concentration rose by 250 microM and reached a full oxygen saturation. The present study demonstrated that heated red meat homogenized in human gastric fluid, at pH 3.0, generated hydroperoxides and malondialdehyde. The cross-reaction between free radicals produced during this reaction cooxidized vitamin E, beta-carotene, and vitamin C. Both lipid peroxidation and cooxidation of vitamin E and beta-carotene were inhibited at pH 3.0 by red wine polyphenols. Ascorbic acid (44 mg) at a concentration that represented the amount that could be ingested during a meal inhibited lipid peroxidation only slightly. Red wine polyphenols failed to prevent ascorbic acid oxidation significantly but, in conjunction with ascorbic acid, did inhibit lipid peroxidation. In the presence of catechin, a well-known polyphenol found in red wine, ascorbic acid at pH 3.0 works in a synergistic manner preventing lipid peroxidation and beta-carotene cooxidation. The present data may explain the major benefits to our health and the crucial role of consuming food products rich in dietary antioxidants such as fruits, vegetables, red wines, or green tea during the meal.

  10. Inhibition of eicosanoid signaling leads to increased lipid peroxidation in a host/parasitoid system.

    PubMed

    Büyükgüzel, Ender; Erdem, Meltem; Tunaz, Hasan; Küçük, Ceyhun; Atılgan, Utku Can; Stanley, David; Büyükgüzel, Kemal

    2017-02-01

    We posed the hypothesis that inhibition of eicosanoid biosynthesis leads to increased lipid peroxidation in insects. Here we report that rearing the greater wax moth, Galleria mellonella, on media supplemented with selected inhibitors of eicosanoid biosynthesis throughout the larval, pupal and adult life led to major alterations in selected oxidative and antioxidative parameters of wax moth and its ectoparasitoid, Bracon hebetor. The highest dietary dexamethasone (Dex), esculetin (Esc) and phenidone (Phe) led to increased malondialdehyde (MDA) levels and to elevated catalase (CAT) and glutathione-S-transferase (GST) activities in all developmental stages of host larvae. Dietary Phe resulted in increased MDA levels, and CAT activity in G. mellonella adults by about 4-fold and about 2-fold, respectively. The Phe effect on GST activity in all stages of the wax moth was expressed in a dose-dependent manner, increased to 140nmol/mg protein/min in larvae. MDA levels were increased by over 30-fold in adult wasps reared on Dex- and Esc-treated hosts. CAT and GST activities were increased in adult parasitoids reared on Esc-and Phe-treated hosts. GST activity of Dex-treated parasitoid larvae increased from about 4 to over 30nmol/mg protein/min. Dietary Phe led to increased GST activity, by about 25-fold, in adult wasps. These data indicate that chronic inhibition of eicosanoid biosynthesis leads to increased oxidative stress, strongly supporting our hypothesis. The significance of this work lies in understanding the roles of eicosanoids in insect biology. Aside from other well-known eicosanoids actions, we propose that eicosanoids mediate reductions in oxidative stress. Copyright © 2016 Elsevier Inc. All rights reserved.

  11. Digestibility of Quinoa (Chenopodium quinoa Willd.) Protein Concentrate and Its Potential to Inhibit Lipid Peroxidation in the Zebrafish Larvae Model.

    PubMed

    Vilcacundo, R; Barrio, D; Carpio, C; García-Ruiz, A; Rúales, J; Hernández-Ledesma, B; Carrillo, W

    2017-08-22

    Quinoa protein concentrate (QPC) was extracted and digested under in vitro gastrointestinal conditions. The protein content of QPC was in the range between 52.40 and 65.01% depending on the assay used. Quinoa proteins were almost completely hydrolyzed by pepsin at pH of 1.2, 2.0, and 3.2. At high pH, only partial hydrolysis was observed. During the duodenal phase, no intact proteins were visible, indicating their susceptibility to the in vitro simulated digestive conditions. Zebrafish larvae model was used to evaluate the in vivo ability of gastrointestinal digests to inhibit lipid peroxidation. Gastric digestion at pH 1.2 showed the highest lipid peroxidation inhibition percentage (75.15%). The lipid peroxidation activity increased after the duodenal phase. The digest obtained at the end of the digestive process showed an inhibition percentage of 82.10%, comparable to that showed when using BHT as positive control (87.13%).

  12. Epicatechin inhibits human plasma lipid peroxidation caused by haloperidol in vitro.

    PubMed

    Dietrich-Muszalska, Anna; Kontek, Bogdan; Olas, Beata; Rabe-Jabłońska, Jolanta

    2012-03-01

    Epicatechin belongs to flavonoids protecting cells against oxidative/nitrative stress. Oxidative/nitrative stress observed in schizophrenia may be caused partially by the treatment of patients with various antipsychotics. The aim of our study was to establish the effects of epicatechin and antipsychotics action (the first generation antipsychotic (FGA)--haloperidol and the second generation antipsychotic (SGA)--amisulpride) on peroxidation of plasma lipids in vitro. Lipid peroxidation in human plasma was measured by the level of thiobarbituric acid reactive species (TBARS). The properties of epicatechin were also compared with the action of a well characterized antioxidative commercial polyphenol-resveratrol (3,4',5-trihydroxystilbene) and quercetin (3,5,7,3',4'-pentahydroxyflavone). Amisulpride, contrary to haloperidol (after 1 and 24 h) does not significantly influence the increase of plasma TBARS level in comparison with control samples (P > 0.05). After incubation (1 and 24 h) of plasma with haloperidol in the presence of epicatechin we observed a significantly decreases the level of TBARS (P < 0.001, P < 0.001, respectively). In our other experiments, we found that epicatechin also decreased the amount of TBARS in human plasma treated with amisulpride. In conclusion, the presented results indicate that epicatechin-the major polyphenolic component of green tea reduced significantly human plasma lipid peroxidation caused by haloperidol. Moreover, epicatechin was found to be a more effective antioxidant, than the solution of pure resveratrol or quercetin.

  13. Fixed oil of Nigella sativa and derived thymoquinone inhibit eicosanoid generation in leukocytes and membrane lipid peroxidation.

    PubMed

    Houghton, P J; Zarka, R; de las Heras, B; Hoult, J R

    1995-02-01

    Samples of the expressed fixed oil from different sources of Nigella sativa seeds were examined by thin-layer and gas chromatography for content of fixed oils and thymoquinone, and these substances were tested as possible inhibitors of eicosanoid generation and membrane lipid peroxidation. The crude fixed oil and pure thymoquinone both inhibited the cyclooxygenase and 5-lipoxygenase pathways of arachidonate metabolism in rat peritoneal leukocytes stimulated with calcium ionophore A23187, as shown by dose-dependent inhibition of thromboxane B2 and leukotriene B4, respectively. Thymoquinone was very potent, with approximate IC50 values against 5-lipoxygenase and cyclo-oxygenase of < 1 microgram/ml and 3.5 micrograms/ml, respectively. Both substances also inhibited non-enzymatic peroxidation in ox brain phospholipid liposomes, but thymoquinone was about ten times more potent. However, the inhibition of eicosanoid generation and lipid peroxidation by the fixed oil of N. sativa is greater than is expected from its content of thymoquinone (ca. 0.2% w/v), and it is possible that other components such as the unusual C20:2 unsaturated fatty acids may contribute also to its anti-eicosanoid and antioxidant activity. These pharmacological properties of the oil support the traditional use of N. sativa and its derived products as a treatment for rheumatism and related inflammatory diseases.

  14. Radiation-induced peroxidation of lipid dissolved in organic solvent and its inhibition by alpha-tocopherol and cepharanthine

    SciTech Connect

    Shiraishi, N.; Joja, I.; Kuroda, M.; Fujishima, M.; Miyake, M.; Aono, K.

    1985-01-01

    Effects of cepharanthine and alpha-tocopherol on radiation-induced peroxidation of lipids dissolved in methanol(MeOH)-chloroform (CHCl3)-H2O(v/v, 2/1/0.8) were examined. alpha-Tocopherol strongly inhibited radiation-induced peroxidation of lipids dissolved in MeOH-CHCl3-H2O. However, cepharanthine exhibited a weak inhibitory action in this system. The change in the absorption spectrum of alpha-tocopherol and cepharanthine by X-irradiation was measured. The reagents were dissolved in 95% EtOH acidified with 20 mM HCl and in MeOH-CHCl3-H2O. alpha-Tocopherol exhibited the change in its absorption spectrum in both systems, and seemed to be oxidized at a high rate by free radicals. However, cepharanthine slightly exhibited the change in its spectrum in MeOH-CHCl3-H2O, but not in acidified EtOH.

  15. Lipid peroxide formation in microsomes. Relationship of hydroxylation to lipid peroxide formation

    PubMed Central

    Wills, E. D.

    1969-01-01

    1. Aminopyrine strongly inhibits NADPH-induced lipid peroxide formation in rat liver microsomes, but ascorbate-induced peroxidation is inhibited to a smaller extent. 2. Aminopyrine oxidation is stimulated by Mg2+ but inhibited by Ca2+. Concentrated solutions (10mm) of iron-chelating agents inhibit aminopyrine oxidation, but the more dilute solutions (0·5mm) of chelators that block lipid peroxide formation do not inhibit aminopyrine oxidation. Microsomes prepared from sucrose–EDTA homogenates rapidly oxidize aminopyrine, but do not form lipid peroxide when incubated with ascorbate or NADPH. 3. Aminopyrine oxidation is strongly inhibited by p-chloromercuribenzoate, less by iodoacetamide and weakly by N-ethylmaleimide. The site of action of these compounds is considered to be a ferredoxin-type protein. GSH and cysteine also inhibit. 4. Other drugs oxidized by microsomes such as caffeine, phenobarbitone and hexobarbitone had either no or little effect on lipid peroxide formation, but codeine inhibited. 5. Most aliphatic hydrocarbons, alcohols, ketones and aldehydes did not affect lipid peroxide formation, but chloroform and carbon tetrachloride inhibited. 6. Many aromatic compounds inhibited lipid peroxide formation. Only aromatic acids were without any effect and phenols and amines were very strong inhibitors. 7. Induction of lipid peroxide formation in microsomes by incubation with ascorbate or NADPH or by treatment with ionizing radiation leads to a sharp decline in the ability of microsomes to oxidize aminopyrine or hydroxylate aniline. 8. It is considered that the two processes of hydroxylation and lipid peroxide formation are closely linked in microsomes. They probably depend on the same electron-transport chain, and peroxide formation, which involves membrane disintegration, may be part of the normal membrane remodelling process. PMID:4390103

  16. Inhibition of membrane lipid peroxidation by a radical scavenging mechanism: a novel function for hydroxyl-containing ionophores.

    PubMed

    Grijalba, M T; Andrade, P B; Meinicke, A R; Castilho, R F; Vercesi, A E; Schreier, S

    1998-03-01

    In the present study we show that K+/H+ hydroxyl-containing ionophores lasalocid-A (LAS) and nigericin (NIG) in the nanomolar concentration range, inhibit Fe2+-citrate and 2,2'-azobis(2-amidinopropane) dihydrochloride (ABAP)-induced lipid peroxidation in intact rat liver mitochondria and in egg phosphatidylcholine (PC) liposomes containing negatively charged lipids--dicetyl phosphate (DCP) or cardiolipin (CL)--and KCl as the osmotic support. In addition, monensin (MON), a hydroxyl-containing ionophore with higher affinity for Na+ than for K+, promotes a similar effect when NaCl is the osmotic support. The protective effect of the ionophores is not observed when the osmolyte is sucrose. Lipid peroxidation was evidenced by mitochondrial swelling, antimycin A-insensitive O2 consumption, formation of thiobarbituric acid-reactive substances (TBARS), conjugated dienes, and electron paramagnetic resonance (EPR) spectra of an incorporated lipid spin probe. A time-dependent decay of spin label EPR signal is observed as a consequence of lipid peroxidation induced by both inductor systems in liposomes. Nitroxide destruction is inhibited by butylated hydroxytoluene, a known antioxidant, and by the hydroxyl-containing ionophores. In contrast, valinomycin (VAL), which does not possess alcoholic groups, does not display this protective effect. Effective order parameters (Seff), determined from the spectra of an incorporated spin label are larger in the presence of salt and display a small increase upon addition of the ionophores, as a result of the increase of counter ion concentration at the negatively charged bilayer surface. This condition leads to increased formation of the ion-ionophore complex, the membrane binding (uncharged) species. The membrane-incorporated complex is the active species in the lipid peroxidation inhibiting process. Studies in aqueous solution (in the absence of membranes) showed that NIG and LAS, but not VAL, decrease the Fe2+-citrate-induced production

  17. Conjugated eicosapentaenoic acid (EPA) inhibits transplanted tumor growth via membrane lipid peroxidation in nude mice.

    PubMed

    Tsuzuki, Tsuyoshi; Igarashi, Miki; Miyazawa, Teruo

    2004-05-01

    Both conjugated linoleic acid (CLA) and eicosapentaenoic acid (EPA) have an antitumor effect. Hence, we hypothesized that a combination of conjugated double bonds and an (n-3) highly unsaturated fatty acid would produce stronger bioactivity. To verify the antitumor effect of conjugated EPA (CEPA), we transplanted DLD-1 human colon tumor cells into nude mice, and compared the tumor growth between CEPA-fed mice and CLA- and EPA-fed mice. After tumor cell inoculation, mice were assigned to 1 of 4 groups (control, CLA, EPA, and CEPA) consisting of 10 mice each. The control group received only safflower oil fatty acids, whereas the remaining groups received a mixture of safflower oil fatty acids and 20 g/100 g of total fatty acids as CLA, EPA, or CEPA. Mice were fed once every 2 d for 4 wk at a dose of 50 mg/mouse at each feeding. After 4 wk, tumor growth in CEPA-fed mice was significantly suppressed, compared with that in CLA- (P < 0.005) and EPA-fed mice (P < 0.001). DNA fragmentation in the tumor tissues of the CEPA-fed mice occurred more frequently than in the CLA- (P < 0.001) and EPA-fed mice (P < 0.001), suggesting that CEPA induced apoptosis in the tumor tissues. To further investigate the mechanism, the level of oxidative stress in the tumor tissues was determined. The CEPA-fed mice showed significant lipid peroxidation, compared with the CLA- (P < 0.001) and EPA-fed mice (P < 0.001). Therefore, we verified that CEPA has a stronger in vivo antitumor effect than EPA and CLA, and that CEPA acts through induction of apoptosis via lipid peroxidation.

  18. Carotenoids inhibit lipid peroxidation and hemoglobin oxidation, but not the depletion of glutathione induced by ROS in human erythrocytes.

    PubMed

    Chisté, Renan Campos; Freitas, Marisa; Mercadante, Adriana Zerlotti; Fernandes, Eduarda

    2014-03-18

    Despite the presence of endogenous antioxidants in erythrocytes, these cells are highly susceptible to oxidative damage and some exogenous antioxidants, such as carotenoids, are able to inhibit the pro-oxidant effect provided by reactive oxygen species. In this study, we evaluated the potential of carotenoids usually detected in human blood plasma (β-carotene, zeaxanthin, lutein, β-cryptoxanthin and lycopene) to prevent the oxidative damage in erythrocytes. Human erythrocytes were subjected to induced oxidative damage and the following biomarkers of oxidative stress were monitored: lipid peroxidation [induced by tert-butyl hydroperoxide (tBHP) or by 2,2'-azobis (2-methylpropionamidine) dihydrochloride (AAPH)] and AAPH-induced oxidation of hemoglobin and depletion of glutathione. When tBHP was used to induce lipid peroxidation, lycopene was the most efficient carotenoid (IC50=2.2 ± 0.4 μM), while lutein was the most efficient (IC50=2.5 ± 0.7 μM) when peroxyl radicals (ROO) were generated by AAPH. In relation to the hemoglobin oxidation induced by AAPH, β-carotene and zeaxanthin were the most efficient antioxidants (IC50=2.9 ± 0.3 μM and 2.9 ± 0.1 μM, respectively). Surprisingly β-cryptoxanthin and lycopene did not inhibit hemoglobin oxidation or lipid peroxidation when induced by AAPH, even at the highest tested concentration (3 μM). Additionally, the tested carotenoids did not prevent ROO-mediated GSH depletion and GSSG formation probably due to the lack of interaction between carotenoids (apolar) and glutathione (polar). Our study contributes with important insights that carotenoids may exert therapeutical potential to act as a natural antioxidant to prevent ROO-induced toxicity in human erythrocytes. Copyright © 2014 Elsevier Inc. All rights reserved.

  19. Inhibition of Oxidative Stress and Lipid Peroxidation by Anthocyanins from Defatted Canarium odontophyllum Pericarp and Peel Using In Vitro Bioassays

    PubMed Central

    Khoo, Hock Eng; Azlan, Azrina; Ismail, Amin; Abas, Faridah; Hamid, Muhajir

    2014-01-01

    Canarium odontophyllum, also known as CO, is a highly nutritious fruit. Defatted parts of CO fruit are potent sources of nutraceutical. This study aimed to determine oxidative stress and lipid peroxidation effects of defatted CO pericarp and peel extracts using in vitro bioassays. Cell cytotoxic effect of the CO pericarp and peel extracts were also evaluated using HUVEC and Chang liver cell lines. The crude extracts of defatted CO peel and pericarp showed cytoprotective effects in t-BHP and 40% methanol-induced cell death. The crude extracts also showed no toxic effect to Chang liver cell line. Using CD36 ELISA, NAD+ and LDL inhibition assays, inhibition of oxidative stress were found higher in the crude extract of defatted CO peel compared to the pericarp extract. Hemoglobin and LDL oxidation assays revealed both crude extracts had significantly reduced lipid peroxidation as compared to control. TBARS values among defatted CO pericarp, peel, and cyanidin-3-glucoside showed no significant differences for hemoglobin and LDL oxidation assays. The protective effects of defatted CO parts, especially its peel is related to the presence of high anthocyanin that potentially offers as a pharmaceutical ingredient for cardioprotection. PMID:24416130

  20. Lipid peroxidation in cell death.

    PubMed

    Gaschler, Michael M; Stockwell, Brent R

    2017-01-15

    Disruption of redox homeostasis is a key phenotype of many pathological conditions. Though multiple oxidizing compounds such as hydrogen peroxide are widely recognized as mediators and inducers of oxidative stress, increasingly, attention is focused on the role of lipid hydroperoxides as critical mediators of death and disease. As the main component of cellular membranes, lipids have an indispensible role in maintaining the structural integrity of cells. Excessive oxidation of lipids alters the physical properties of cellular membranes and can cause covalent modification of proteins and nucleic acids. This review discusses the synthesis, toxicity, degradation, and detection of lipid peroxides in biological systems. Additionally, the role of lipid peroxidation is highlighted in cell death and disease, and strategies to control the accumulation of lipid peroxides are discussed. Copyright © 2016 The Author(s). Published by Elsevier Inc. All rights reserved.

  1. Curcumin Blocks Naproxen-Induced Gastric Antral Ulcerations through Inhibition of Lipid Peroxidation and Activation of Enzymatic Scavengers in Rats.

    PubMed

    Kim, Jeong-Hwan; Jin, Soojung; Kwon, Hyun Ju; Kim, Byung Woo

    2016-08-28

    Curcumin is a polyphenol derived from the plant Curcuma longa, which is used for the treatment of diseases associated with oxidative stress and inflammation. The present study was undertaken to determine the protective effect of curcumin against naproxen-induced gastric antral ulcerations in rats. Different doses (10, 50, and 100 mg/kg) of curcumin or vehicle (curcumin, 0 mg/kg) were pretreated for 3 days by oral gavage, and then gastric mucosal lesions were caused by 80 mg/kg naproxen applied for 3 days. Curcumin significantly inhibited the naproxen-induced gastric antral ulcer area and lipid peroxidation in a dose-dependent manner. In addition, curcumin markedly increased activities of radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase in a dose-dependent manner. Specifically, 100 mg/kg curcumin completely protected the gastric mucosa against the loss in the enzyme, resulting in a drastic increase of activities of radical scavenging enzymes up to more than the level of untreated normal rats. Histological examination obviously showed that curcumin prevents naproxen-induced gastric antral ulceration as a result of direct protection of the gastric mucosa. These results suggest that curcumin blocks naproxen-induced gastric antral ulcerations through prevention of lipid peroxidation and activation of radical scavenging enzymes, and it may offer a potential remedy of gastric antral ulcerations.

  2. Antioxidant, lipid peroxidation inhibition and free radical scavenging efficacy of a diterpenoid compound sugiol isolated from Metasequoia glyptostroboides.

    PubMed

    Bajpai, Vivek K; Sharma, Ajay; Kang, Sun Chul; Baek, Kwang-Hyun

    2014-01-01

    To investigate the antioxidant efficacy of a biologically active diterpenoid compound sugiol isolated from Metasequoia glyptostroboides (M. glyptostroboides) in various antioxidant models. An abietane type diterpenoid sugiol, isolated from ethyl acetate extract of M. glyptostroboides cones, was analyzed for its antioxidant efficacy as reducing power ability and lipid peroxidation inhibition as well as its ability to scavenge free radicals such as 1,1-diphenyl-2-picryl hydrazyl, nitric oxide, superoxide and hydroxyl radicals. The sugiol showed significant and concentration-dependent antioxidant and free radical scavenging activities. Consequently, the sugiol exerted lipid peroxidation inhibitory effect by 76.5% as compared to α-tocopherol (80.13%) and butylated hydroxyanisole (76.59%). In addition, the sugiol had significant scavenging activities of 1,1-diphenyl-2-picryl hydrazyl, nitric oxide, superoxide and hydroxyl free radicals in a concentration-dependent manner by 78.83%, 72.42%, 72.99% and 85.04%, when compared to the standard compound ascorbic acid (81.69%, 74.62%, 73.00% and 73.79%) and α-tocopherol/butylated hydroxyanisole (84.09%, 78.61%, 74.45% and 70.02%), respectively. These findings justify the biological and traditional uses of M. glyptostroboides or its secondary metabolites as confirmed by its promising antioxidant efficacy. Copyright © 2014 Hainan Medical College. Published by Elsevier B.V. All rights reserved.

  3. Lipid Peroxidation Is an Early Symptom Triggered by Aluminum, But Not the Primary Cause of Elongation Inhibition in Pea Roots1

    PubMed Central

    Yamamoto, Yoko; Kobayashi, Yukiko; Matsumoto, Hideaki

    2001-01-01

    Pea (Pisum sativum) roots were treated with aluminum in a calcium solution, and lipid peroxidation was investigated histochemically and biochemically, as well as other events caused by aluminum exposure. Histochemical stainings were observed to distribute similarly on the entire surface of the root apex for three events (aluminum accumulation, lipid peroxidation, and callose production), but the loss of plasma membrane integrity (detected by Evans blue uptake) was localized exclusively at the periphery of the cracks on the surface of root apex. The enhancement of four events (aluminum accumulation, lipid peroxidation, callose production, and root elongation inhibition) displayed similar aluminum dose dependencies and occurred by 4 h. The loss of membrane integrity, however, was enhanced at lower aluminum concentrations and after longer aluminum exposure (8 h). The addition of butylated hydroxyanisole (a lipophilic antioxidant) during aluminum treatment completely prevented lipid peroxidation and callose production by 40%, but did not prevent or slow the other events. Thus lipid peroxidation is a relatively early symptom induced by the accumulation of aluminum and appears to cause, in part, callose production, but not the root elongation inhibition; by comparison, the loss of plasma membrane integrity is a relatively late symptom caused by cracks in the root due to the inhibition of root elongation. PMID:11154329

  4. Lipid peroxidation of fish oils.

    PubMed

    Godwin, Angela; Prabhu, H Ramachandra

    2006-03-01

    Fish and fish oils are the richest sources of ω-3 fatty acids. However, they are susceptible to lipid peroxidation due to their high degree of unsaturation. In the present study, the level of thiobarbituric acid reactive material in various fish oils available in the market with and without added Vitamin E was determined. The peroxide levels in fish oil heated to food frying temperature of 180°C and the effect of addition of vitamin E has also been studied. The results indicate that the peroxide levels in almost all the products available in the market were abnormally high irrespective of their Vitamin E content. This might be due to the inefficient methods used for processing and storage of fish oils. Addition of vitamin E was found to have a significant effect in lowering the rate of peroxidation of fish oil during thermal stress, showing that association of antioxidants with ω-3 fatty acids lowers the rate of lipid peroxidation.

  5. Fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, scavenges free radicals and inhibits lipid peroxidation in rat liver microsomes.

    PubMed

    Yamamoto, A; Hoshi, K; Ichihara, K

    1998-11-13

    We investigated the effect of fluvastatin sodium (fluvastatin) and pravastatin, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, on the formation of thiobarbituric acid reactive substances both in vivo and in vitro in rat liver microsomes and on active oxygen species. Oral administration of fluvastatin at low doses (3.13 and 6.25 mg/kg) inhibited the formation of thiobarbituric acid reactive substances in rat liver microsomes, but high doses (12.5 and 25 mg/kg) did not change the formation of thiobarbituric acid reactive substances. Fluvastatin at any dose used had no effect on the content of cytochrome P-450 and the activity of NADPH-cytochrome P-450 reductase. In in vitro experiments, concentrations of fluvastatin ranging from 1 x 10(-6) - 1 x 10(-4) M markedly inhibited NADPH-dependent lipid peroxidation in liver microsomes, but pravastatin weakly inhibited lipid peroxidation. The order of magnitude of inhibition of each drug on in vitro lipid peroxidation was butylated hydroxytoluene > probucol > or = fluvastatin > pravastatin. Moreover, fluvastatin chemically scavenged active oxygen species such as hydroxyl radicals and superoxide anion generated by the Fenton reaction and by the xanthine-xanthine oxidase system, respectively, but pravastatin showed no scavenging of superoxide anion. These results indicate that the suppression of in vivo and in vitro lipid peroxidation in liver microsomes may be, at least in part, due to the scavenging by fluvastatin of free radicals.

  6. Topical alpha-tocotrienol supplementation inhibits lipid peroxidation but fails to mitigate increased transepidermal water loss after benzoyl peroxide treatment of human skin.

    PubMed

    Weber, Stefan U; Thiele, Jens J; Han, Nancy; Luu, Chate; Valacchi, Giuseppe; Weber, Stefanie; Packer, Lester

    2003-01-15

    Benzoyl peroxide (BPO) is a commonly used drug in the treatment of acne vulgaris, but it induces unwanted side effects related to stratum corneum (SC) function. Since it has been recently shown to oxidize SC antioxidants, it was hypothesized that antioxidant supplementation may mitigate the BPO-induced SC changes. To test this, 11 subjects were selected to be topically supplemented with alpha-tocotrienol (5% w/vol) for 7 d on defined regions of the upper back, while the contralateral region was used for vehicle-only controls. Starting on day 8, all test sites were also treated with BPO (10%) for 7 d; the alpha-tocotrienol supplementation was continued throughout the study. A single dose of BPO depleted 93.2% of the total vitamin E. While continuing the BPO exposure for 7 d further depleted vitamin E in both vehicle-only and alpha-tocotrienol-treated sites, significantly more vitamin E remained in the alpha-tocotrienol-treated areas. Seven BPO applications increased lipid peroxidation. Alpha-tocotrienol supplementation significantly mitigated the BPO-induced lipid peroxidation. The transepidermal water loss was increased 1.9-fold by seven BPO applications, while there was no difference between alpha-tocotrienol treatment and controls. The data suggest that alpha-tocotrienol supplementation counteracts the lipid peroxidation but not the barrier perturbation in the SC induced by 10% BPO.

  7. Application of simulation modeling to lipid peroxidation processes.

    PubMed

    Tappel, A L; Tappel, A A; Fraga, C G

    1989-01-01

    A quantitative simulation model was developed that utilized present knowledge of lipid peroxidation in biological systems. The simulation model incorporated the following features: peroxidizability of polyunsaturated lipids, activation of inducers and their initiation of lipid peroxidation, concurrent autoxidation, inhibition of lipid peroxidation by vitamin E, reduction of some of the hydroperoxides by glutathione peroxidase, and formation of thiobarbituric acid-reactive substances. Simulation calculations were done using a computer spreadsheet program. When the simulation program was applied to tissue slice and microsomal peroxidizing systems, the results of the stimulation were in agreement with the experimental data.

  8. Antioxidant effect of bisphosphonates and simvastatin on chondrocyte lipid peroxidation

    SciTech Connect

    Dombrecht, E.J.; De Tollenaere, C.B.; Aerts, K.; Cos, P.; Schuerwegh, A.J.; Bridts, C.H.; Van Offel, J.F.; Ebo, D.G.; Stevens, W.J. . E-mail: immuno@ua.ac.be; De Clerck, L.S.

    2006-09-22

    The objective of this study was to evaluate the effect of bisphosphonates (BPs) and simvastatin on chondrocyte lipid peroxidation. For this purpose, a flow cytometrical method using C11-BODIPY{sup 581/591} was developed to detect hydroperoxide-induced lipid peroxidation in chondrocytes. Tertiary butylhydroperoxide (t-BHP) induced a time and concentration dependent increase in chondrocyte lipid peroxidation. Addition of a Fe{sup 2+}/EDTA complex to t-BHP or hydrogen peroxide (H{sub 2}O{sub 2}) clearly enhanced lipid peroxidation. The lipophilic simvastatin demonstrated a small inhibition in the chondrocyte lipid peroxidation. None of three tested BPs (clodronate, pamidronate, and risedronate) had an effect on chondrocyte lipid peroxidation induced by t-BHP. However, when Fe{sup 2+}/EDTA complex was added to t-BHP or H{sub 2}O{sub 2}, BPs inhibited the lipid peroxidation process varying from 25% to 58%. This study demonstrates that BPs have antioxidant properties as iron chelators, thereby inhibiting the chondrocyte lipid peroxidation. These findings add evidence to the therapeutic potential of bisphosphonates and statins in rheumatoid arthritis.

  9. From balsamic to healthy: traditional balsamic vinegar melanoidins inhibit lipid peroxidation during simulated gastric digestion of meat.

    PubMed

    Verzelloni, Elena; Tagliazucchi, Davide; Conte, Angela

    2010-01-01

    In this work traditional balsamic vinegar (TBV) melanoidins were characterized for chemical composition and antioxidant activity and their anti-peroxidative effect during an in vitro gastric digestion of turkey meat was studied. The most important constituents of TBV melanoidins were carbohydrates (51% w/w) of which glucose (35% w/w) and fructose (10% w/w) are the main representatives, hydroxymethylfurfural (7.2% w/w), phenolic groups (4.6% w/w) and proteins (1.2% w/w). The antioxidant capacity of melanoidins was studied, measuring lipid hydroperoxides and secondary lipoxidation products formed during in vitro gastric digestion of turkey meat. The most important mechanisms in their antioxidant activity resulted radical scavenging and Fe(2+)-chelating activities. Pepsin inhibiting ability has been excluded. TBV melanoidins were also able to bind heme under gastric conditions potentially preventing its absorption and prooxidant and cytotoxic effects. Our results support the idea that TBV melanoidins may have a role in oxidative damage prevention. Fe(2+)-chelating and heme-binding activities as well as mechanisms of antioxidant activity of TBV melanoidins were also compared with coffee, barley coffee and dark beer melanoidins.

  10. Inhibition of eicosanoid signaling leads to increased lipid peroxidation in a host/parasitoid system

    USDA-ARS?s Scientific Manuscript database

    We posed the hypothesis that eicosanoids act in reduction of oxidative stress in insects. Here we report that inhibiting eicosanoid biosynthesis throughout the larval, pupal and adult life led to major alterations on some oxidative and antioxidative parameters of the greater wax moth, Galleria mello...

  11. Water-soluble compounds of lettuce inhibit DNA damage and lipid peroxidation induced by glucose/serum deprivation in N2a cells.

    PubMed

    Asadpour, Elham; Ghorbani, Ahmad; Sadeghnia, Hamid R

    2014-01-01

    Oxidative stress, increase of lipid peroxidation and resultant DNA damage are associated with pathophysiology of many human diseases such as acute and chronic CNS injuries and diseases, cancer, and also aging. This work was done to investigate whether water fraction from the hydroalcoholic extract of green leaf lettuce (Lactuca sativa L.) can protect N2a cells against glucose/serum deprivation (GSD)-induced lipid peroxidation and DNA fragmentation. The cells were cultivated for 12 h in GSD condition in the absence or presence of the lettuce fraction. The total antioxidant ability of the lettuce water fraction was determined using ferric reducing antioxidant power (FRAP) assay. The intracellular lipid peroxidation was evaluated by malondialdehyde (MDA) level. DNA damage was determined using single cell gel electrophoresis. Using FRAP assay, the antioxidant activity of lettuce water fraction was found to be 574 micromol/g, which is equivalent to 64.1 mg of pure ascorbic acid. Exposure of the cells to GSD condition led to a significant increase of MDA level and DNA fragmentation. Lettuce extract at 400 microg/mL could decrease the elevated intracellular lipid peroxidation and DNA damage. The present study demonstrates that lettuce exerts genoprotective effect through inhibition of oxidative stress.

  12. Propofol inhibits inflammation and lipid peroxidation following cerebral ischemia/reperfusion in rabbits☆

    PubMed Central

    Wei, Xiaodong; Wan, Xing; Zhao, Bo; Hou, Jiabao; Liu, Min; Cheng, Bangchang

    2012-01-01

    The present study established a rabbit model of global cerebral ischemia using the ‘six-vessel’ method, which was reperfused after 30 minutes of ischemia. Rabbits received intravenous injection of propofol at 5 mg/kg prior to ischemia and 20 mg/kg per hour after ischemia until samples were prepared. Results revealed that propofol inhibited serum interleukin-8, endothelin-1 and malondialdehyde increases and promoted plasma superoxide dismutase activity after cerebral ischemia/reperfusion. In addition, cerebral cortex edema was attenuated with little neuronal nuclear degeneration and pyknosis with propofol treatment. The cross-sectional area of neuronal nuclei was, however, increased following propofol treatment. These findings suggested that propofol could improve anti-oxidant activity and inhibit synthesis of inflammatory factors to exert a protective effect on cerebral ischemia/reperfusion injury. PMID:25737711

  13. Promethazine inhibits the formation of aldehydic products of lipid peroxidation but not covalent binding resulting from the exposure of rat liver fractions to CCl4.

    PubMed Central

    Poli, G; Cheeseman, K H; Biasi, F; Chiarpotto, E; Dianzani, M U; Esterbauer, H; Slater, T F

    1989-01-01

    Promethazine is known to have protective activity in relation to CCl4-induced liver necrosis. This hepatoprotective property has been investigated with regard to the free radical scavenging and antioxidant properties of promethazine using isolated hepatocytes and microsomal suspensions. CCl4 is activated in both systems to free radical metabolites that bind covalently to lipid and protein, and initiate lipid peroxidation. A large number of carbonyl products is produced during CCl4-induced lipid peroxidation; promethazine strongly inhibits the production of all classes of carbonyl compounds in both microsomal suspensions and isolated hepatocytes. In contrast, promethazine is a very weak inhibitor of the covalent binding of metabolites of CCl4. We conclude that promethazine acts by scavenging the trichloromethylperoxyl radical and lipid peroxyl radicals, and is a weak scavenger of the trichloromethyl radical. These data, when considered together with the hepatoprotective effects of promethazine, suggest that lipid peroxidation is of relatively more importance than covalent binding in the pathogenesis of CCl4-induced liver necrosis. PMID:2604730

  14. Quantitative Structure-Activity Relationships Predicting the Antioxidant Potency of 17β-Estradiol-Related Polycyclic Phenols to Inhibit Lipid Peroxidation

    PubMed Central

    Prokai, Laszlo; Rivera-Portalatin, Nilka M.; Prokai-Tatrai, Katalin

    2013-01-01

    The antioxidant potency of 17β-estradiol and related polycyclic phenols has been well established. This property is an important component of the complex events by which these types of agents are capable to protect neurons against the detrimental consequences of oxidative stress. In order to relate their molecular structure and properties with their capacity to inhibit lipid peroxidation, a marker of oxidative stress, quantitative structure-activity relationship (QSAR) studies were conducted. The inhibition of Fe3+-induced lipid peroxidation in rat brain homogenate, measured through an assay detecting thiobarbituric acid reactive substances for about seventy compounds were correlated with various molecular descriptors. We found that lipophilicity (modeled by the logarithm of the n-octanol/water partition coefficient, logP) was the property that influenced most profoundly the potency of these compounds to inhibit lipid peroxidation in the biological medium studied. Additionally, the important contribution of the bond dissociation enthalpy of the phenolic O–H group, a shape index, the solvent-accessible surface area and the energy required to remove an electron from the highest occupied molecular orbital were also confirmed. Several QSAR equations were validated as potentially useful exploratory tools for identifying or designing novel phenolic antioxidants incorporating the structural backbone of 17β-estradiol to assist therapy development against oxidative stress-associated neurodegeneration. PMID:23344051

  15. Quantitative structure-activity relationships predicting the antioxidant potency of 17β-estradiol-related polycyclic phenols to inhibit lipid peroxidation.

    PubMed

    Prokai, Laszlo; Rivera-Portalatin, Nilka M; Prokai-Tatrai, Katalin

    2013-01-11

    The antioxidant potency of 17β-estradiol and related polycyclic phenols has been well established. This property is an important component of the complex events by which these types of agents are capable to protect neurons against the detrimental consequences of oxidative stress. In order to relate their molecular structure and properties with their capacity to inhibit lipid peroxidation, a marker of oxidative stress, quantitative structure-activity relationship (QSAR) studies were conducted. The inhibition of Fe3+-induced lipid peroxidation in rat brain homogenate, measured through an assay detecting thiobarbituric acid reactive substances for about seventy compounds were correlated with various molecular descriptors. We found that lipophilicity (modeled by the logarithm of the n-octanol/water partition coefficient, logP) was the property that influenced most profoundly the potency of these compounds to inhibit lipid peroxidation in the biological medium studied. Additionally, the important contribution of the bond dissociation enthalpy of the phenolic O-H group, a shape index, the solvent-accessible surface area and the energy required to remove an electron from the highest occupied molecular orbital were also confirmed. Several QSAR equations were validated as potentially useful exploratory tools for identifying or designing novel phenolic antioxidants incorporating the structural backbone of 17β-estradiol to assist therapy development against oxidative stress-associated neurodegeneration.

  16. Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation

    PubMed Central

    Che, Xia; Wang, Xin; Zhang, Junyan; Peng, Chengfeng; Zhen, Yilan; Shao, Xu; Zhang, Gongliang; Dong, Liuyi

    2016-01-01

    Purpose: The aim of this study was to explore the cardioprotective effect of vitexin on chronic myocardial ischemia/reperfusion injury in rats and potential mechanisms. Methods: A chronic myocardial ischemia/reperfusion injury model was established by ligating left anterior descending coronary for 60 minutes, and followed by reperfusion for 14 days. After 2 weeks ischemia/reperfusion, cardiac function was measured to assess myocardial injury. The level of ST segment was recorded in different periods by electrocardiograph. The change of left ventricular function and myocardial reaction degree of fibrosis of heart was investigated by hematoxylin and eosin (HE) staining and Sirius red staining. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. The blood samples were collected to measure the levels of MDA, the activities of SOD and NADPH in serum. Epac1, Rap1, Bax and Bcl-2 were examined by using Western Blotting. Results: Vitexin exerted significant protective effect on chronic myocardial ischemia/reperfusion injury, improved obviously left ventricular diastolic function and reduced myocardial reactive fibrosis degree in rats of myocardial ischemia. Medium and high-dose vitexin groups presented a significant decrease in Bax, Epac1 and Rap1 production and increase in Bcl-2 compared to the I/R group. It may be related to preventing myocardial cells from apoptosis, improving myocardial diastolic function and inhibiting lipid peroxidation. Conclusions: Vitexin is a cardioprotective herb, which may be a promising useful complementary and alternative medicine for patients with coronary heart disease. PMID:27648122

  17. Polyphenols from Lonicera caerulea L. berry attenuate experimental nonalcoholic steatohepatitis by inhibiting proinflammatory cytokines productions and lipid peroxidation.

    PubMed

    Wu, Shusong; Yano, Satoshi; Hisanaga, Ayami; He, Xi; He, Jianhua; Sakao, Kozue; Hou, De-Xing

    2017-04-01

    Nonalcoholic steatohepatitis (NASH) is a common disease, which is closely associated with inflammation and oxidative stress, and Lonicera caerulea L. polyphenols (LCP) are reported to possess both antioxidant and anti-inflammatory properties. This study aimed to investigate the protective effects and mechanisms of LCP on NASH in a high-fat diet plus carbon tetrachloride (CCL4 ) induced mouse model. Mice were fed with high-fat diet containing LCP (0.5-1%) or not, and then administrated with CCL4 to induce NASH. Liver sections were stained by hematoxylin-eosin stain, serum transaminases and lipids were measured by clinical analyzer, insulin was examined by ELISA, cytokines were determined by multiplex technology, and hepatic proteins were detected by Western blotting. LCP improved histopathological features of NASH with lower levels of lipid peroxidation and cytokines including granulocyte colony-stimulating factor, IL-3, IL-4, macrophage inflammatory protein-1β, IL-6, IL-5, keratinocyte-derived cytokine, tumor necrosis factor-alpha, IL-2, IL-1β, monocytes chemotactic protein-1, IL-13, IFN-γ, IL-10, IL-12(p70), IL-1α, eotaxin, granulocyte-macrophage colony-stimulating factor, macrophage inflammatory protein-1α, IL-17, and RANTES. Further molecular analysis revealed that LCP increased the expression of nuclear factor (erythroid-derived 2)-like 2 and manganese-dependent superoxide dismutase, but decreased forkhead box protein O1 and heme oxygenase-1 in the liver of NASH mice. Dietary supplementation of LCP ameliorates inflammation and lipid peroxidation by upregulating nuclear factor (erythroid-derived 2)-like 2 and manganese-dependent superoxide dismutase, and downregulating forkhead box protein O1 and heme oxygenase-1 in NASH. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  18. [Nitric oxide and lipid peroxidation].

    PubMed

    Cristol, J P; Maggi, M F; Guérin, M C; Torreilles, J; Descomps, B

    1995-01-01

    Nitric oxide (NO) is a free radical produced enzymatically in biological systems from the guanidino group of L-arginine. Its large spectrum of biological effects is achieved through chemical interactions with different targets including oxygen (O2), superoxide (O2o-) and other oxygen reactive species (ROS), transition metals and thiols. Superoxide anions and other ROS have been reported to react with NO to produce peroxynitrite anions that can decompose to form nitrogen dioxide (NO2) and hydroxyl radial (OHo). Thus, NO has been reported to have a dual effect on lipid peroxidation (prooxidant via the peroxynitrite or antioxydant via the chelation of ROS). In the present study we have investigated in different models the in vitro and in vivo action of NO on lipid peroxidation. Copper-induced LDL oxidation were used as an in vitro model. Human LDL (100 micrograms ApoB/ml) were incubated in oxygene-saturated PBS buffer in presence or absence of Cu2+ (2.5 microM) with increasing concentrations of NO donnors (sodium nitroprussiate or nitroso-glutathione). LDL oxidation was monitored continuously for conjugated diene formation (234 nm) and 4-hydroxynonenal (HNE) accumulation. Exogenous NO prevents in a dose dependent manner the progress of copper-induced oxidation. Ischaemia-reperfusion injury (I/R), characterized by an overproduction of ROS, is used as an in vivo model. Anaesthetized rats were submitted to 1 hour renal ischaemia following by 2 hours of reperfusion. Sham-operated rats (SOP) were used as control. Lipid peroxidation was evaluated by measuring the HNE accumulated in rats kidneys in presence or absence of L-arginine or D-arginine infusion. L-arginine, but not D-arginine, enhances HNE accumulation in I/R but not in SOP (< 0.050 pmol/g tissue in SOP versus 0.6 nmol/g tissue in I/R), showing that, in this experimental conditions, NO produced from L-arginine, enhances the toxicity of ROS. This study shows that the pro- or antioxydant effects of NO are different

  19. Lipid peroxidation induced by indomethacin with horseradish peroxidase and hydrogen peroxide: involvement of indomethacin radicals.

    PubMed

    Miura, Toshiaki; Muraoka, Sanae; Fujimoto, Yukio

    2002-06-01

    Some of the side-effects of using indomethacin (IM) involve damage to the gastric mucosa and liver mitochondria. On the other hand, neutrophils infiltrate inflammatory sites to damage the tissues through the generation of reactive oxygen species by myeloperoxidase. The stomach and intestine have large amounts of peroxidase. These findings suggest that peroxidases are involved in tissue damage induced by IM. To clarify the basis for the tissue damage induced by IM in the presence of horseradish peroxidase (HRP) and H2O2 (HRP-H2O2), lipid peroxidation was investigated. When IM was incubated with liver microsomes in the presence of HRP-H2O2 and ADP-Fe3+, lipid peroxidation was time-dependent. Catalase and desferrioxamine almost completely inhibited lipid peroxidation, indicating that H2O2 and iron are necessary for lipid peroxidation. Of interest, superoxide dismutase strongly inhibited lipid peroxidation, and it also inhibited the formation of bathophenanthroline-Fe2+, indicating that reduction of the ferric ion was due to superoxide (O2-). ESR signals of IM radicals were detected during the interaction of IM with HRP-H2O2. However, the IM radical by itself did not reduce the ferric ion. These results suggest that O2- may be generated during the interaction of IM radicals with H2O2. Ferryl species, which are formed during the reduction of iron by O2-, probably are involved in lipid peroxidation.

  20. [Indices of oxidative stress. 2. Lipid peroxides].

    PubMed

    Lushchak, V I; Bahniukova, T V; Luzhna, L I

    2006-01-01

    Two methods of the determination of lipid peroxidation products have been compared which are based on Fe(II) oxidation by them at acid pH values in the presence of xylenol orange which binds Fe(III) have been compared. The first method uses cumene hydropeoxide as an internal standard. In the second one, lipid peroxides are previously reduced by triphenylphosphine and these substances content is measured as a difference of the production of complexes with xylenol orange and iron ions in the control (with reduction) and experimental sample (without reduction). The optimization of measurement conditions is described. The levels of lipid peroxides in goldfish tissues assayed simultaneously by two methods were similar. The method with cumene hydroperoxide needs less amounts of biological material; moreover, there is no necessity in a calibration curve. Effects of hyperoxia on lipid peroxide levels in goldfish tissues were studied with the cumene method. Within the first hours of hyperoxia this index increased 13-times in the liver and 2-times in the brain and muscle. The further exposure rebounded this parameter to the initial level. Levels of lipid peroxides positively correlated with levels of end products of lipid peroxidation (thiobarbiturate acid reactive substances) in the goldfish tissues. The method of quantification of lipid peroxides with cumene is recommended for wide using in biological investigations.

  1. Metallothionein-II Inhibits Lipid Peroxidation and Improves Functional Recovery after Transient Brain Ischemia and Reperfusion in Rats

    PubMed Central

    Diaz-Ruiz, Araceli; Vacio-Adame, Patricia; Monroy-Noyola, Antonio; Méndez-Armenta, Marisela; Ortiz-Plata, Alma; Rios, Camilo

    2014-01-01

    After transient cerebral ischemia and reperfusion (I/R), damaging mechanisms, such as excitotoxicity and oxidative stress, lead to irreversible neurological deficits. The induction of metallothionein-II (MT-II) protein is an endogenous mechanism after I/R. Our aim was to evaluate the neuroprotective effect of MT-II after I/R in rats. Male Wistar rats were transiently occluded at the middle cerebral artery for 2 h, followed by reperfusion. Rats received either MT (10 μg per rat i.p.) or vehicle after ischemia. Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; also, neurological deficit was evaluated after ischemia, using the Longa scoring scale. Infarction area was analyzed 72 hours after ischemia. Results showed increased LP in frontal cortex (30.7%) and hippocampus (26.4%), as compared to control group; this effect was fully reversed by MT treatment. Likewise, we also observed a diminished neurological deficit assessed by the Longa scale in those animals treated with MT compared to control group values. The MT-treated group showed a significant (P < 0.05) reduction of 39.9% in the infarction area, only at the level of hippocampus, as compared to control group. Results suggest that MT-II may be a novel neuroprotective treatment to prevent ischemia injury. PMID:24719677

  2. β-Estradiol-3-benzoate confers neuroprotection in Parkinson MPP(+) rat model through inhibition of lipid peroxidation.

    PubMed

    Aguirre-Vidal, Yoshajandith; Monroy-Noyola, Antonio; Anaya-Ramos, Laura; Arteaga-Silva, Marcela; Mendez-Armenta, Marisela; Ostoa-Saloma, Pedro; Díaz-Zaragoza, Mariana; Morales-Montor, Jorge; Ríos, Camilo; Montes, Sergio

    2017-10-01

    Estradiol (E2), in addition to its known hormone function, is a neuroactive steroid that has shown neuroprotective profile in several models of neurological diseases. The present study explores the antioxidant effect of β-estradiol-3-benzoate (EB) on the neurotoxicity elicited by MPP(+) in rat striatum. Male Wistar rats, that were gonadectomized 30days prior to EB, were given 100µgEB per rat every 48h for 11days and animals were infused with MPP(+) via intrastriatal at day six after beginning EB treatment. EB treatment completely prevented the fall in dopamine caused by MPP(+), such result was related with decreased lipid peroxidation, a marker of oxidative stress; diminished number of ipsilateral-to-lesion turns and increased signal of the dopamine-synthesizing enzyme Tyrosin Hydroxylase in substantia nigra. The protection elicited by EB was not related to Mn or Cu-Zn superoxide dismutase enzymatic activities or glutathione modulation since none of these parameters were influenced by EB at the times assayed. Whereas, increased expression of PON2 as a result of EB treatment was observed, this phenomenon could be one of the mechanism by which the steroid conferred protection to dopaminergic cells against MPP(+) injury. Copyright © 2017 Elsevier Inc. All rights reserved.

  3. Teprenone promotes the healing of acetic acid-induced chronic gastric ulcers in rats by inhibiting neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues.

    PubMed

    Kobayashi, T; Ohta, Y; Yoshino, J; Nakazawa, S

    2001-01-01

    Teprenone, an anti-ulcer drug, has been reported to promote the healing of acetic acid-induced chronic gastric ulcers in rats by stimulating gastric mucus synthesis and secretion. Recently, it has been implicated that neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues have an inhibitory effect on the healing of acetic acid-induced chronic gastric ulcers in rats. Therefore, we attempted to clarify whether teprenone exerts a healing-promoting effect on acetic acid-induced chronic gastric ulcers through its inhibitory effect on neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues. In rats with chronic gastric ulcers made by applying acetic acid to the stomach, gastric ulcer healing started later than 3 days after the acetic acid application. Gastric mucosal myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, and lipid peroxide content were higher in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application. Gastric mucosal non-protein SH content was lower in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application, and gastric mucosal adherent mucus content was lower in the ulcerated region than in the intact region on the 8th and 15th day. Daily oral administration of teprenone (100 mg kg(-1)x 2) for 7 or 14 days, starting on the 8th day after the application of acetic acid to the stomach, enhanced the reduction of the ulcer area with attenuation of all these biochemical changes found in the ulcerated region. The teprenone administration caused a decrease in MPO activity and an increase in adherent mucus content in the gastric mucosa of the intact region. These results suggest that the healing-promoting effect of teprenone on acetic acid-induced chronic gastric ulcers in rats could be due not only to stimulation of gastric mucus secretion but also to inhibition of neutrophil infiltration

  4. AFB1 hepatocarcinogenesis is via lipid peroxidation that inhibits DNA repair, sensitizes mutation susceptibility and induces aldehyde-DNA adducts at p53 mutational hotspot codon 249

    PubMed Central

    Hu, Yu; Mehta, Manju; Desai, Dhimant; Amin, Shantu; Zheng, Yi; Tang, Moon-Shong

    2017-01-01

    Aflatoxin B1 (AFB1) contamination in the food chain is a major cause of hepatocellular carcinoma (HCC). More than 60% of AFB1 related HCC carry p53 codon 249 mutations but the causal mechanism remains unclear. We found that 1) AFB1 induces two types of DNA adducts in human hepatocytes, AFB1-8,9-epoxide-deoxyguanosine (AFB1-E-dG) induced by AFB1-E and cyclic α-methyl-γ-hydroxy-1,N2-propano-dG (meth-OH-PdG) induced by lipid peroxidation generated acetaldehyde (Acet) and crotonaldehyde (Cro); 2) the level of meth-OH-PdG is >30 fold higher than the level of AFB1-E-dG; 3) AFB1, Acet, and Cro, but not AFB1-E, preferentially induce DNA damage at codon 249; 4) methylation at –CpG- sites enhances meth-OH-PdG formation at codon 249; and 5) repair of meth-OH-PdG at codon 249 is poor. AFB1, Acet, and Cro can also inhibit DNA repair and enhance hepatocyte mutational sensitivity. We propose that AFB1-induced lipid peroxidation generated aldehydes contribute greatly to hepatocarcinogenesis and that sequence specificity of meth-OH-PdG formation and repair shape the codon 249 mutational hotspot. PMID:28212554

  5. Evaluation of the antioxidant activity of root extract of pepper fruit (Dennetia tripetala), and it's potential for the inhibition of lipid peroxidation.

    PubMed

    Okolie, Ngozi Paulinus; Falodun, Abiodun; Davids, Oluseyi

    2014-01-01

    The antioxidant properties of ethanolic root extract of pepper fruit (Donnetia tripetala), and its effect on lipid peroxidation of some fresh beef tissues during frozen storage were investigated. The antioxidant parameters were assessed using standard methods, while malondialdehyde levels of different fresh beef tissue sections treated with the extract prior to freezing, were estimated in a colorimetric reaction with thiobarbituric acid. The H2O2-scavenging ability of the extract was similar to that of ascorbic acid, with a maximum scavenging power of 55.61 ±4.98%, and an IC50 value of 86µg/ml. The extract exhibited a concentration-dependent ferric ion-reducing power, although this was significantly lower relative to that of the ascorbic acid (p < 0.05). The total phenolic content was 212.5 ± 0.002 mg/g, while the nitric oxide-scavenging ability was 64.33 ± 0.2% after 150 min. The capacity of the extract to inhibit lipid peroxidation in frozen heart muscle slices was significantly higher than that of vitamin C (p < 0 .05), but comparable to vitamins C and E in frozen testes and kidney slices. These results suggest that the root extract of D. tripetala is rich in antioxidants which can be applied to meat preservation during refrigerated storage.

  6. Inhibition of key enzymes linked to type 2 diabetes and sodium nitroprusside induced lipid peroxidation in rats' pancreas by phenolic extracts of avocado pear leaves and fruit.

    PubMed

    Oboh, Ganiyu; Isaac, Adelusi Temitope; Akinyemi, Ayodele Jacobson; Ajani, Richard Akinlolu

    2014-09-01

    Persea americana fruit and leaves had been known in folk medicine for their anti-diabetic prowess. Therefore, this study sought to investigate the inhibitory effect of phenolic extract from avocado pear (Persea americana) leaves and fruits on some key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase); and sodium nitroprusside (SNP) induced lipid peroxidation in rats' pancreas in vitro. The phenolic extracts of Persea americana fruit and leaves were extracted using methanol and 1M HCl (1:1 v/v). Thereafter, their inhibitory effects on sodium nitroprusside induced lipid peroxidation and key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) were determined in vitro. The result revealed that the leaves had fruit of avocado pear inhibit both α-amylase and α-glucosidase activities in a dose dependent manner. However, the Peel had the highest α-amylase inhibitory activity while the leaf had the highest α-glucosidase inhibitory activity as revealed by their IC50 value. Furthermore, incubation of the rat pancreas in the presence of 5 mM SNP caused an increase in the malondialdehyde (MDA) content in the tissue, however, introduction of the phenolic extracts inhibited MDA produced in a dose dependent manner. The additive and/or synergistic action of major phenolic compounds such as syringic acid, eugenol, vnillic acid, isoeugenol, guaiacol, kaemferol, catechin, ρ-hydroxybenzoic acid, ferulic acid, apigenin, naringenin, epigallocatechin, epicatechin, lupeol and epigallocatechin-3-O-gallate in avocado pear using gas chromatography (GC) could have contributed to the observed medicinal properties of the plant. Therefore, inhibition of some key enzymes linked to type 2 diabetes and prevention of oxidative stress in the pancreas could be some of the possible mechanism by which they exert their anti-diabetic properties.

  7. Inhibition of Key Enzymes Linked to Type 2 Diabetes and Sodium Nitroprusside Induced Lipid Peroxidation in Rats’ Pancreas by Phenolic Extracts of Avocado Pear Leaves and Fruit

    PubMed Central

    Oboh, Ganiyu; Isaac, Adelusi Temitope; Akinyemi, Ayodele Jacobson; Ajani, Richard Akinlolu

    2014-01-01

    Persea americana fruit and leaves had been known in folk medicine for their anti-diabetic prowess. Therefore, this study sought to investigate the inhibitory effect of phenolic extract from avocado pear (Persea americana) leaves and fruits on some key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase); and sodium nitroprusside (SNP) induced lipid peroxidation in rats’ pancreas in vitro. The phenolic extracts of Persea americana fruit and leaves were extracted using methanol and 1M HCl (1:1 v/v). Thereafter, their inhibitory effects on sodium nitroprusside induced lipid peroxidation and key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) were determined in vitro. The result revealed that the leaves had fruit of avocado pear inhibit both α-amylase and α-glucosidase activities in a dose dependent manner. However, the Peel had the highest α-amylase inhibitory activity while the leaf had the highest α-glucosidase inhibitory activity as revealed by their IC50 value. Furthermore, incubation of the rat pancreas in the presence of 5 mM SNP caused an increase in the malondialdehyde (MDA) content in the tissue, however, introduction of the phenolic extracts inhibited MDA produced in a dose dependent manner. The additive and/or synergistic action of major phenolic compounds such as syringic acid, eugenol, vnillic acid, isoeugenol, guaiacol, kaemferol, catechin, ρ-hydroxybenzoic acid, ferulic acid, apigenin, naringenin, epigallocatechin, epicatechin, lupeol and epigallocatechin-3-O-gallate in avocado pear using gas chromatography (GC) could have contributed to the observed medicinal properties of the plant. Therefore, inhibition of some key enzymes linked to type 2 diabetes and prevention of oxidative stress in the pancreas could be some of the possible mechanism by which they exert their anti-diabetic properties PMID:25324703

  8. Lipid peroxidation in experimental uveitis: sequential studies.

    PubMed

    Goto, H; Wu, G S; Chen, F; Kristeva, M; Sevanian, A; Rao, N A

    1992-06-01

    Previously we have detected the occurrence of retinal lipid peroxidation initiated by phagocyte-derived oxygen radicals in experimental autoimmune uveitis (EAU). In the current studies, the confirmation of inflammation-mediated lipid peroxidation was proceeded further to include measurement of multiple parameters, including conjugated dienes, ketodienes, thiobarbituric acid reactive substances and fluorescent chromolipids. The assay for myeloperoxidase, a measure for the number of polymorphonuclear leukocytes in the inflammatory sites was also carried out. The levels of all these parameters were followed through the course of EAU development. The sequential evaluation of histologic changes using both light and electron microscopy was also carried out and the results were correlated with lipid peroxidation indices. These data suggest that the retinal lipid peroxidation plays a causative role in the subsequent retinal degeneration.

  9. Acetaminophen attenuates lipid peroxidation in children undergoing cardiopulmonary bypass.

    PubMed

    Simpson, Scott A; Zaccagni, Hayden; Bichell, David P; Christian, Karla G; Mettler, Bret A; Donahue, Brian S; Roberts, L Jackson; Pretorius, Mias

    2014-07-01

    Hemolysis, occurring during cardiopulmonary bypass, is associated with lipid peroxidation and postoperative acute kidney injury. Acetaminophen inhibits lipid peroxidation catalyzed by hemeproteins and in an animal model attenuated rhabdomyolysis-induced acute kidney injury. This pilot study tests the hypothesis that acetaminophen attenuates lipid peroxidation in children undergoing cardiopulmonary bypass. Single-center prospective randomized double-blinded study. University-affiliated pediatric hospital. Thirty children undergoing elective surgical correction of a congenital heart defect. Patients were randomized to acetaminophen (OFIRMEV [acetaminophen] injection; Cadence Pharmaceuticals, San Diego, CA) or placebo every 6 hours for four doses starting before the onset of cardiopulmonary bypass. Markers of hemolysis, lipid peroxidation (isofurans and F2-isoprostanes), and acute kidney injury were measured throughout the perioperative period. Cardiopulmonary bypass was associated with a significant increase in free hemoglobin (from a prebypass level of 9.8 ± 6.2 mg/dL to a peak of 201.5 ± 42.6 mg/dL postbypass). Plasma and urine isofuran and F2-isoprostane concentrations increased significantly during surgery. The magnitude of increase in plasma isofurans was greater than the magnitude in increase in plasma F2-isoprostanes. Acetaminophen attenuated the increase in plasma isofurans compared with placebo (p = 0.02 for effect of study drug). There was no significant effect of acetaminophen on plasma F2-isoprostanes or urinary makers of lipid peroxidation. Acetaminophen did not affect postoperative creatinine, urinary neutrophil gelatinase-associated lipocalin, or prevalence of acute kidney injury. Cardiopulmonary bypass in children is associated with hemolysis and lipid peroxidation. Acetaminophen attenuated the increase in plasma isofuran concentrations. Future studies are needed to establish whether other therapies that attenuate or prevent the effects of free

  10. Acetaminophen Attenuates Lipid Peroxidation in Children Undergoing Cardiopulmonary Bypass

    PubMed Central

    Simpson, Scott A.; Zaccagni, Hayden; Bichell, David P.; Christian, Karla G.; Mettler, Bret A.; Donahue, Brian S.; Roberts, L. Jackson; Pretorius, Mias

    2014-01-01

    Objective Hemolysis, occurring during cardiopulmonary bypass (CPB), is associated with lipid peroxidation and postoperative acute kidney injury (AKI). Acetaminophen (ApAP) inhibits lipid peroxidation catalyzed by hemeproteins and in an animal model attenuated rhabdomyolysis-induced AKI. This pilot study tests the hypothesis that ApAP attenuates lipid peroxidation in children undergoing CPB. Design Single center prospective randomized double blinded study. Setting University-affiliated pediatric hospital. Patients Thirty children undergoing elective surgical correction of a congenital heart defect. Interventions Patients were randomized to ApAP (OFIRMEV® (acetaminophen) injection, Cadence Pharmaceuticals, San Diego, CA) or placebo every 6 hours for 4 doses starting before the onset of CPB. Measurement and Main Results Markers of hemolysis, lipid peroxidation (isofurans and F2-isoprostanes) and AKI were measured throughout the perioperative period. CPB was associated with a significant increase in free hemoglobin (from a pre-bypass level of 9.8±6.2 mg/dl to a peak of 201.5±42.6 mg/dl post-bypass). Plasma and urine isofuran and F2-isoprostane concentrations increased significantly during surgery. The magnitude of increase in plasma isofurans was greater than the magnitude in increase in plasma F2-isoprostanes. ApAP attenuated the increase in plasma isofurans compared to placebo (P=0.02 for effect of study drug). There was no significant effect of ApAP on plasma F2-isoprostanes or urinary makers of lipid peroxidation. ApAP did not affect postoperative creatinine, urinary neutrophil gelatinase-associated lipocalin or prevalence of AKI. Conclusion CPB in children is associated with hemolysis and lipid peroxidation. ApAP attenuated the increase in plasma isofuran concentrations. Future studies are needed to establish whether other therapies that attenuate or prevent the effects of free hemoglobin result in more effective inhibition of lipid peroxidation in patients

  11. A Trypsin Inhibitor from Tecoma stans Leaves Inhibits Growth and Promotes ATP Depletion and Lipid Peroxidation in Candida albicans and Candida krusei

    PubMed Central

    Patriota, Leydianne L. S.; Procópio, Thamara F.; de Souza, Maria F. D.; de Oliveira, Ana Patrícia S.; Carvalho, Lidiane V. N.; Pitta, Maira G. R.; Rego, Moacyr J. B. M.; Paiva, Patrícia M. G.; Pontual, Emmanuel V.; Napoleão, Thiago H.

    2016-01-01

    Tecoma stans (yellow elder) has shown medicinal properties and antimicrobial activity. Previous reports on antifungal activity of T. stans preparations and presence of trypsin inhibitor activity from T. stans leaves stimulated the investigation reported here. In this work, we proceeded to the purification and characterization of a trypsin inhibitor (TesTI), which was investigated for anti-Candida activity. Finally, in order to determine the potential of TesTI as a new natural chemotherapeutic product, its cytotoxicity to human peripheral blood mononuclear cells (PBMCs) was evaluated. TesTI was isolated from saline extract by ammonium sulfate fractionation followed by ion exchange and gel filtration chromatographies. Antifungal activity was evaluated by determining the minimal inhibitory (MIC) and fungicide (MFC) concentrations using fungal cultures containing only yeast form or both yeast and hyphal forms. Candida cells treated with TesTI were evaluated for intracellular ATP levels and lipid peroxidation. Cytotoxicity of TesTI to PBMCs was evaluated by MTT assay. TesTI (39.8 kDa, pI 3.41, Ki 43 nM) inhibited similarly the growth of both C. albicans and C. krusei culture types at MIC of 100 μg/mL. The MFCs were 200 μg/mL for C. albicans and C. krusei. Time-response curves revealed that TesTI (at MIC) was more effective at inhibiting the replication of C. albicans cells. At MIC, TesTI promoted reduction of ATP levels and lipid peroxidation in the Candida cells, being not cytotoxic to PBMCs. In conclusion, TesTI is an antifungal agent against C. albicans and C. krusei, without toxicity to human cells. PMID:27199940

  12. 4-Hydroxynonenal, a lipid peroxidation byproduct of spinal cord injury, is cytotoxic for oligodendrocyte progenitors and inhibits their responsiveness to PDGF.

    PubMed

    Gard, A L; Solodushko, V G; Waeg, G; Majic, T

    2001-03-15

    Oligodendroglial reactions to compression injury of spinal cord include apoptosis, secondary demyelination, and remyelination failure. Within hours after contusion, the membrane lipid peroxidation (MLP) byproduct, 4-hydroxynonenal (HNE), increases rapidly in gray matter and thereafter in white matter tracts beyond the initial lesion level. Considering that HNE is a mediator and marker of neuronal MLP toxicity in various neurodegenerative conditions, the present study examined its effect on the regeneration potential of oligodendrocyte progenitors, as defined by their capacity to survive, proliferate and migrate in primary culture. Treatment of oligodendroblasts with HNE evoked a time- and dose-dependent cytotoxicity resembling apoptosis at aldehyde concentrations known to be produced by neurons and achieved in tissue undergoing peroxidative injury. In addition, sublethal concentrations of HNE inhibited the mitogenic and chemotactic responses of more immature progenitors to platelet-derived growth factor. These effects appear to be mediated in part by the formation of HNE adducts with progenitor proteins located within the plasma membrane and cytoplasmic compartments. Our data are the first to show that HNE can have direct, deleterious effects on oligodendrocyte precursors. The present study also suggests a mechanism by which the striking accumulation of HNE in white matter tracts surrounding the site of spinal cord compression injury and in other ischemic-hypoxic insults associated with MLP could suppress the potential regenerative response of endogenous oligodendrocyte progenitor cells.

  13. Lipid Peroxidation and Its Toxicological Implications

    PubMed Central

    Nam, Tae-gyu

    2011-01-01

    Lipid peroxidation is a free radical oxidation of polyunsaturated fatty acids such as linoleic acid or arachidonic acid. This process has been related with various pathologies and disease status mainly because of the oxidation products formed during the process. The oxidation products include reactive aldehydes such as malondialdehyde and 4-hydroxynonenal. These reactive aldehydes can form adducts with DNAs and proteins, leading to the alterations in their functions to cause various diseases. This review will provide a short summary on the implication of lipid peroxidation on cancer, atherosclerosis, and neurodegeneration as well as chemical and biochemical mechanisms by which these adducts affect the pathological conditions. In addition, select examples will be presented where antioxidants were used to counteract oxidative damage caused by lipid peroxidation. At the end, isoprostanes are discussed as a gold standard for the assessment of oxidative damages. PMID:24278542

  14. Lipid peroxidation and its toxicological implications.

    PubMed

    Nam, Tae-Gyu

    2011-03-01

    Lipid peroxidation is a free radical oxidation of polyunsaturated fatty acids such as linoleic acid or arachidonic acid. This process has been related with various pathologies and disease status mainly because of the oxidation products formed during the process. The oxidation products include reactive aldehydes such as malondialdehyde and 4-hydroxynonenal. These reactive aldehydes can form adducts with DNAs and proteins, leading to the alterations in their functions to cause various diseases. This review will provide a short summary on the implication of lipid peroxidation on cancer, atherosclerosis, and neurodegeneration as well as chemical and biochemical mechanisms by which these adducts affect the pathological conditions. In addition, select examples will be presented where antioxidants were used to counteract oxidative damage caused by lipid peroxidation. At the end, isoprostanes are discussed as a gold standard for the assessment of oxidative damages.

  15. Ferroptosis: Death by Lipid Peroxidation.

    PubMed

    Yang, Wan Seok; Stockwell, Brent R

    2016-03-01

    Ferroptosis is a regulated form of cell death driven by loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4) and subsequent accumulation of lipid-based reactive oxygen species (ROS), particularly lipid hydroperoxides. This form of iron-dependent cell death is genetically, biochemically, and morphologically distinct from other cell death modalities, including apoptosis, unregulated necrosis, and necroptosis. Ferroptosis is regulated by specific pathways and is involved in diverse biological contexts. Here we summarize the discovery of ferroptosis, the mechanism of ferroptosis regulation, and its increasingly appreciated relevance to both normal and pathological physiology.

  16. [Effects of manganese, zircon and lithium alone on rat liver lipid peroxidation].

    PubMed

    Li, S; Long, S

    2001-05-01

    Lipid peroxide (LPO) in rat liver was detected by malondiadehyde (MDA) colorimetry. The effect of manganese, zircon and lithium alone on lipid peroxidation in rat liver was also studied. The results showed that manganese and zircon at the doses of (9.862-1.972) x 10(-4) and (0.1972-9.862) x 10(-5) nmol/L respectively decreased LPO in rat liver(P < 0.01). Lithium inhibited lipid peroxidation at the dose of (19.72-1.972) x 10(-4) nmol/L, and induced lipid peroxidation at higher concentration.

  17. Involvement of striatal lipid peroxidation and inhibition of calcium influx into brain slices in neurobehavioral alterations in a rat model of short-term oral exposure to manganese.

    PubMed

    Avila, Daiana Silva; Gubert, Priscila; Fachinetto, Roselei; Wagner, Caroline; Aschner, Michael; Rocha, João Batista Teixeira; Soares, Félix Alexandre Antunes

    2008-11-01

    Manganese is an essential element for biological systems, nevertheless occupational exposure to high levels of Mn can lead to neurodegenerative disorder, characterized by excessive Mn accumulation, especially in astrocytes of basal ganglia and symptoms closely resembling idiopathic Parkinson's disease (PD). The purpose of this study was to evaluate behavioral and biochemical alterations in adult rats exposed for 30 days to 10 and 25mg/mL of MnCl(2) in their drinking water. MnCl(2) intoxicated rats showed impaired locomotor activity in comparison to control animals. Furthermore, lipid peroxidation were increased, delta-aminolevulinate dehydratase (delta-ALA-D, an enzyme sensitive to pro-oxidant situations) activity was inhibited and (45)Ca(2+) influx into striatal slices was decreased in rats exposed to 25mg/mL of Mn, indicating that this brain region was markedly affected by short-term Mn exposure. In contrast, Mn exposure was not associated with characteristic extrapyramidal effects and did not modify protein oxidation, suggesting that the striatal damage represents early stages of Mn-induced damage. In addition, treatment with Mn was associated with reduced body weight gain, but there were no discernible alterations in liver and kidney function. In conclusion, Mn caused increased oxidative stress and decreased (45)Ca(2+) influx into the striatum, which are likely linked to impaired locomotor activity, but not with the occurrence of orofacial dyskinesia.

  18. Acetaminophen and aspirin inhibit superoxide anion generation and lipid peroxidation, and protect against 1-methyl-4-phenyl pyridinium-induced dopaminergic neurotoxicity in rats.

    PubMed

    Maharaj, D S; Saravanan, K S; Maharaj, H; Mohanakumar, K P; Daya, S

    2004-04-01

    We assessed the antioxidant activity of non-narcotic analgesics, acetaminophen and aspirin in rat brain homogenates and neuroprotective effects in vivo in rats intranigrally treated with 1-methyl-4-phenyl pyridinium (MPP+). Both drugs inhibited cyanide-induced superoxide anion generation, as well as lipid peroxidation in rat brain homogenates, the combination of the agents resulting in a potentiation of this effect. Acetaminophen or aspirin when administered alone or in combination, did not alter dopamine (DA) levels in the forebrain or in the striatum. Intranigral infusion of MPP+ in rats caused severe depletion of striatal DA levels in the ipsilateral striatum in rats by the third day. Systemic post-treatment of acetaminophen afforded partial protection, whereas similar treatment of aspirin resulted in complete blockade of MPP+-induced striatal DA depletion. While these findings suggest usefulness of non-narcotic analgesics in neuroprotective therapy in neurodegenerative diseases, aspirin appears to be a potential candidate in prophylactic as well as in adjuvant therapy in Parkinson's disease.

  19. Peroxide-induced cell death and lipid peroxidation in C6 glioma cells.

    PubMed

    Linden, Arne; Gülden, Michael; Martin, Hans-Jörg; Maser, Edmund; Seibert, Hasso

    2008-08-01

    Peroxides are often used as models to induce oxidative damage in cells in vitro. The aim of the present study was to elucidate the role of lipid peroxidation in peroxide-induced cell death. To this end (i) the ability to induce lipid peroxidation in C6 rat astroglioma cells of hydrogen peroxide (H2O2), cumene hydroperoxide (CHP) and t-butyl hydroperoxide (t-BuOOH) (ii) the relation between peroxide-induced lipid peroxidation and cell death in terms of time and concentration dependency and (iii) the capability of the lipid peroxidation chain breaking alpha-tocopherol to prevent peroxide-induced lipid peroxidation and/or cell death were investigated. Lipid peroxidation was characterised by measuring thiobarbituric acid reactive substances (TBARS) and, by HPLC, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE) and hexanal. Within 2 h CHP, t-BuOOH and H2O2 induced cell death with EC50 values of 59+/-9 microM, 290+/-30 microM and 12+/-1.1 mM, respectively. CHP and t-BuOOH, but not H2O2 induced lipid peroxidation in C6 cells with EC50 values of 15+/-14 microM and 130+/-33 microM, respectively. The TBARS measured almost exclusively consisted of MDA. 4-HNE was mostly not detectable. The concentration of hexanal slightly increased with increasing concentrations of organic peroxides. Regarding time and concentration dependency lipid peroxidation preceded cell death. Pretreatment with alpha-tocopherol (10 microM, 24 h) prevented both, peroxide-induced lipid peroxidation and cell death. The results strongly indicate a major role of lipid peroxidation in the killing of C6 cells by organic peroxides but also that lipid peroxidation is not involved in H2O2 induced cell death.

  20. Oxygen concentration dependence of lipid peroxidation and lipid-derived radical generation: application of profluorescent nitroxide switch.

    PubMed

    Mito, Fumiya; Kitagawa, Kana; Yamasaki, Toshihide; Shirahama, Chisato; Oishi, Taketoshi; Ito, Yuko; Yamato, Mayumi; Yamada, Ken-Ichi

    2011-09-01

    Lipid-derived radicals and peroxides are involved in the pathogenesis of oxidative stress diseases and, although lipid peroxide production is a required reaction between a lipid radical and molecular oxygen, a useful lipid radical detection method has remained tentative. Also, the effect of oxygen concentration on lipid peroxide production must be considered because of the hypoxic conditions in cancer and ischemic regions. In this study, the focus was on nitroxide reactivity, which allows spin trapping with carbon-centred radicals via radical-radical reactions and fluorophore quenching through interactions with nitroxide's unpaired electron. Thus, the aim here was to demonstrate a useful detection method for lipid-derived radicals as well as to clarify the effects of oxygen concentration on lipid peroxide production using profluorescent nitroxide. This latter compound reacted with lipid-derived radicals in a manner inversely dependent on oxygen concentration, resulting in fluorescence due to alkoxyamine formation and, conversely, lipid peroxide concentrations decreased with lower oxygen in the reaction system. Furthermore, nitroxide inhibited lipid peroxide production and stopped oxygen consumption in the same solution. These results suggested that the novel application of profluorescent nitroxide could directly and sensitively detect lipid-derived radicals and that radical and peroxide production were dependent on oxygen concentration.

  1. Membrane lipid peroxidation by UV-A: Mechanism and implications

    SciTech Connect

    Bose, B.; Agarwal, S.; Chatterjee, S.N. )

    1990-10-01

    UV-A produced a dose-dependent linear increase of lipid peroxidation in liposomal membrane, as detected by the assay of (i) conjugated dienes, (ii) lipid hydroperoxides, (iii) malondialdehydes (MDA), and (iv) the fluorescent adducts formed by the reaction of MDA with glycine and also a linear dose-dependent increase of ({sup 14}C)glucose efflux from the liposomes. UV-A-induced MDA production could not be inhibited by any significant degree by sodium formate, dimethyl sulfoxide, EDTA, or superoxide dismutase but was very significantly inhibited by butylated hydroxytoluene, alpha-tocopherol, sodium azide, L-histidine, dimethylfuran, and beta-carotene. MDA formation increased with an increase in the D{sub 2}O content in water, leading to a maximal amount of nearly 50% enhancement of lipid peroxidation in 100% D{sub 2}O vis-a-vis water used as dispersion medium. The experimental findings indicate the involvement of singlet oxygen as the initiator of the UV-A-induced lipid peroxidation.

  2. Down-regulation of Notch1 expression is involved in HL-60 cell growth inhibition induced by 4-hydroxynonenal, a product of lipid peroxidation.

    PubMed

    Pizzimenti, Stefania; Barrera, Giuseppina; Calzavara, Elisabetta; Mirandola, Leonardo; Toaldo, Cristina; Dianzani, Mario Umberto; Comi, Paola; Chiaramonte, Raffaella

    2008-11-01

    The role of the Notch1 pathway has been well assessed in leukemia. Notch1 mutations are the most common ones in T acute lymphoblastic leukaemia patients which carry either oncogenic Notch1 forms or ineffective ubiquitin ligase implicated in Notch1 turnover. Abnormalities in the Notch1-Jagged1 system have been reported also in acute myelogenous leukaemia (AML) patients where Jagged1 is frequently over-expressed. Moreover, activating Notch1 mutations, as well, can occur in human AML and in leukemia cases with lineage infidelity. As a result, Notch1 signalling inhibition is an attractive goal in leukaemia therapy. Blockage/delay in cell differentiation and/or increase of proliferation are the main results of Notch1 signalling activation in several leukemic cell lines. Moreover, specific genes involved in cell growth control have been identified as Notch1 transcriptional targets, i.e. Cyclin D1 and c-Myc. 4-Hydroxynonenal (HNE), an aldehyde produced during lipid peroxidation, is involved in several pathological and physiological conditions, including inflammation; atherosclerosis; and neurodegenerative and chronic liver diseases. Moreover HNE has an antiproliferative/ differentiative effect in several cell lines, by affecting the expression of key genes, such as oncogenes (e.g. c-Myc, c-Myb), cyclins and telomerase. This prompted us to study the effect of HNE on Notch1 expression and its related signalling in HL-60 cells, a leukemic cell line widely used for differentiation studies. RT-PCR as well as Western blot assay showed Notch1down-regulation in HNE-treated HL-60 cells. The expression of Hes1, a Notch1 target gene, was concomitantly down-regulated by HNE treatment, reflecting Notch1 signalling inhibition. DAPT, an inhibitor of Notch activity, when added contemporary to HNE, further increased cell growth inhibition, without affecting apoptosis. Moreover, DAPT treatment reversed the HNE-induced differentiation. Overall these results suggest that Notch1 is a target

  3. Inhibition of iron/ascorbate-induced lipid peroxidation by an N-terminal peptide of bovine lactoferrin and its acylated derivatives.

    PubMed

    Wakabayashi, H; Matsumoto, H; Hashimoto, K; Teraguchi, S; Takase, M; Hayasawa, H

    1999-05-01

    Bovine lactoferrin (LF) and lactoferricin B (LFcin B), an antimicrobial peptide derived from bovine LF, inhibited thiobarbituric acid-reactive substance (TBARS) formation in a iron/ascorbate-induced liposomal phospholipid peroxidation system. The inhibition of TBARS formation occurred with N-acylated 9-mer peptides with a core sequence of LFcin B and, compared to LFcin B, their antioxidant effect was clearly observed at a concentration almost 100 times lower.

  4. Lipid peroxidation of rabbit small intestinal microvillus membrane vesicles by iron complexes.

    PubMed

    Fodor, I; Marx, J J

    1988-07-01

    Fe(II)- and Fe(III)-induced lipid peroxidation of rabbit small intestinal microvillus membrane vesicles was studied. Ferrous ammonium sulphate, ferrous ascorbate at a molar ratio of 10:1, and ferric citrate, at molar ratios of 1:1 and 1:20, did not stimulate lipid peroxidation. Ferrous ascorbate, 1:1, induced low stimulation, while ferrous ascorbate, 1:20 gave higher stimulation of lipid peroxidation. These results show that in our experimental system, ascorbate is a promotor rather than an inhibitor of lipid peroxidation. Ferric nitrilotriacetate (at molar ratios of 1:2 and 1:10), at an iron concentration of 200 microM, was by far the most effective in inducing lipid peroxidation. Superoxide dismutase, mannitol and glutathione had no effect, while catalase, thiourea and vitamin E markedly decreased ferrous ascorbate 1:20-induced lipid peroxidation. Ferric nitrilotriacetate-induced lipid peroxidation was slightly reduced by catalase and mannitol, significantly reduced by superoxide dismutase, and completely inhibited by thiourea. Glutathione caused a 100% increase in the ferric nitrilotriacetate-induced lipid peroxidation. These results suggest that Fe(II) in the presence of trace amounts of Fe(III), or an oxidizing agent and Fe(III) in the presence of Fe(II) or a reducing agent, are potent stimulators of lipid peroxidation of microvillus membrane vesicles. Addition of deferoxamine completely inhibited both ferrous ascorbate, 1:20 and ferric nitrilotriacetate-induced lipid peroxidation, demonstrating the requirement for iron for its stimulation. Iron-induced peroxidation of microvillus membrane may have physiological significance because it could already be demonstrated at 2 microM iron concentration.

  5. Chronic intermittent hypoxia-induced neuronal apoptosis in the hippocampus is attenuated by telmisartan through suppression of iNOS/NO and inhibition of lipid peroxidation and inflammatory responses.

    PubMed

    Yuan, Xiao; Guo, Xueling; Deng, Yan; Zhu, Die; Shang, Jin; Liu, Huiguo

    2015-01-30

    Obstructive sleep apnea syndrome (OSAS) plays a critical role in the initiation and progression of Alzheimer׳s disease (AD), but little is known about the precise mechanism of OSAS-induced AD. Nitric oxide synthase (NOS) and nitric oxide (NO) are known to play key roles in the development of AD. Several studies have confirmed that an angiotensin II type 1 receptor blocker, telmisartan, beneficially regulates NOS and NO. Here, we examined the neuroprotective effects of telmisartan against hippocampal apoptosis induced by chronic intermittent hypoxia (CIH), the most characteristic pathophysiological change of OSAS. Adult male Sprague Dawley rats were subjected to 8h of intermittent hypoxia per day with or without telmisartan for eight weeks. Neuronal apoptosis in the hippocampal CA1 region, NOS activity, NO content, and the presence of inflammatory agents and radical oxygen species in the hippocampus were determined. The results showed that CIH activated inducible nitric oxide synthase (iNOS), increased NO content, and enhanced lipid peroxidation and inflammatory responses in the hippocampus. Treatment with telmisartan inhibited excessive iNOS and NO generation and reduced lipid peroxidation and inflammatory responses. In addition, telmisartan significantly ameliorated the hippocampal apoptosis induced by CIH. In conclusion, Pre-CIH telmisartan administration attenuated CIH-induced hippocampal apoptosis partly by regulating NOS activity, inhibiting excessive NO generation, and reducing lipid peroxidation and inflammatory responses. Copyright © 2014 Elsevier B.V. All rights reserved.

  6. Inhibition of key enzymes linked to type 2 diabetes and sodium nitroprusside-induced lipid peroxidation in rat pancreas by water-extractable phytochemicals from unripe pawpaw fruit (Carica papaya).

    PubMed

    Oboh, Ganiyu; Olabiyi, Ayodeji A; Akinyemi, Ayodele J; Ademiluyi, Adedayo O

    2014-02-01

    Various parts of unripe pawpaw (Carica papaya Linn) fruit have been reportedly used for the management or treatment of diabetes mellitus in folklore medicine. Therefore, the present study sought to investigate the inhibitory effects of the aqueous extract of different parts of unripe pawpaw fruit on key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) and sodium nitroprusside (SNP)-induced lipid peroxidation in rat pancreas in vitro. The aqueous extracts of the unripe pawpaw (C. papaya) fruit parts were prepared (1:20 w/v) and the ability of the extracts to inhibit α-amylase, α-glucosidase and SNP-induced lipid peroxidation in rat pancreas in vitro was investigated. The results revealed that all the extracts inhibited α-amylase (IC50=0.87-1.11 mg/mL), α-glucosidase (IC50=1.76-2.64 mg/mL) and SNP-induced lipid peroxidation (IC50=1.99-2.42 mg/mL) in a dose-dependent manner. However, combination of the flesh, seed and peel in equal amounts had the highest inhibitory effect on α-amylase and α-glucosidase activities. Strong inhibitory activities of the unripe pawpaw fruit against key enzymes linked to type 2 diabetes and SNP-induced lipid peroxidation in rat pancreas could be part of the mechanism by which unripe pawpaw is used in the management/prevention of diabetes mellitus in folk medicine. However, combining the unripe pawpaw fruit parts in equal amounts exhibited synergistic properties on α-amylase and α-glucosidase inhibitory activities.

  7. The lipid peroxidation in breast cancer patients.

    PubMed

    Kedzierska, Magdalena; Olas, Beata; Wachowicz, Barbara; Jeziorski, Arkadiusz; Piekarski, Janusz

    2010-06-01

    The aim of our study was to estimate oxidative stress (by using different biomarkers of lipid peroxidation--isoprostanes and thiobarbituric acid reactive substances (TBARS)) in patients with invasive breast cancer, patients with benign breast diseases and in a control group. We observed a statistically increased level of TBARS in plasma and isoprostanes in urine of patients with invasive breast cancer in comparison with a control group. The concentration of tested biomarkers in plasma or urine from patients with invasive breast cancer was also higher than in patients with benign breast diseases. Moreover, the levels of tested markers in patients with benign breast diseases and in a control group did not differ. Considering the data presented in this study, we suggest that free radicals induce peroxidation of unsaturated fatty acid in patients with breast cancer.

  8. [Lipid peroxidation processes in chronic bronchitis].

    PubMed

    Ignatova, G L; Volchegorskiĭ, I A; Volkova, E G; Kazachkov, E L; Kolesnikov, O L

    1998-01-01

    Comparison of the levels of lipid peroxidation (LPO) products in condensate of the exhaled air (CEA) and in the biopsy samples from the inflammation focus. Extraction spectrophotometry was used to measure LPO products in CEA and biopsies from 30 males aged 30-60 years suffering from chronic bronchitis and 30 healthy controls of the same age. There was activation of local accumulation of isopropanol-soluble LPO products in the bronchopulmonary system accompanied by lowered content of lipoperoxides and high antioxidant activity in CEA. Chronic bronchitis is characterized by multidirectional shifts in LPO in the inflammation focus and CEA.

  9. Differential anti-lipid peroxidative activity of melatonin

    NASA Astrophysics Data System (ADS)

    Kawanishi, Shinya; Sakurai, Hiromu

    2002-01-01

    Scavenging activities of melatonin, which is a pineal secretory product and functions in circadian biology, and its related compounds against reactive oxygen species such as superoxide anion radical, hydrogen peroxide, hydroxyl radical and singlet oxygen as well as organic peroxide radical (t-BuOO•) were evaluated chemically by using electron spin resonance-spin trap and chemiluminescence methods. Antioxidative activity of the compounds was estimated by IC50 value (µM), 50% inhibiting concentration of a compound against reactive oxygen species formed in each system, and the second-order rate constants ( k 2) for the reactions of the compounds and superoxide anion radical or hydroxyl radical. Because melatonin has exhibited the highest scavenging activity against t-BuOO•, the biochemical anti-lipid peroxide radical scavenging activities of melatonin were examined. We found that melatonin exhibits higher anti-lipid peroxidative activity in the rat brain microsomes than in the rat liver microsomal and liposomal systems, suggesting that melatonin may function as a treatment for reactive oxygen species-related diseases of the brain.

  10. Aqueous extracts of two varieties of ginger (Zingiber officinale) inhibit angiotensin I-converting enzyme, iron(II), and sodium nitroprusside-induced lipid peroxidation in the rat heart in vitro.

    PubMed

    Akinyemi, Ayodele J; Ademiluyi, Adedayo O; Oboh, Ganiyu

    2013-07-01

    Ginger has reportedly been used in folk medicine for the management and prevention of hypertension and other cardiovascular diseases. Therefore, this study sought to investigate the inhibitory effect of aqueous extracts of two varieties of ginger on a key enzyme linked to hypertension (angiotensin I-converting enzyme [ACE]), and on pro-oxidants [Fe(2+) and sodium nitroprusside (SNP)] which have been shown to induce lipid peroxidation in the rat's isolated heart in vitro. Aqueous extracts (0.05 mg/mL) of red ginger (Zingiber officinale var. Rubra) and white ginger (Zingiber officinale Roscoe) were prepared and the ability of the extracts to inhibit ACE along with Fe(2+)- and SNP-induced lipid peroxidation was determined in rat's heart in vitro. Results revealed that both extracts inhibited ACE in a dose-dependent manner (25-125 μg/mL). However, red ginger extract (EC50=27.5 μg/mL) had a significantly (P<.05) higher inhibitory effect on ACE than white ginger extract (EC50=87.0 μg/mL). Furthermore, incubation of the rat's heart in the presence of Fe(2+) and SNP caused a significant increase (P<.05) in the malondialdehyde (MDA) content of the heart homogenates, while the introduction of the ginger extracts (78-313 μg/mL) caused a dose-dependent decrease in the MDA content of the stressed heart homogenates. This suggests that the possible mechanism through which ginger exerts its antihypertensive properties may be through inhibition of ACE activity and prevention of lipid peroxidation in the heart. Furthermore, red ginger showed stronger inhibition of ACE than white ginger. Additionally, it should be noted that these protective properties of the ginger varieties could be attributed to their polyphenol contents.

  11. Lipid peroxidation, calcium, iron, and TCDD toxicity in rats

    SciTech Connect

    Al-Bayati, Z.A.F.

    1986-01-01

    2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been studied as a prototype of halogenated aromatic hydrocarbons. Previous studies have shown that TCDD enhances hepatic lipid peroxidation. This study on TCDD administration to rats was conducted to: measure induction of lipid peroxidation in hepatic and extrahepatic tissues; compare lipid peroxidation between sexes; determine the contributions of H/sub 2/O/sub 2/ and other reactive oxygen species and associated enzymes on hepatic lipid peroxidation: determine the role of iron in TCDD-induced lipid peroxidation; and investigate the relationship between TCDD-induced alterations in lipid peroxidation, calcium homeostasis, reduced glutathione content (GSH) and selenium-dependent glutathione peroxidase activity (GSH-Px). The results demonstrated that TCDD induces changes in microsomal lipid peroxidation in hepatic and extrahepatic tissues. The rates of microsomal lipid peroxidation in male rats were less than in microsomes from female rats. TCDD treatment produced a significant increase in lipid peroxidation which preceded an increase in whole homogenate and mitochondrial calcium content, but paralleled an increase in microsomal calcium content. TCDD treatment produced dose and time dependent decreases in hepatic GSH content and GSH-Px activity in female rats. H/sub 2/O/sub 2/ and possibly hydroxyl radical and singlet oxygen are involved in TCDD-induced hepatic microsomal lipid peroxidation. The results support the hypothesis that the toxicity of TCDD and its lack of tissue selectivity in male and female rats may be due in part to lipid peroxidation. Lipid peroxidation may alter membrane permeability to calcium and lead to sequestration of calcium.

  12. Silica radical-induced DNA damage and lipid peroxidation.

    PubMed Central

    Shi, X; Mao, Y; Daniel, L N; Saffiotti, U; Dalal, N S; Vallyathan, V

    1994-01-01

    In recent years, more attention has been given to the mechanism of disease induction caused by the surface properties of minerals. In this respect, specific research needs to be focused on the biologic interactions of oxygen radicals generated by mineral particles resulting in cell injury and DNA damage leading to fibrogenesis and carcinogenesis. In this investigation, we used electron spin resonance (ESR) and spin trapping to study oxygen radical generation from aqueous suspensions of freshly fractured crystalline silica. Hydroxyl radical (.OH), superoxide radical (O2.-) and singlet oxygen (1O2) were all detected. Superoxide dismutase (SOD) partially inhibited .OH yield, whereas catalase abolished .OH generation. H2O2 enhanced .OH generation while deferoxamine inhibited it, indicating that .OH is generated via a Haber-Weiss type reaction. These spin trapping measurements provide the first evidence that aqueous suspensions of silica particles generate O2.- and 1O2. Oxygen consumption measurements indicate that freshly fractured silica uses molecular oxygen to generate O2.- and 1O2. Electrophoretic assays of in vitro DNA strand breakages showed that freshly fractured silica induced DNA strand breakage, which was inhibited by catalase and enhanced by H2O2. In an argon atmosphere, DNA damage was suppressed, showing that molecular oxygen is required for the silica-induced DNA damage. Incubation of freshly fractured silica with linoleic acid generated linoleic acid-derived free radicals and caused dose-dependent lipid peroxidation as measured by ESR spin trapping and malondialdehyde formation. SOD, catalase, and sodium benzoate inhibited lipid peroxidation by 49, 52, and 75%, respectively, again showing the role of oxygen radicals in silica-induced lipid peroxidation.(ABSTRACT TRUNCATED AT 250 WORDS) Images Figure 7. PMID:7705289

  13. Lipid peroxidation in rats chronically fed ethanol.

    PubMed Central

    Teare, J P; Greenfield, S M; Watson, D; Punchard, N A; Miller, N; Rice-Evans, C A; Thompson, R P

    1994-01-01

    Chronic alcohol consumption induces cytochrome P450IIE1, enabling habitual abusers to consume far greater quantities of alcohol than normal subjects. This pathway of metabolism leads to the production of free radical species, which cause tissue damage through peroxidation of cell membranes. Groups of Wistar rats of equal male: female ratio (n = 24) were fed alcohol by gavage twice daily to achieve a dosage of 15 g/kg body weight. Mean peak blood alcohol concentrations of 186 mg% were produced in males and 156 mg% in females. The animals were allowed free access to standard laboratory chow and water. Control animals were pair-fed to the alcoholic group and fed isocaloric glucose by gavage. Groups of animals were killed between 9 and 11 am on consecutive mornings, after nocturnal feeding, since it has previously been shown that fasting rapidly depletes hepatic glutathione concentrations. Hepatic glutathione was measured by a spectrophotometric enzymatic recycling procedure. As a marker of lipid peroxidation hepatic malonaldehyde (MDA) was measured by high performance liquid chromatography. Hepatic MDA was increased in the alcoholic group (p < 0.001), as was total hepatic glutathione (p < 0.0001). Plasma concentrations of alpha-tocopherol were increased in the alcoholic group, but ascorbic acid and superoxide dismutase values were not affected. No sex differences were detected. The increased MDA production in the alcohol group is strong evidence that lipid peroxidation is a mechanism of alcoholic tissue damage. The rise in hepatic glutathione may be an adaptive response to free radical production that protects the rat against tissue damage. PMID:7828990

  14. Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

    PubMed

    Ayala, Antonio; Muñoz, Mario F; Argüelles, Sandro

    2014-01-01

    Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970-1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010-2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

  15. Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

    PubMed Central

    Muñoz, Mario F.; Argüelles, Sandro

    2014-01-01

    Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown. PMID:24999379

  16. Lipoprotein-specific transport of circulating lipid peroxides.

    PubMed

    Ahotupa, Markku; Suomela, Jukka-Pekka; Vuorimaa, Timo; Vasankari, Tommi

    2010-10-01

    Serum lipoproteins, the carriers of cholesterol and other lipophilic substances in blood, are known to contain variable amounts of lipid peroxides. We investigated the transport of food-derived and endogenously formed lipid peroxides by serum lipoproteins under physiological conditions. Five independent trials were conducted in which different groups of healthy volunteers either consumed a test meal (a standard hamburger meal rich in lipid peroxides) or underwent strenuous physical exercise. The transport function was characterized by analyzing the kinetics of lipid peroxides in lipoprotein fractions. For evaluation of their potential involvement, indicators of oxidative stress (8-isoprostanes, malondialdehyde, 8-oxo-deoxyguanosine), antioxidant functions (total antioxidant potential, paraoxonase activity), and serum lipids were also analyzed. We found that food lipid peroxides are incorporated into serum triglyceride-rich lipoproteins and low-density lipoprotein, directing the flow of lipid peroxides towards peripheral tissues. High-density lipoprotein appears to have an opposite and protective function, and is able to respond to oxidative stress by substantially increasing the reverse transport of lipid peroxides. We propose that the specific atherosclerosis-related effects of serum lipoproteins are not explained by cholesterol transport alone and may rather result from the transport of the more directly atherogenic lipid peroxides.

  17. The involvement of superoxide and iron ions in the NADPH-dependent lipid peroxidation in human placental mitochondria.

    PubMed

    Klimek, J

    1988-01-19

    Incubation of human term placental mitochondria with Fe2+ and a NADPH-generating system initiated high levels of lipid peroxidation, as measured by the production of malondialdehyde. Malondialdehyde formation was accompanied by a corresponding decrease of the unsaturated fatty acid content. This NADPH-dependent lipid peroxidation was strongly inhibited by superoxide dismutase and singlet oxygen scavengers, markedly stimulated by paraquat, but was not affected by hydroxyl radical scavengers. Catalase enhanced the production of malondialdehyde by placental mitochondria. The effects of catalase and hydroxyl radical scavengers suggest that the initiation of NADPH-dependent lipid peroxidation is not dependent upon the hydroxyl radical produced via an iron-catalyzed Fenton reaction. These studies provide evidence that hydrogen peroxide strongly inhibits NADPH-dependent mitochondrial lipid peroxidation. The inhibitory effect of superoxide dismutase and stimulatory effect of paraquat, which was abolished by the addition of superoxide dismutase, suggests that superoxide may promote NADPH-dependent lipid peroxidation in human placental mitochondria.

  18. Promotion of iron-induced rat liver microsomal lipid peroxidation by copper.

    PubMed

    Beckman, J K; Borowitz, S M; Greene, H L; Burr, I M

    1988-06-01

    Although copper has been demonstrated to promote lipid peroxidation in a number of systems, the mechanisms involved have not been fully defined. In this study, the role of copper in modifying lipid peroxidation has been explored in rat hepatic microsomes. In an in vitro system containing reduced glutathione (GSH, 200 microM) and Tris buffer, pH 7.4, cupric sulfate (1-50 microM) potentiated lipid peroxidation induced by ferrous sulfate (10 microM) but was unable to elicit peroxidation in the absence of iron. Higher levels of cupric sulfate (100 microM or greater) were inhibitory. The nature as well as the extent of the peroxidative response of microsomes to cupric sulfate were dependent on glutathione levels in addition to those of iron. Cupric sulfate (100 microM) strongly potentiated ferrous ion-induced lipid peroxidation in the presence of 400-800 microM GSH, while it inhibited peroxidation at lower levels of GSH (0-200 microM) and did not affect ferrous ion-induced peroxidation with glutathione levels of 3-10 mM. The potentiating effect of copper on ferrous ion-induced lipid peroxidation was further explored by investigating: (1) potential GSH-mediated reduction of cupric ions; (2) potential copper/GSH-mediated reduction of ferric ions (formed by oxidation during incubation); and (3) possible promotion of propagation reactions by copper/GSH. Our results indicate that cupric ions are reduced by GSH and thus are converted from an inhibitor to an enhancer of iron-induced lipid peroxidation. Cuprous ions appear to potentiate lipid peroxidation by reduction of ferric ions, rather than by promoting propagation reactions. Iron (in a specific Fe+2/Fe+3 ratio) is then an effective promoter of initiation reactions.

  19. Modulation of radiation induced lipid peroxidation by phospholipase A 2 and calmodulin antagonists: Relevance to detoxification

    NASA Astrophysics Data System (ADS)

    Varshney, Rajeev; Kale, R. K.

    1995-04-01

    Ghost membranes prepared from erythrocytes of Swiss albino mice were irradiated with 0.9 Gy s -1. Lipid peroxidation initiated by ionizing radiation was enhanced by phospholipase A 2, and required both phospholipase A 2 and GSH-peroxidase for consecutive action to convert fatty acid peroxides into corresponding alcohols. The ability of phospholipase A 2 to enhance lipid peroxidation was increased in presence of Ca 2+. However, in combination, phospholipase A 2 and GSH-peroxidase were effective in inhibiting lipid peroxidation. These findings show that free fatty acid peroxides considerably increase the peroxidation. Calmodulin antagonists inhibit lipid peroxidation and decrease the radiation induced release of Ca 2+ from the membranes. Our results suggest the importance of Ca 2+ dependent phospholipase A 2 in detoxification of fatty acid peroxides in the membranes. It is quite possible that scavenging of free radicals by calmodulin antagonists lower the formation of hydroperoxides, resulting in the decrease in activity of phospholipase A 2. Alternatively, decrease in Ca 2+ release due to the calmodulin antagonists might have affected the activity of phospholipase A 2. Our observations might be of considerable significance in the understanding of post irradiation effect on biological membranes.

  20. In vitro inhibition activity of polyphenol-rich extracts from Syzygium aromaticum (L.) Merr. & Perry (Clove) buds against carbohydrate hydrolyzing enzymes linked to type 2 diabetes and Fe2+-induced lipid peroxidation in rat pancreas

    PubMed Central

    Adefegha, Stephen Adeniyi; Oboh, Ganiyu

    2012-01-01

    Objective To investigate and compare the inhibitory properties of free and bound phenolic extracts of clove bud against carbohydrate hydrolyzing enzymes (alpha-amylase & alpha-glucosidase) and Fe2+-induced lipid peroxidation in rat pancreas in vitro. Methods The free phenolics were extracted with 80% (v/v) acetone, while bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate. Then, the interaction of the extracts with alpha-amylase and alpha-glucosidase was subsequently assessed. Thereafter, the total phenolic contents and antioxidant activities of the extracts were determined. Results The result revealed that both extracts inhibited alpha-amylase and alpha-glucosidase in a dose-dependent manner. However, the alpha-glucosidase inhibitory activity of the extracts were significantly (P<0.05) higher than their alpha-amylase inhibitory activity. The free phenolics (31.67 mg/g) and flavonoid (17.28 mg/g) contents were significantly (P<0.05) higher than bound phenolic (23.52 mg/g) and flavonoid (13.70 mg/g) contents. Both extracts also exhibited high antioxidant activities as typified by their high reducing power, 1,1 diphenyl-2- picrylhydrazyl (DPPH) and 2, 2-azinobis-3-ethylbenzo-thiazoline-6-sulfonate (ABTS) radical scavenging abilities, as well as inhibition of Fe2+-induced lipid peroxidation in rat pancreas in vitro. Conclusions This study provides a biochemical rationale by which clove elicits therapeutic effect on type 2 diabetes. PMID:23569846

  1. In vitro inhibition activity of polyphenol-rich extracts from Syzygium aromaticum (L.) Merr. & Perry (Clove) buds against carbohydrate hydrolyzing enzymes linked to type 2 diabetes and Fe(2+)-induced lipid peroxidation in rat pancreas.

    PubMed

    Adefegha, Stephen Adeniyi; Oboh, Ganiyu

    2012-10-01

    To investigate and compare the inhibitory properties of free and bound phenolic extracts of clove bud against carbohydrate hydrolyzing enzymes (alpha-amylase & alpha-glucosidase) and Fe(2+)-induced lipid peroxidation in rat pancreas in vitro. The free phenolics were extracted with 80% (v/v) acetone, while bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate. Then, the interaction of the extracts with alpha-amylase and alpha-glucosidase was subsequently assessed. Thereafter, the total phenolic contents and antioxidant activities of the extracts were determined. The result revealed that both extracts inhibited alpha-amylase and alpha-glucosidase in a dose-dependent manner. However, the alpha-glucosidase inhibitory activity of the extracts were significantly (P<0.05) higher than their alpha-amylase inhibitory activity. The free phenolics (31.67 mg/g) and flavonoid (17.28 mg/g) contents were significantly (P<0.05) higher than bound phenolic (23.52 mg/g) and flavonoid (13.70 mg/g) contents. Both extracts also exhibited high antioxidant activities as typified by their high reducing power, 1,1 diphenyl-2- picrylhydrazyl (DPPH) and 2, 2-azinobis-3-ethylbenzo-thiazoline-6-sulfonate (ABTS) radical scavenging abilities, as well as inhibition of Fe(2+)-induced lipid peroxidation in rat pancreas in vitro. This study provides a biochemical rationale by which clove elicits therapeutic effect on type 2 diabetes.

  2. Acid phosphatase and lipid peroxidation in human cataractous lens epithelium.

    PubMed

    Vasavada, A R; Thampi, P; Yadav, S; Rawal, U M

    1993-12-01

    The anterior lens epithelial cells undergo a variety of degenerative and proliferative changes during cataract formation. Acid phosphatase is primarily responsible for tissue regeneration and tissue repair. The lipid hydroperoxides that are obtained by lipid peroxidation of polysaturated or unsaturated fatty acids bring about deterioration of biological membranes at cellular and tissue levels. Acid phosphatase and lipid peroxidation activities were studied on the lens epithelial cells of nuclear cataract, posterior subcapsular cataract, mature cataract, and mixed cataract. Of these, mature cataractous lens epithelium showed maximum activity for acid phosphatase (516.83 moles of p-nitrophenol released/g lens epithelium) and maximum levels of lipid peroxidation (86.29 O.D./min/g lens epithelium). In contrast, mixed cataractous lens epithelium showed minimum activity of acid phosphatase (222.61 moles of p-nitrophenol released/g lens epithelium) and minimum levels of lipid peroxidation (54.23 O.D./min/g lens epithelium). From our study, we correlated the maximum activity of acid phosphatase in mature cataractous lens epithelium with the increased areas of superimposed cells associated with the formation of mature cataract. Likewise, the maximum levels of lipid peroxidation in mature cataractous lens epithelium was correlated with increased permeability of the plasma membrane. Conversely, the minimum levels of lipid peroxidation in mixed cataractous lens epithelium makes us presume that factors other than lipid peroxidation may also account for the formation of mixed type of cataract.

  3. NADPH- and linoleic acid hydroperoxide-induced lipid peroxidation and destruction of cytochrome P-450 in hepatic microsomes.

    PubMed

    Iba, M M; Mannering, G J

    1987-05-01

    Temporal aspects of the effects of inhibitors on hepatic cytochrome P-450 destruction and lipid peroxidation induced by NADPH and linoleic acid hydroperoxide (LAHP) were compared. In the absence of added Fe2+, NADPH-induced lipid peroxidation in hepatic microsomes exhibited a slow phase followed by a fast phase. The addition of Fe2+ eliminated the slow phase, thus demonstrating that iron is a rate-limiting component in the reaction. EDTA, which complexes iron, and p-chloromercurobenzoate (pCMB), which inhibits NADPH-cytochrome P-450 reductase, inhibited both phases of the reaction. Catalase as well as scavengers of hydroxyl radical, inhibited NADPH-induced lipid peroxidation almost completely. GSH also inhibited the NADPH-dependent reaction but only when added at the beginning of the reaction. In contrast with NADPH-dependent lipid peroxidation, the autocatalytic reaction induced by LAHP was not biphasic, NADPH-dependent or iron-dependent, nor was it inhibited by hydroxyl radical scavengers, catalase or GSH. A synergistic effect on lipid peroxidation was observed when both NADPH and LAHP were added to microsomes. It is concluded that both the fast and slow phases of NADPH-dependent microsomal lipid peroxidation are catalyzed enzymatically and are dependent upon Fe2+, whereas LAHP-dependent lipid peroxidation is autocatalytic. Since the fast phase of enzymatic lipid peroxidation occurred during the fast phase of destruction of cytochrome P-450, it is postulated that iron made available from cytochrome P-450 is sufficient to promote optimal lipid peroxidation. Since catalase and hydroxyl radical scavengers inhibited NADPH-dependent but not LAHP-dependent lipid peroxidation, it is concluded that the hydroxyl radical derived from H2O2 is the initiating active-oxygen species in the enzymatic reaction but not in the autocatalytic reaction.

  4. Lipid peroxidation induced by maternal cadmium exposure in mouse pups

    SciTech Connect

    Baohui Xu |; Yapin Jin; Zhaoliang Feng; Zhaofa Xu; Matsushita, Toshio

    1993-11-01

    Cadmium as an environmental pollutant has received considerable attention and its toxic effects have been studied extensively in human and adult animals. Moreover, an International Task Group on Metal Accumulation (1973) has established that although it is in a limited quantity cadmium can be transported across placenta and excreted through milk in animals. Likewise, it can pass through placenta in humans. Furthermore, the fact is that women in the cadmium-polluted areas are continuously exposed to cadmium during gestation and lactation. Even if they are removed from the exposure, the body burden of cadmium probably remains high because of the very long biological half-time of cadmium which is estimated to be between 17.6 and 33 years. Thus, it is possible that fetuses and pups may be exposed to cadmium during maternal gestation and lactation. Although placenta affords some protection from cadmium exposure, cadmium exposure prior to day 10-11 when placenta forms may be deleterious. Cadmium exposure during pregnancy and its effects on offsprings, which were mainly focused on litter size, pup survival, pup growth and cadmium contents in pups following maternal cadmium exposure have been reported. Lipid peroxide has been considered as a sensitive toxicological index for environmental pollutants. The inhibited antioxidant enzymes and enhanced lipid peroxidation due to cadmium exposure have been demonstrated both in humans and animals. Therefore, the present study was designed to evaluate the toxic effects of maternal cadmium exposure on mouse pups using both the indices used in the previous studies and determinations of lipid peroxide concentrations in various pup organs. In conclusion, data from the present study indicate that the detection of LPO concentration in selected pup tissues is a sensitive index for evaluating the effects of maternal cadmium exposure on mouse pups. 16 refs., 4 tabs.

  5. Inhibition of lipid peroxidation and enhancement of GST activity by cardamom and cinnamon during chemically induced colon carcinogenesis in Swiss albino mice.

    PubMed

    Bhattacharjee, Shamee; Rana, Tapasi; Sengupta, Archana

    2007-01-01

    Globally, colorectal cancer is the third commonest cancer in men since 1975.The present study focuses on the preventive strategies aimed at reducing the incidences and mortality of large bowel cancer. Chemoprevention of colon cancer appears to be a very realistic possibility because various intermediate stages have been identified preceding the development of malignant colonic tumors. Several studies have demonstrated that generous consumption of vegetables reduces the risk of colon cancer. This idea has prompted the present investigation to search for some novel plant products, which may have possible anticarcinogenic activity. It has already been proved from various experiments that chemopreventive agents, by virtue of their anti-oxidant, anti-inflammatory, anti-proliferative, apoptosis-inducing activity, act at various levels including molecular, cellular, tissue and organ levels to interfere with carcinogens. Previous studies from our laboratory have already reported the inhibitory effect of cinnamon and cardamom on azoxymethane induced colon carcinogenesis by virtue of their anti-inflammatory, anti-proliferative and pro-apoptotic activity. This particular experiment was carried out to assess the anti-oxidative potential of these spices. Aqueous suspensions of cinnamon and cardamom have been shown to enhance the level of detoxifying enzyme (GST activity) with simultaneous decrease in lipid peroxidation levels in the treatment groups when compared to that of the carcinogen control group.

  6. Synthetically prepared Aamadori-glycated phosphatidylethanolaminecan trigger lipid peroxidation via free radical reactions.

    PubMed

    Oak, J; Nakagawa, K; Miyazawa, T

    2000-09-08

    This study for the first time confirmed the peroxidative role of the Amadori product derived from the glycation of phosphatidylethanolamine (PE), namely Amadori-PE. The product was synthesized from the reaction of dioleoyl PE with D-glucose, and then purified by a solid-phase extraction procedure, which was a key step in the next HPLC technique for the isolation of essentially pure Amadori-PE. When the synthetically prepared Amadori-PE was incubated with linoleic acid in the presence of Fe(3+) in micellar system, a remarkable formation of thiobarbituric acid reactive substances was observed together with increases in lipid hydroperoxides. In addition, the lipid peroxidation caused by Amadori-PE was effectively inhibited by superoxide dismutase, mannitol, catalase and metal chelator. These results indicated that Amadori-PE triggers oxidative modification of lipids via the generation of superoxide, and implied the involvement of 'lipid glycation' along with membrane lipid peroxidation in the pathogenesis of diabetes and aging.

  7. Hydrogen peroxide inhibition of bicupin oxalate oxidase

    PubMed Central

    Goodwin, John M.; Rana, Hassan; Ndungu, Joan; Chakrabarti, Gaurab

    2017-01-01

    Oxalate oxidase is a manganese containing enzyme that catalyzes the oxidation of oxalate to carbon dioxide in a reaction that is coupled with the reduction of oxygen to hydrogen peroxide. Oxalate oxidase from Ceriporiopsis subvermispora (CsOxOx) is the first fungal and bicupin enzyme identified that catalyzes this reaction. Potential applications of oxalate oxidase for use in pancreatic cancer treatment, to prevent scaling in paper pulping, and in biofuel cells have highlighted the need to understand the extent of the hydrogen peroxide inhibition of the CsOxOx catalyzed oxidation of oxalate. We apply a membrane inlet mass spectrometry (MIMS) assay to directly measure initial rates of carbon dioxide formation and oxygen consumption in the presence and absence of hydrogen peroxide. This work demonstrates that hydrogen peroxide is both a reversible noncompetitive inhibitor of the CsOxOx catalyzed oxidation of oxalate and an irreversible inactivator. The build-up of the turnover-generated hydrogen peroxide product leads to the inactivation of the enzyme. The introduction of catalase to reaction mixtures protects the enzyme from inactivation allowing reactions to proceed to completion. Circular dichroism spectra indicate that no changes in global protein structure take place in the presence of hydrogen peroxide. Additionally, we show that the CsOxOx catalyzed reaction with the three carbon substrate mesoxalate consumes oxygen which is in contrast to previous proposals that it catalyzed a non-oxidative decarboxylation with this substrate. PMID:28486485

  8. Hydrogen peroxide inhibition of bicupin oxalate oxidase.

    PubMed

    Goodwin, John M; Rana, Hassan; Ndungu, Joan; Chakrabarti, Gaurab; Moomaw, Ellen W

    2017-01-01

    Oxalate oxidase is a manganese containing enzyme that catalyzes the oxidation of oxalate to carbon dioxide in a reaction that is coupled with the reduction of oxygen to hydrogen peroxide. Oxalate oxidase from Ceriporiopsis subvermispora (CsOxOx) is the first fungal and bicupin enzyme identified that catalyzes this reaction. Potential applications of oxalate oxidase for use in pancreatic cancer treatment, to prevent scaling in paper pulping, and in biofuel cells have highlighted the need to understand the extent of the hydrogen peroxide inhibition of the CsOxOx catalyzed oxidation of oxalate. We apply a membrane inlet mass spectrometry (MIMS) assay to directly measure initial rates of carbon dioxide formation and oxygen consumption in the presence and absence of hydrogen peroxide. This work demonstrates that hydrogen peroxide is both a reversible noncompetitive inhibitor of the CsOxOx catalyzed oxidation of oxalate and an irreversible inactivator. The build-up of the turnover-generated hydrogen peroxide product leads to the inactivation of the enzyme. The introduction of catalase to reaction mixtures protects the enzyme from inactivation allowing reactions to proceed to completion. Circular dichroism spectra indicate that no changes in global protein structure take place in the presence of hydrogen peroxide. Additionally, we show that the CsOxOx catalyzed reaction with the three carbon substrate mesoxalate consumes oxygen which is in contrast to previous proposals that it catalyzed a non-oxidative decarboxylation with this substrate.

  9. Lipid peroxidation-DNA damage by malondialdehyde.

    PubMed

    Marnett, L J

    1999-03-08

    Malondialdehyde is a naturally occurring product of lipid peroxidation and prostaglandin biosynthesis that is mutagenic and carcinogenic. It reacts with DNA to form adducts to deoxyguanosine and deoxyadenosine. The major adduct to DNA is a pyrimidopurinone called M1G. Site-specific mutagenesis experiments indicate that M1G is mutagenic in bacteria and is repaired by the nucleotide excision repair pathway. M1G has been detected in liver, white blood cells, pancreas, and breast from healthy human beings at levels ranging from 1-120 per 108 nucleotides. Several different assays for M1G have been described that are based on mass spectrometry, 32P-postlabeling, or immunochemical techniques. Each technique offers advantages and disadvantages based on a combination of sensitivity and specificity. Application of each of these techniques to the analysis of M1G is reviewed and future needs for improvements are identified. M1G appears to be a major endogenous DNA adduct in human beings that may contribute significantly to cancer linked to lifestyle and dietary factors. High throughput methods for its detection and quantitation will be extremely useful for screening large populations. Copyright 1999 Elsevier Science B.V.

  10. Interaction of aldehydes derived from lipid peroxidation and membrane proteins

    PubMed Central

    Pizzimenti, Stefania; Ciamporcero, Eric; Daga, Martina; Pettazzoni, Piergiorgio; Arcaro, Alessia; Cetrangolo, Gianpaolo; Minelli, Rosalba; Dianzani, Chiara; Lepore, Alessio; Gentile, Fabrizio; Barrera, Giuseppina

    2013-01-01

    A great variety of compounds are formed during lipid peroxidation of polyunsaturated fatty acids of membrane phospholipids. Among them, bioactive aldehydes, such as 4-hydroxyalkenals, malondialdehyde (MDA) and acrolein, have received particular attention since they have been considered as toxic messengers that can propagate and amplify oxidative injury. In the 4-hydroxyalkenal class, 4-hydroxy-2-nonenal (HNE) is the most intensively studied aldehyde, in relation not only to its toxic function, but also to its physiological role. Indeed, HNE can be found at low concentrations in human tissues and plasma and participates in the control of biological processes, such as signal transduction, cell proliferation, and differentiation. Moreover, at low doses, HNE exerts an anti-cancer effect, by inhibiting cell proliferation, angiogenesis, cell adhesion and by inducing differentiation and/or apoptosis in various tumor cell lines. It is very likely that a substantial fraction of the effects observed in cellular responses, induced by HNE and related aldehydes, be mediated by their interaction with proteins, resulting in the formation of covalent adducts or in the modulation of their expression and/or activity. In this review we focus on membrane proteins affected by lipid peroxidation-derived aldehydes, under physiological and pathological conditions. PMID:24027536

  11. Effects of Ferulago angulata Extract on Serum Lipids and Lipid Peroxidation

    PubMed Central

    Rafieian-kopaei, Mahmoud; Shahinfard, Najmeh; Rouhi-Boroujeni, Hojjat; Gharipour, Mojgan; Darvishzadeh-Boroujeni, Pariya

    2014-01-01

    Background. Nowadays, herbs they are considered to be the main source of effective drugs for lowering serum lipids and lipid peroxidation. The present experimental animal study aimed to assess the impact of Ferulago angulata on serum lipid profiles, and on levels of lipid peroxidation. Methods. Fifty male Wistar rats, weighing 250–300 g, were randomly divided into five equal groups (ten rats in each). The rat groups received different diets as follows: Group I: fat-rich diet; Group II: fat-rich diet plus hydroalcoholic extracts of Ferulago angulata at a dose of 400 mg/kg; Group III: fat-rich diet plus hydroalcoholic extracts of Ferulago angulata at a dose of 600 mg/kg; Group IV: fat-rich diet plus atorvastatin; Group V: common stock diet. The levels of serum glucose and lipids and the atherogenic index were measured. In addition, malondialdehyde (MDA), thiol oxidation, carbonyl concentrations, C-reactive proteins, and antioxidant capacity were evaluated in each group of rats. Results. Interestingly, by adding a hydroalcoholic extract of Ferulago angulata to the high-fat diet, the levels of total cholesterol and low-density lipoproteins (LDL) in the high-fat diet rats were both significantly reduced. This result was considerably greater compared to when atorvastatin was added as an antilipid drug. The beneficial effects of the Ferulago angulata extract on lowering the level of triglycerides was observed only when a high dosage of this plant extraction was added to a high fat diet. Furthermore, the level of malondialdehyde, was significantly affected by the use of the plant extract in a high-fat diet, compared with a normal regimen or high-fat diet alone. Conclusion. Administration of a hydroalcoholic extract of Ferulago angulata can reduce serum levels of total cholesterol, triglycerides, and LDL. It can also inhibit lipid peroxidation. PMID:24707310

  12. Lipid peroxidation and haemoglobin degradation in red blood cells exposed to t-butyl hydroperoxide. The relative roles of haem- and glutathione-dependent decomposition of t-butyl hydroperoxide and membrane lipid hydroperoxides in lipid peroxidation and haemolysis.

    PubMed

    Trotta, R J; Sullivan, S G; Stern, A

    1983-06-15

    Red cells exposed to t-butyl hydroperoxide undergo lipid peroxidation, haemoglobin degradation and hexose monophosphate-shunt stimulation. By using the lipid-soluble antioxidant 2,6-di-t-butyl-p-cresol, the relative contributions of t-butyl hydroperoxide and membrane lipid hydroperoxides to oxidative haemoglobin changes and hexose monophosphate-shunt stimulation were determined. About 90% of the haemoglobin changes and all of the hexose monophosphate-shunt stimulation were caused by t-butyl hydroperoxide. The remainder of the haemoglobin changes appeared to be due to reactions between haemoglobin and lipid hydroperoxides generated during membrane peroxidation. After exposure of red cells to t-butyl hydroperoxide, no lipid hydroperoxides were detected iodimetrically, whether or not glucose was present in the incubation. Concentrations of 2,6-di-t-butyl-p-cresol, which almost totally suppressed lipid peroxidation, significantly inhibited haemoglobin binding to the membrane but had no significant effect on hexose monophosphate shunt stimulation, suggesting that lipid hydroperoxides had been decomposed by a reaction with haem or haem-protein and not enzymically via glutathione peroxidase. The mechanisms of lipid peroxidation and haemoglobin oxidation and the protective role of glucose were also investigated. In time-course studies of red cells containing oxyhaemoglobin, methaemoglobin or carbonmono-oxyhaemoglobin incubated without glucose and exposed to t-butyl hydroperoxide, haemoglobin oxidation paralleled both lipid peroxidation and t-butyl hydroperoxide consumption. Lipid peroxidation ceased when all t-butyl hydroperoxide was consumed, indicating that it was not autocatalytic and was driven by initiation events followed by rapid propagation and termination of chain reactions and rapid non-enzymic decomposition of lipid hydroperoxides. Carbonmono-oxyhaemoglobin and oxyhaemoglobin were good promoters of peroxidation, whereas methaemoglobin relatively spared the

  13. Involvement of lipid peroxidation and organic peroxides in UVA-induced matrix metalloproteinase-1 expression.

    PubMed

    Polte, Tobias; Tyrrell, Rex M

    2004-06-15

    Ultraviolet A (UVA) irradiation causes human skin aging and skin cancer at least partially through the activation of matrix metalloproteinases (MMPs). MMP-1, the interstitial collagenase, is responsible for the degradation of collagen and is involved in tumor progression in human skin. The present study uses human skin fibroblast cells (FEK4) to investigate the involvement of lipid peroxidation and the role of peroxides as possible mediators in MMP-1 activation by UVA. Preincubation with the antioxidants butylated hydroxytoluene and Trolox reduced UVA-dependent MMP-1 upregulation, suggesting that peroxidation of membrane lipids is involved. Blocking the iron-driven generation of lipid peroxides and hydroxyl radicals by different iron chelators led to a decrease in UVA-induced MMP-1 mRNA accumulation. Moreover, modulation of glutathione peroxidase activity by use of the specific inhibitor mercaptosuccinate (MS) or by the depletion of glutathione (using buthionine-S, R-sulfoximine, BSO), enhanced the UVA-dependent MMP-1 response. Finally, UVA irradiation generated a significant increase in intracellular peroxide levels which is augmented by pretreatment of the cells with BSO or MS. Our results demonstrate that lipid peroxidation and the production of peroxides are important events in the signalling pathway of MMP-1 activation by UVA.

  14. Induction of lipid peroxidation by hexachlorocyclohexane, dieldrin, TCDD, carbon tetrachloride, and hexachlorobenzene in rats

    SciTech Connect

    Goel, M.R.; Shara, M.A.; Stohs, S.J.

    1988-02-01

    Hexachlorobenzene (HCB), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), hexachlorocyclohexane (HCCH) and dieldrin are all halogenated lipophilic environmental contaminants. A common biologic property of these compounds is their ability to induce hepatic microsomal drug metabolizing enzymes. Furthermore, exposure of laboratory animals to these xenobiotics elicits a number of similar effects including porphyria, hypothyroidism, a wasting syndrome and lethality. Perturbation of membrane lipids and lipid peroxidation may be responsible for at least part of the toxic effects of HCCH. TCDD has been shown to induce lipid peroxidation in hepatic and extrahepatic tissues. Based on the similar toxic manifestations of HCB, HCCH, TCDD and dieldrin, the authors have examined the effects of these xenobiotics on hepatic lipid peroxidation following an acutely toxic dose. Lipid peroxidation was assessed by determining the content of thiobarbituric acid reactive substance (TBARS) in the liver, employing malondialdehyde as the standard. Animals were also treated with carbon tetrachloride, a well know inducer of lipid peroxidation, as a positive control. Furthermore, the ability of these xenobiotics to inhibit selenium dependent glutathione peroxidase (GSHPX) activity was determined.

  15. In vitro curcumin modulates ferric nitrilotriacetate (Fe-NTA) and hydrogen peroxide (H2O2)-induced peroxidation of microsomal membrane lipids and DNA damage.

    PubMed

    Iqbal, Mohammad; Okazaki, Yasumasa; Okada, Shigeru

    2003-01-01

    A number of investigations have implicated the involvement of free radicals in various pathogenic process including initiation/promotion stages of carcinogenesis and antioxidants have been considered to be a protective agent for this reason. An iron chelate, ferric nitrilotriacetate (Fe-NTA), is a potent nephrotoxic agent and induces acute and subacute renal proximal tubular necrosis by catalyzing the decomposition of hydrogen peroxide-derived production of hydroxyl radicals, which are known to cause lipid peroxidation and DNA damage. The latter is associated with a high incidence of renal adenocarcinoma in rodents. Lipid peroxidation and DNA damage are the principal manifestation of Fe-NTA-induced toxicity, which could be mitigated by antioxidants. In this study, we therefore investigated the effect of curcumin, a polyphenolic compound from Curcuma longa for a possible protection against lipid peroxidation and DNA damage induced by Fe-NTA and hydrogen peroxide in vitro. Incubation of renal microsomal membrane/and or calf thymus DNA with hydrogen peroxide (40 mM) in the presence of Fe-NTA (0.1 mM) induces renal microsomal lipid peroxidation and DNA damage to about 2.2-and 5.6-fold, respectively, as compared to saline treated control (P<0.001). Induction of renal microsomal lipid peroxidation and DNA damage was modulated by curcumin dose dependently. In lipid peroxidation protection studies, curcumin treatment showed a dose-dependent strong inhibition (18-80% inhibition, P<0.05-0.001) of Fe-NTA and hydrogen peroxide-induced lipid peroxidation as measured by MDA formation in renal microsomes. Similarly, in DNA-sugar damage protection studies, curcumin treatment also showed a dose dependent inhibition (22-57% inhibition, P<0.05-0.001) of DNA-sugar damage. From these studies, it was concluded that curcumin modulates Fe-NTA and hydrogen peroxide-induced peroxidation of microsomal membrane lipids and DNA damage. Curcumin might, therefore, be a suitable candidate for the

  16. The protective effect of Aloysia triphylla aqueous extracts against brain lipid-peroxidation.

    PubMed

    Lasagni Vitar, Romina M; Reides, Claudia G; Ferreira, Sandra M; Llesuy, Susana F

    2014-03-01

    In a normal diet, the use of herbs may contribute significantly to the total intake of plant antioxidants and even be a better source of dietary antioxidants than many other food groups. Therefore, the aims of this study were to evaluate the protective effect of aqueous extracts of Aloysia triphylla (infusion and decoction) against lipid-peroxidation of brain homogenates and to determine changes in the prooxidant/antioxidant balance when the plant material is added. In order to elucidate a possible antioxidant mechanism in vitro evaluation of total antioxidant capacity, oxygen species scavenging ability and reducing power (RP) were studied. Tested extracts had shown a strong inhibition of lipid-peroxidation measured as thiobarbituric acid-reactive products of lipid-peroxidation (TBARS) and chemiluminescence. Furthermore, infusion and decoction exhibited free radical trapping ability, expressed by the capacity to scavenge superoxide and hydrogen peroxide. Additionally, both aqueous extracts presented antioxidant activity measured as total reactive antioxidant potential (TRAP), 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and 2,2'-azino-bis(3-ethylbenzthiazoline)-6-sulfonic acid radical (ABTS) scavenging activity and RP. These results suggest that the lipid-peroxidation inhibition mechanism proposed is that the antioxidants present in Aloysia triphylla could act as strong scavengers of reactive oxygen species not only at the initiation of the lipid-peroxidation chain reaction, but also at the propagation step. Therefore, they could be used as prophylactic and therapeutic agents for those diseases where the occurrence of oxidative stress and lipid-peroxidation contributes to the progression of damage.

  17. Methods to create thermally oxidized lipids and comparison of analytical procedures to characterize peroxidation

    USDA-ARS?s Scientific Manuscript database

    The objective of this experiment was to evaluate peroxidation in 4 lipids, each with 3 degrees of peroxidation. Lipid sources were: corn oil (CN), canola oil (CA), poultry fat, and tallow. Peroxidation levels were: original lipids (OL), slow-oxidized lipids (SO), and rapid-oxidized lipids (RO). To p...

  18. A possible mechanism for initiation of lipid peroxidation by ascorbate in rat liver microsomes.

    PubMed

    Casalino, E; Sblano, C; Landriscina, C

    1996-02-01

    The mechanism by which lipid peroxidation progresses has been known for years, but there is disagreement regarding the mode of its initiation. The aim of this study was to examine: (a) the role of endogenous iron in the initiation of ascorbate-induced lipid peroxidation in microsomal and liposomal membranes; (b) the role of oxygen-free radicals in this process; and (c) the redox state of ascorbate during the course of lipid peroxidation. Ascorbate-induced lipid peroxidation was assessed by measuring hydroperoxide and thiobarbituric acid reactive substances (TBARS) formation in membranes after incubation in Tris-HCl buffer (pH 7.4) for 15 min. To confirm the role of endogenous iron and oxygen-free radicals, the effect of iron chelating agents (EDTA and thiourea) and radical scavengers (benzoate, mannitol, catalase and SOD) on lipid peroxidation was examined. Spectrophotometric measurements and ESR spectra have made it possible to determine ascorbate concentration and its redox state. Ascorbate promoted lipid peroxidation in both rat liver microsomes and liposomes without addition of exogenous iron. Iron chelating agents such as EDTA and thiourea inhibited lipid peroxidation, while SOD, catalase, mannitol and benzoate had no effect. The addition of 5 microM Fe2+ (or Fe3+) to the incubation mixture did not significantly alter hydroperoxide production, but that of TBARS was increased. Lipid peroxidation significantly altered the fatty acid profile in microsomes and liposomes, the most affected being the C20:4 and C22:6 species. Ascorbate in Tris-HCl buffer (pH 7.4) autoxidized very slowly. Its oxidation was catalyzed by Fe3+ ions at a rate determined by incubation time and iron concentration. In contrast, no ascorbate oxidation occurred in the presence of microsomes when lipid peroxidation was proceeding at a maximal rate. Under these conditions a typical ascorbyl radical ESR spectrum signal greater than that arising from ascorbate alone was obtained and the magnitude

  19. Essential Oil from Clove Bud (Eugenia aromatica Kuntze) Inhibit Key Enzymes Relevant to the Management of Type-2 Diabetes and Some Pro-oxidant Induced Lipid Peroxidation in Rats Pancreas in vitro.

    PubMed

    Oboh, Ganiyu; Akinbola, Ifeoluwa A; Ademosun, Ayokunle O; Sanni, David M; Odubanjo, Oluwatoyin V; Olasehinde, Tosin A; Oyeleye, Sunday I

    2015-01-01

    The inhibition of enzymes involved in the breakdown of carbohydrates is considered a therapeutic approach to the management of type-2 diabetes. This study sought to investigate the effects of essential oil from clove bud on α-amylase and α-glucosidase activities. Essential oil from clove bud was extracted by hydrodistillation, dried with anhydrous Na2SO4 and characterized using gas chromatography-mass spectrometry (GC-MS). The effects of the essential oil on α-amylase and α-glucosidase activities were investigated. The antioxidant properties of the oil and the inhibition of Fe(2+) and sodium nitroprusside-induced malondialdehyde (MDA) production in rats pancreas homogenate were also carried out. The essential oil inhibited α-amylase (EC50=88.9 μl/L) and α-glucosidase (EC50=71.94 μl/L) activities in a dose-dependent manner. Furthermore, the essential oil inhibited Fe(2+) and SNP-induced MDA production and exhibited antioxidant activities through their NO*, OH*, scavenging and Fe(2+)- chelating abilities. The total phenolic and flavonoid contents of the essential oil were 12.95 mg/g and 6.62 mg/g respectively. GC-MS analysis revealed the presence of α-pinene, β-pinene, neral, geranial, gamma terpinene, cis-ocimene, allo ocimene, 1,8-cineole, linalool, borneol, myrcene and pinene-2-ol in significant amounts. Furthermore, the essential oils exhibited antioxidant activities as typified by hydroxyl (OH) and nitric oxide (NO)] radicals scavenging and Fe(2+)-chelating abilities. The inhibition of α-amylase and α-glucosidase activities, inhibition of pro-oxidant induced lipid peroxidation in rat pancreas and antioxidant activities could be possible mechanisms for the use of the essential oil in the management and prevention of oxidative stress induced type-2 diabetes.

  20. Protective effect of phytic acid hydrolysis products on iron-induced lipid peroxidation of liposomal membranes.

    PubMed

    Miyamoto, S; Kuwata, G; Imai, M; Nagao, A; Terao, J

    2000-12-01

    Beneficial effects of dietary phytic acid (myo-inositol hexaphosphate; IP6) have often been explained by its strong iron ion-chelating ability, which possibly suppresses iron ion-induced oxidative damage in the gastrointestinal tract. Because phytic acid is hydrolyzed during digestion, this work aimed to know whether its hydrolysis products (IP2, IP3, IP4, and IP5) could still prevent iron ion-induced lipid peroxidation. Studies using liposomal membranes demonstrated that hydrolysis products containing three or more phosphate groups are able to inhibit iron ion-induced lipid peroxidation although their effectiveness decreased with dephosphorylation. Similarly, they also prevented iron ion-induced decomposition of phosphatidylcholine hydroperoxide. These results demonstrate that intermediate products of phytic acid hydrolysis still possess iron ion-chelating ability, and thus they can probably prevent iron ion-induced lipid peroxidation in biological systems.

  1. Turmeric and black pepper spices decrease lipid peroxidation in meat patties during cooking

    PubMed Central

    Zhang, Yanjun; Henning, Susanne M.; Lee, Ru-Po; Huang, Jianjun; Zerlin, Alona; Li, Zhaoping; Heber, David

    2015-01-01

    Abstract Spices are rich in natural antioxidants and have been shown to be potent inhibitors of lipid peroxidation during cooking of meat. Turmeric contains unique conjugated curcuminoids with strong antioxidant activity. Piperine, one of the main constituents of black pepper, is known to increase the bioavailability of curcuminoids in mouse and human studies when consumed with turmeric. We investigated whether adding black pepper to turmeric powder may further inhibit lipid peroxidation when added to meat patties prior to cooking. The addition of black pepper to turmeric significantly decreased the lipid peroxidation in hamburger meat. When investigating the antioxidant activity of the main chemical markers, we determined that piperine did not exhibit any antioxidant activity. Therefore, we conclude that other black pepper ingredients are responsible for the increased antioxidant activity of combining black pepper with turmeric powder. PMID:25582173

  2. Turmeric and black pepper spices decrease lipid peroxidation in meat patties during cooking.

    PubMed

    Zhang, Yanjun; Henning, Susanne M; Lee, Ru-Po; Huang, Jianjun; Zerlin, Alona; Li, Zhaoping; Heber, David

    2015-05-01

    Spices are rich in natural antioxidants and have been shown to be potent inhibitors of lipid peroxidation during cooking of meat. Turmeric contains unique conjugated curcuminoids with strong antioxidant activity. Piperine, one of the main constituents of black pepper, is known to increase the bioavailability of curcuminoids in mouse and human studies when consumed with turmeric. We investigated whether adding black pepper to turmeric powder may further inhibit lipid peroxidation when added to meat patties prior to cooking. The addition of black pepper to turmeric significantly decreased the lipid peroxidation in hamburger meat. When investigating the antioxidant activity of the main chemical markers, we determined that piperine did not exhibit any antioxidant activity. Therefore, we conclude that other black pepper ingredients are responsible for the increased antioxidant activity of combining black pepper with turmeric powder.

  3. Lipid peroxidation causes endosomal antigen release for cross-presentation

    PubMed Central

    Dingjan, Ilse; Verboogen, Daniëlle RJ; Paardekooper, Laurent M; Revelo, Natalia H; Sittig, Simone P; Visser, Linda J; Mollard, Gabriele Fischer von; Henriet, Stefanie SV; Figdor, Carl G; ter Beest, Martin; van den Bogaart, Geert

    2016-01-01

    Dendritic cells (DCs) present foreign antigen in major histocompatibility complex (MHC) class I molecules to cytotoxic T cells in a process called cross-presentation. An important step in this process is the release of antigen from the lumen of endosomes into the cytosol, but the mechanism of this step is still unclear. In this study, we show that reactive oxygen species (ROS) produced by the NADPH-oxidase complex NOX2 cause lipid peroxidation, a membrane disrupting chain-reaction, which in turn results in antigen leakage from endosomes. Antigen leakage and cross-presentation were inhibited by blocking ROS production or scavenging radicals and induced when using a ROS-generating photosensitizer. Endosomal antigen release was impaired in DCs from chronic granulomatous disease (CGD) patients with dysfunctional NOX2. Thus, NOX2 induces antigen release from endosomes for cross-presentation by direct oxidation of endosomal lipids. This constitutes a new cellular function for ROS in regulating immune responses against pathogens and cancer. PMID:26907999

  4. Lipid peroxidation causes endosomal antigen release for cross-presentation.

    PubMed

    Dingjan, Ilse; Verboogen, Daniëlle Rj; Paardekooper, Laurent M; Revelo, Natalia H; Sittig, Simone P; Visser, Linda J; Mollard, Gabriele Fischer von; Henriet, Stefanie Sv; Figdor, Carl G; Ter Beest, Martin; van den Bogaart, Geert

    2016-02-24

    Dendritic cells (DCs) present foreign antigen in major histocompatibility complex (MHC) class I molecules to cytotoxic T cells in a process called cross-presentation. An important step in this process is the release of antigen from the lumen of endosomes into the cytosol, but the mechanism of this step is still unclear. In this study, we show that reactive oxygen species (ROS) produced by the NADPH-oxidase complex NOX2 cause lipid peroxidation, a membrane disrupting chain-reaction, which in turn results in antigen leakage from endosomes. Antigen leakage and cross-presentation were inhibited by blocking ROS production or scavenging radicals and induced when using a ROS-generating photosensitizer. Endosomal antigen release was impaired in DCs from chronic granulomatous disease (CGD) patients with dysfunctional NOX2. Thus, NOX2 induces antigen release from endosomes for cross-presentation by direct oxidation of endosomal lipids. This constitutes a new cellular function for ROS in regulating immune responses against pathogens and cancer.

  5. Lipid peroxidation and cytotoxicity induced by respirable volcanic ash.

    PubMed

    Cervini-Silva, Javiera; Antonio-Nieto-Camacho; Gomez-Vidales, Virginia; Ramirez-Apan, María Teresa; Palacios, Eduardo; Montoya, Ascención; Kaufhold, Stephan; Abidin, Zeanal; Theng, Benny K G

    2014-06-15

    This paper reports that the main component of respirable volcanic ash, allophane, induces lipid peroxidation (LP), the oxidative degradation of lipids in cell membranes, and cytotoxicity in murin monocyle/macrophage cells. Naturally-occurring allophane collected from New Zealand, Japan, and Ecuador was studied. The quantification of LP was conducted using the Thiobarbituric Acid Reactive Substances (TBARS) assay. The cytotoxic effect was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide colorimetric assay. Electron-Paramagnetic Resonance (EPR) determinations of naturally-occurring allophane confirmed the incorporation in the structure and clustering of structural Fe(3+), and nucleation and growth of small-sized Fe (oxyhydr)oxide or gibbsite. LP induced by allophane varied with time, and solid concentration and composition, reaching 6.7 ± 0.2 nmol TBARS mg prot(-1). LP was surface controlled but not restricted by structural or surface-bound Fe(3+), because redox processes induced by soluble components other than perferryl iron. The reactivity of Fe(3+) soluble species stemming from surface-bound Fe(3+) or small-sized Fe(3+) refractory minerals in allophane surpassed that of structural Fe(3+) located in tetrahedral or octahedral sites of phyllosilicates or bulk iron oxides. Desferrioxamine B mesylate salt (DFOB) or ethylenediaminetetraacetic acid (EDTA) inhibited LP. EDTA acted as a more effective inhibitor, explained by multiple electron transfer pathways. Registered cell-viability values were as low as 68.5 ± 6.7%.

  6. Lipid peroxidation induced by trichloroethylene in rat liver

    SciTech Connect

    Ogino, Keiki; Hobara, Tatuya; Kobayashi, Haruo; Ishiyama, Hironobu; Gotoh, Masayuki; Imamura, Akihisa; Egami, Norio )

    1991-03-01

    It is well-known that trichloroethylene (TRI) is metabolized by cytochrome P-450 to TRI oxide, which binds irreversibly to cell macromolecules to generates hepatic damage. TRI oxide was metabolized to Chloral and Chloral hydrate, as an intramolecular rearrangement product of TRI oxide. However, recent studies have demonstrated that TRI oxide is not an obligate intermediate in the conversion of TRI to chloral. Therefore, there is no satisfactory explanation about the hepatic toxicity of TRI. On the other hand, the hepatic toxicity of halogenated compounds, may be closely related to lipid peroxidation, TRI enhances carbon tetrachloride hepatotoxicity in association with lipid peroxidation. In this report, the authors studied the effect of TRI on lipid peroxidation in vivo and in vitro.

  7. Effects of (+)-1,2-bis(3,5-dioxopiperazin-1-yl)propane (ADR-529) on iron-catalyzed lipid peroxidation.

    PubMed

    Ryan, T P; Samokyszyn, V M; Dellis, S; Aust, S D

    1990-01-01

    ADR-529 [(+)-1,2-bis(3,5-dioxopiperazin-1-yl)propane], a nonpolar, cyclic analogue of EDTA, protects against anthracycline cardiotoxicity in vivo. The protective mechanism presumably involves chelation of iron by a hydrolysis product of ADR-529, thus preventing the formation of reactive iron/oxygen species which can damage membrane lipids. We investigated the effects of ADR-529 and its hydrolysis products (the tetraacid and the diacid diamide) on NADPH- and ADP-Fe(3+)-dependent lipid peroxidation of rat liver microsomes and liposomes in the presence of cytochrome P-450 reductase. Hydrolyzed ADR-529 products caused inhibition of lipid peroxidation when in excess of the iron concentration. However, no inhibition of lipid peroxidation was detected by similar concentrations of nonhydrolyzed ADR-529. Microsomes did not affect the inhibition of lipid peroxidation, suggesting that rat liver microsomes do not hydrolyze ADR-529. Similarly, the diacid diamide hydrolysis product of ADR-529 inhibited ferritin- and adriamycin-iron-dependent liposomal lipid peroxidation in a concentration-dependent manner. No correlation between partially reduced oxygen species (O2.- and .OH; as measured by electron spin resonance) and lipid peroxidation (as assayed by malondialdehyde formation) was observed, suggesting that liposomal lipid peroxidation was strictly an iron-dependent phenomenon. These results suggest that inhibition of lipid peroxidation by iron chelation may be related to the protective effects of ADR-529 on in vivo anthracycline toxicity.

  8. Cumene peroxide and Fe(2+)-ascorbate-induced lipid peroxidation and effect of phosphoglucose isomerase.

    PubMed

    Agadjanyan, Z S; Dugin, S F; Dmitriev, L F

    2006-09-01

    Malondialdehyde (MDA) is one of cytotoxic aldehydes produced in cells as a result of lipid peroxidation and further MDA metabolism in cytoplasm is not known. In our experiments the liver fraction 10,000 g containing phosphoglucose isomerase and enzymes of the glyoxalase system was used and obtained experimental data shows that in this fraction there is an aggregate of reactions taking place both in membranes (lipid peroxidation) and outside membranes. MDA accumulation is relatively slow because MDA is a substrate of aldehyde isomerase (MDA <--> methylglyoxal). The well known enzyme phosphoglucose isomerase acts as an aldehyde isomerase (Michaelis constant for this enzyme Km = 133 +/- 8 microM). MDA conversion to methylglyoxal and further to neutral product D-lactate (with GSH as a cofactor) occurs in cytoplasm and D-lactate should be regarded as the end product of two different parametabolic reactions: lipid peroxidation or protein glycation.

  9. Novel interference in thiobarbituric acid assay for lipid peroxidation.

    PubMed

    Baumgartner, W A; Baker, N; Hill, V A; Wright, E T

    1975-05-01

    The thiobarbituric acid test for lipid peroxidation, when applied to a mixture of acetaldehyde and sucrose, produces a 532 nm aborbing chromogen which is indistinguishable from that formed by malonaldehyde and thiobarbituric acid. Unless special procedures are adopted to correct for this effect, the combined action of acetaldehyde and sucrose interferes seriously with the assay of lipid peroxidation reactions, notably those implicated in alcohol-induced liver injuries. However, this unusual thiobarbituric acid effect also can be used as a sensitive method for the detection of acetaldehyde.

  10. Effect of asbestos on lipid peroxidation in the red cells.

    PubMed Central

    Gabor, S; Anca, Z

    1975-01-01

    In vitro exposure of red cells to vie International Union against Cancer (UICC) standard reference asbestos samples resulted in an increase of thiobarbituric acid substances. Chrysotiles developed the largest amounts of lipid peroxides, followed by anthophyllite, amosite, and crocidolite in decreasing order. Compared with the control samples erythrocytes free of dusts, all types of the asbestos examined disclosed significant differences. The results obtained provide support for the cytotoxic potential of amosite and crocidolite and, on the other hand, suggest that a lipid peroxidation of unsaturated fatty acids may be involved in the mechanisms(s) of membrane-damaging effects of asbestos dusts. PMID:1125126

  11. Beta-glucan from Saccharomyces cerevisiae reduces plasma lipid peroxidation induced by haloperidol.

    PubMed

    Dietrich-Muszalska, Anna; Olas, Beata; Kontek, Bogdan; Rabe-Jabłońska, Jolanta

    2011-07-01

    Since oxidative stress observed in schizophrenia may be caused partially by the treatment of patients with various antipsychotics, the aim of the study was to establish the effects of beta-d-glucan, polysaccharide derived from the yeast cell walls of species such as Saccharomyces cerevisiae, and the antipsychotics (the first generation antipsychotic (FGA) - haloperidol and the second generation antipsychotic (SGA) - amisulpride) action on plasma lipid peroxidation in vitro. Lipid peroxidation in human plasma was measured by the level of thiobarbituric acid reactive species (TBARS). The samples of plasma from healthy subjects were incubated with haloperidol or amisulpride in the presence of beta-glucan (4 μg/ml). The action of beta-d-glucan was also compared with the properties of a well characterized commercial monomeric polyphenol - resveratrol (3,4',5-trihydroxystilbene, the final concentration - 4 μg/ml). The two-way analysis variance showed that the differences in TBARS levels were depended on the type of tested drugs (p=7.9 × 10(-6)). We observed a statistically increase of the level of biomarker of lipid peroxidation such as TBARS after 1 and 24h incubation of plasma with haloperidol compared to the control samples (p<0.01, p<0.02, respectively). Amisulpride, contrary to haloperidol (after 1 and 24h) did not cause plasma lipid peroxidation (p>0.05). We showed that in the presence of beta-glucan, lipid peroxidation in plasma samples treated with haloperidol was significantly decreased. Moreover, we did not observe the synergistic action of beta-glucan and amisulpride on the inhibition of plasma lipid peroxidation. However, the beta-d-glucan was found to be more effective antioxidant, than the solution of pure resveratrol. The presented results indicate that beta-glucan seems to have distinctly protective effects against the impairment of plasma lipid molecules induced by haloperidol.

  12. Dietary fiber and lipid peroxidation: effect of dietary fiber on levels of lipids and lipid peroxides in high fat diet.

    PubMed

    Thampi, B S; Manoj, G; Leelamma, S; Menon, V P

    1991-06-01

    Effect of feeding coconut and blackgram fiber isolated as neutral detergent fiber (NDF) on the levels of lipids and lipid peroxides was studied in rats given a high fat diet. Concentration of cholesterol, free falty acid and phospholipids showed significant decrease in the serum, liver aorta and intestine of coconut and blackgram fiber groups. Concentration of malondialdehyde (MDA) and conjugated dienes was significantly decreased in liver and intestine of both fiber groups, while hydroperoxides showed significant increase in liver and heart of both the fiber groups. SOD and catalase activity was found to be increased in liver, intestine, heart proximal colon and distal colon of both the fiber groups. Serum ceruloplasmin levels showed a slight increase in animals fed coconut and blackgram fiber groups. Glutathione levels in liver, intestine proximal colon, distal colon and heart also showed a significant decrease in the animals of both the fiber groups.

  13. Effect of quercetin and genistein on copper- and iron-induced lipid peroxidation in methyl linolenate.

    PubMed

    Boadi, William Y; Iyere, Peter A; Adunyah, Samuel E

    2003-01-01

    The single and combined effects of two abundant flavonoids, namely quercetin and genistein, were investigated according to their ability to inhibit the oxidation of methyl linolenate via Fenton's pathway. Antioxidative activity was determined by oxidizing methyl linolenate suspended in a buffer solution with either Fe2+ (50 microM) or Cu2+ (50 microM) and hydrogen peroxide (0.01 mM) without or with a flavonoid sample (10 or 20 microM). Lipid peroxidation products were measured by the thiobarbituric acid (TBA) assay and the amounts of thiobarbituric acid-reactive substances (TBARS) were calculated from a calibration curve using 1,1,3,3-tetraethoxypropane as the standard. Both quercetin and genistein at the 10 or 20 microM level decreased lipid peroxidation significantly compared with their respective controls. Of the two flavonoids tested, quercetin had a more marked effect on inhibiting lipid peroxides. Peroxidation products for the control samples were higher for the Fe2+-treated samples compared with the Cu2+ samples. Combination of both flavonoids at the same dose levels continued to decrease lipid peroxidation, the effect being the same for both metal ions. The data suggest that the combined flavonoids offered better protection than the single treatments and this may be attributed to the better radical scavenging or increased chelating capabilities of the combined over the single treatments. The differences in peroxide levels for the single treatment of quercetin compared with the genistein-treated samples may reflect the structural differences between these compounds in combating oxidative stress.

  14. Mitochondrial lipid peroxidation by cumene hydroperoxide and its prevention by succinate.

    PubMed

    Bindoli, A; Cavallini, L; Jocelyn, P

    1982-09-15

    Rat liver mitochondria form lipid hydroperoxides when they are incubated aerobically with cumene hydroperoxide. The rate of reaction is dependent on the initial concentration of the latter and involves the consumption of oxygen. Gradient-separated and cytochrome c-depleted mitochondria, mitoplasts and submitochondrial fractions also undergo this peroxidation. Mitochondrial lipid peroxidation by cumene hydroperoxide is strongly inhibited by SKF52A (an inhibitor of cytochrome P-450), by antioxidants and to a lesser extent by the enzymes superoxide dismutase and catalase. Conversely, rotenone and N-ethylmaleimide stimulate the reaction. Succinate protects against the lipid peroxidation and in some mitochondrial fractions the associated oxygen uptake is also inhibited. This protection by succinate is prevented by malonate but not by N-ethylmaleimide or antimycin. Lipid hydroperoxides present in previously peroxidised mitochondria are partly lost on reincubation with succinate and this reaction is also unaffected by N-ethylmaleimide but inhibited by both malonate and antimycin. The results suggest that reduction of mitochondrial ubiquinone may prevent the generation of lipid hydroperoxides but that their subsequent removal may require reduction at or beyond cytochrome b.

  15. The effect of alpha-tocopherol on lipid peroxidation of microsomes and mitochondria from rat testis.

    PubMed

    Gavazza, M B; Catalá, A

    2006-04-01

    The testis is a remarkably active metabolic organ; hence it is suitable not only for studies of lipid metabolism in the organ itself but also for the study of lipid peroxidation processes in general. The content of fatty acids in testis is high with a prevalence of polyunsaturated fatty acids (PUFA) which renders this tissue very susceptible to lipid peroxidation. Studies were carried out to evaluate the effect of alpha-tocopherol in vitro on ascorbate-Fe(++) lipid peroxidation of rat testis microsomes and mitochondria. Chemiluminescence and fatty acid composition were used as an index of the oxidative destruction of lipids. Special attention was paid to the changes produced on the highly PUFA [C20:4 n6] and [C22:5 n6]. Lipid peroxidation of testis microsomes or mitochondria induced a significant decrease of both fatty acids. Total chemiluminescence was similar in both kinds of organelles when the peroxidized without (control) and with ascorbate-Fe(++) (peroxidized) groups were compared. Arachidonic acid was protected more efficiently than docosapentaenoic acid at all alpha-tocopherol concentrations tested when rat testis microsomes or mitochondria were incubated with ascorbate-Fe(++). The maximal percentage of inhibition in both organelles was approximately 70%; corresponding to an alpha-tocopherol concentration between 1 and 0.25 mM. IC50 values from the inhibition of alpha-tocopherol on the chemiluminescence were higher in microsomes (0.144 mM) than mitochondria (0.078 mM). The protective effect observed by alpha-tocopherol in rat testis mitochondria was higher compared with microsomes, associated with the higher amount of [C20:4 n6]+[C22:5 n6] in microsomes that in mitochondria. It is proposed that the vulnerability to lipid peroxidation of rat testis microsomes and mitochondria is different because of the different proportion of PUFA in these organelles The peroxidizability index (PI) was positively correlated with the level of long chain fatty acids. The

  16. Inhibitory Response of Raphanus sativus on Lipid Peroxidation in Albino Rats

    PubMed Central

    2008-01-01

    In the present study, inhibitory effect of the methanol extract of Raphanus sativus root on lipid peroxidation has been carried out in normal rats. Graded doses of methanol extract of root of the plant (40, 80 and 120 mg kg−1 body weight) were administered orally for 15 days to experimental treated rats. Distilled water was administered to experimental control rats. At the end of experiment, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substance, reduced glutathione and activity of catalase. Results indicated that the extract of R. sativus root reduced the levels of thiobarbituric acid reactive substance significantly in all experimental treated groups (P < 0.05) as compared to the experimental control group. It also increased the levels of reduced glutathione and increased the activity of catalase. In vitro experiments with the liver of experimental control and experimental treated rats were also carried out against cumene hydroperoxide induced lipid peroxidation. The extract inhibited in vitro cumene hydroperoxide induced lipid peroxidation. R. sativus inhibits lipid peroxidation in vivo and in vitro. It provides protection by strengthening the antioxidants like glutathione and catalase. Inclusion of this plant in every day diet would be beneficial. PMID:18317549

  17. Increased erythrocyte lipid peroxidation in hereditary xerocytosis.

    PubMed

    Harm, W; Fortier, N L; Lutz, H U; Fairbanks, G; Snyder, L M

    1979-12-03

    Xerocytosis is a chronic hemolytic anemia with abnormal membrane function manifested by an increase in passive potassium permeability. Xerocytes demonstrate a greater susceptibility to hydrogen peroxide manifested by the production of malondialdehyde (MDA). Xerocyte membrane phospholipid and fatty acid analysis is normal except for a slight increase in phosphatidyl choline, a commensurate decrease in sphingomyelin, as well as a decrease in linoleic acid. Metabolism and glutathione stability are normal as well as plasma vitamin E levels in patients with xerocytosis. The increased susceptibility to oxidant stress is exaggerated in the "older aged" xerocyte population and correlated well with decreased intracellular potassium concentration.

  18. [Lipid peroxidation indices in children with congenital cleft palate].

    PubMed

    Nagirnyĭ, Ia P

    1989-01-01

    Observed were 66 children with congenital palate clefts and a control group of 25 children. The data suggest that the disease involves the lipid peroxidation disorders and impairment of the antioxydative defence. The results can be used for designing the antioxydant and membrane-stabilizing therapies in out-patient departments.

  19. Nutrient overload, lipid peroxidation and pancreatic beta cell function.

    PubMed

    Sasson, Shlomo

    2017-10-01

    Since the landmark discovery of α,β-unsaturated 4-hydroxyalkenals by Esterbauer and colleagues most studies have addressed the consequences of the tendency of these lipid peroxidation products to form covalent adducts with macromolecules and modify cellular functions. Many studies describe detrimental and cytotoxic effects of 4-hydroxy-2E-nonenal (4-HNE) in myriad tissues and organs and many pathologies. Other studies similarly assigned unfavorable effects to 4-hydroxy-2E-hexenal (4-HHE) and 4-hydroxy-2E,6Z-dodecadienal (4-HDDE). Nutrient overload (e.g., hyperglycemia, hyperlipidemia) modifies lipid metabolism in cells and promotes lipid peroxidation and the generation of α,β-unsaturated 4-hydroxyalkenals. Advances glycation- and lipoxidation end products (AGEs and ALEs) have been associated with the development of insulin resistance and pancreatic beta cell dysfunction and the etiology of type 2 diabetes and its peripheral complications. Less acknowledged are genuine signaling properties of 4-hydroxyalkenals in hormetic processes that provide defense against the consequences of nutrient overload. This review addresses recent findings on such lipohormetic mechanisms that are associated with lipid peroxidation in pancreatic beta cells. This article is part of a Special Issue entitled SI: LIPID OXIDATION PRODUCTS, edited by Giuseppe Poli. Copyright © 2016 Elsevier Inc. All rights reserved.

  20. Assay to detect lipid peroxidation upon exposure to nanoparticles.

    PubMed

    Potter, Timothy M; Neun, Barry W; Stern, Stephan T

    2011-01-01

    This chapter describes a method for the analysis of human hepatocarcinoma cells (HEP G2) for lipid peroxidation products, such as malondialdehyde (MDA), following treatment with nanoparticle formulations. Oxidative stress has been identified as a likely mechanism of nanoparticle toxicity, and cell-based in vitro systems for evaluation of nanoparticle-induced oxidative stress are widely considered to be an important component of biocompatibility screens. The products of lipid peroxidation, lipid hydroperoxides, and aldehydes, such as MDA, can be measured via a thiobarbituric acid reactive substances (TBARS) assay. In this assay, which can be performed in cell culture or in cell lysate, MDA combines with thiobarbituric acid (TBA) to form a fluorescent adduct that can be detected at an excitation wavelength of 530 nm and an emission wavelength of 550 nm. The results are then expressed as MDA equivalents, normalized to total cellular protein (determined by Bradford assay).

  1. Subadditive interactions between antioxidants in the protection against lipid peroxidation.

    PubMed

    Piotrowski, Lukasz; Bartosz, Grzegorz

    2009-01-01

    Synergistic interactions between antioxidants have been postulated but not proven. On the contrary, it has been reported that the antioxidant activity of mixtures of antioxidants can be lower than the sum of the antioxidant activities of individual components. We report that such a situation can be observed in 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)-treated phosphatidylcholine liposomes in which lipid peroxidation was monitored by oxidation of 4,4-difluoro-5-(4-phenyl-1 3-butadienyl)-4-bora-3a,4a-diaza-s-indacene-3-undecanoic acid (C11-BODIPY581/591). Glutathione, present inside liposomes, and hydrophobic antioxidants, present in the lipid bilayer, protected against lipid peroxidation, but their simultaneous action was lower than the sum of individual contributions. A possible explanation for this effect is proposed.

  2. Peroxidation of tobacco membrane lipids by the photosensitizing toxin, cercosporin.

    PubMed

    Daub, M E

    1982-06-01

    Cercosporin, a nonspecific toxin from Cercospora species, is a photosensitizing compound which rapidly kills plant cells in the light. Cell death appears to be due to a cercosporin-mediated peroxidation of membrane lipids. Tobacco leaf discs treated with cercosporin showed a large increase in electrolyte leakage 1 to 2 minutes after irradiation with light. All tobacco protoplasts exposed to cercosporin in the light were damaged within 45 minutes. Chloroform:methanol extracts of toxin-treated suspension cultures gave positive reactions for lipid hydroperoxides in the thiobarbituric acid test. Cercosporin-treated leaf discs emitted high concentrations of ethane 12 to 24 hours after incubation in the light. Cercosporin also oxidized solutions of methyl linolenate as determined by the thiobarbituric acid assay and the emission of ethane. alpha-Tocopherol had an inhibitory effect on the cercosporin-mediated lipid peroxidation.

  3. The involvement of transition metal ions on iron-dependent lipid peroxidation.

    PubMed

    Repetto, Marisa G; Ferrarotti, Nidia F; Boveris, Alberto

    2010-04-01

    The metals iron (Fe) and copper (Cu) are considered trace elements, and the metals cobalt (Co) and nickel (Ni) are known as ultra-trace elements, considering their presence in low to very low quantity in humans. The biologic activity of these transition metals is associated with the presence of unpaired electrons that favor their participation in redox reactions. They are part of important enzymes involved in vital biologic processes. However, these transition metals become toxic to cells when they reach elevated tissue concentrations and produce cellular oxidative damage. Phospholipid liposomes (0.5 mg/ml, phosphatidylcholine (PC)/phosphatidylserine (PS), 60/40) were incubated for 60 min at 37 degrees C with 25 microM of Fe2+ in the absence and in the presence of Cu2+, Co2+, and Ni2+ (0-100 microM) with and without the addition of hydrogen peroxide (H2O2, 5-50 microM). Iron-dependent lipid peroxidation in PC/PS liposomes was assessed by thiobarbituric acid-reactive substances (TBARS) production. Metal transition ions promoted lipid peroxidation by H2O2 decomposition and direct homolysis of endogenous hydroperoxides. The Fe2+-H2O2-mediated lipid peroxidation takes place by a pseudo-second order process, and the Cu2+-mediated process by a pseudo-first order reaction. Co2+ and Ni2+ alone do not induce lipid peroxidation. Nevertheless, when they are combined with Fe2+, Fe2+-H2O2-mediated lipid peroxidation was stimulated in the presence of Ni2+ and was inhibited in the presence of Co2+. The understanding of the effects of transition metal ions on phospholipids is relevant to the prevention of oxidative damage in biologic systems.

  4. Enhancement of lipid peroxidation and its amelioration by vitamin E in a subject with mutations in the SBP2 gene.

    PubMed

    Saito, Yoshiro; Shichiri, Mototada; Hamajima, Takashi; Ishida, Noriko; Mita, Yuichiro; Nakao, Shohei; Hagihara, Yoshihisa; Yoshida, Yasukazu; Takahashi, Kazuhiko; Niki, Etsuo; Noguchi, Noriko

    2015-11-01

    Selenocysteine (Sec) insertion sequence-binding protein 2 (SBP2) is essential for the biosynthesis of Sec-containing proteins, termed selenoproteins. Subjects with mutations in the SBP2 gene have decreased levels of several selenoproteins, resulting in a complex phenotype. Selenoproteins play a significant role in antioxidative defense, and deficiencies in these proteins can lead to increased oxidative stress. However, lipid peroxidation and the effects of antioxidants in subjects with SBP2 gene mutations have not been studied. In the present study, we evaluated the lipid peroxidation products in the blood of a subject (the proband) with mutations in the SBP2 gene. We found that the proband had higher levels of free radical-mediated lipid peroxidation products, such as 7β-hydroxycholesterol, than the control subjects. Treatment of the proband with vitamin E (α-tocopherol acetate, 100 mg/day), a lipid-soluble antioxidant, for 2 years reduced lipid peroxidation product levels to those of control subjects. Withdrawal of vitamin E treatment for 7 months resulted in an increase in lipid peroxidation products. Collectively, these results clearly indicate that free radical-mediated oxidative stress is increased in the subject with SBP2 gene mutations and that vitamin E treatment effectively inhibits the generation of lipid peroxidation products.

  5. Protective effect of propofol against kainic acid-induced lipid peroxidation in mouse brain homogenates: comparison with trolox and melatonin.

    PubMed

    Lee, Hyung; Jang, Young-Ho; Lee, Seong-Ryong

    2005-07-01

    This study compared the effectiveness of propofol with that of trolox and melatonin for reduction of lipid peroxidation in vitro. Lipid peroxidation was induced by addition of kainic acid (KA; 10 mM), hydrogen peroxide (H2O2; 10 mM), or ferrous ammonium sulfate (5 microM) to mouse brain homogenate, and thiobarbituric acid-reactive substances (TBA-RS) were used as a marker of lipid peroxidation. Propofol, trolox, and melatonin reduced KA-, H2O2-, and ferrous ammonium sulfate-induced lipid peroxidation in a concentration-dependent manner. In reducing KA-induced lipid peroxidation, 50% inhibitory concentration (IC50) values of antioxidants were as follows: propofol (11.33 mM), trolox (4.00 mM), and melatonin (9.72 mM). In reducing H2O2-induced lipid peroxidation, IC50 values of antioxidants were as follows: propofol (56.86 mM), trolox (33.34 mM), and melatonin (26.63 mM). In reducing ferrous ion-induced lipid peroxidation, IC50 values of antioxidants were as follows: propofol (49.57 mM), trolox (60.35 mM), and melatonin (22.02 mM). Under the in vitro conditions of this experiment, propofol was an excellent and a very potent antioxidant in inhibiting KA-, H2O2-, and ferrous ion-induced lipid peroxidation in mouse brain homogenates. We conclude that the antioxidant properties of propofol at clinically relevant anesthetic concentrations may have a neuroprotective effect.

  6. Regulation of collagen synthesis in human dermal fibroblasts by ascorbic-induced lipid peroxidation

    SciTech Connect

    Geesin, J.C. Johnson and Johnson Consumer Products, Inc., Skillman, NJ ); Gordon, J.S. ); Gordon, J.S. ); Berg, R.A. )

    1991-03-11

    Ascorbic acid has been shown to stimulate collagen synthesis through the induction of lipid peroxidation which leads to increased transcription of the collagen genes. To test the ability of aldehyde products of lipid peroxidation to mediate this effect, the authors treated cultured fibroblasts with 1-200{mu}M of malondialdehyde, acetaldehyde, glyoxal or hexenal in the presence of lipid peroxidation inducing or noninducing concentrations of ascorbic acid. The treatment process involved either pretreatment of cells for 66hrs with either concentration of ascorbate before a 6hr treatment in the presence of ascorbate and the aldehydes, or 6 or 72hr treatment of the cells in the presence of either concentration of ascorbate plus the aldehydes. No effect of any of these aldehydes was seen on ascorbate-stimulated collagen synthesis. Also, pretreatment of fibroblasts for 24hrs with 100nM phorbol myristate acetate (PMA), which produces down regulation of protein kinase C(PKC), failed to alter the ascorbate-stimulation of collagen synthesis. Additionally, the authors tested the ability of benzamide, a poly ACP ribosylation inhibitor, to inhibit the ascorbate response with no specific effect noted. These results do not support the proposed roles for aldehydes, PKC, or poly ADP ribosylation in the mediation of the lipid peroxidation induced stimulation of collagen synthesis.

  7. A spectrophotometric assay for lipid peroxides in serum lipoproteins using a commercially available reagent.

    PubMed

    el-Saadani, M; Esterbauer, H; el-Sayed, M; Goher, M; Nassar, A Y; Jürgens, G

    1989-04-01

    A method is described for measuring lipid peroxides by means of the color reagent of a commercially available test kit for cholesterol estimation. In principle, this assay makes use of the oxidative capacity of lipid peroxides to convert iodide to iodine, which can be measured photometrically at 365 nm. Calibration curves were obtained using peroxides such as H2O2, t-butyl hydroperoxide, and cumene hydroperoxide. A stoichiometric relationship was observed between the amount of organic peroxides assayed and the concentration of iodine produced. Concentrations of lipid peroxides as small as 1 nmol/ml could be measured. The ability to estimate lipid peroxides of isolated low density lipoprotein was demonstrated.

  8. [Lipid peroxidation processes and activity of brain succinate dehydrogenase in experimental craniocerebral trauma].

    PubMed

    Demchuk, M L; Medvedev, A E; Promyslov, M Sh; Gorkin, V Z

    1993-01-01

    A statistically significant decrease in the activity of succinate dehydrogenase (SDH) was found in the rabbit brain after craniocerebral injury. The decrease in the activity of brain SDH was not shown to result from "competitive inhibition" by malonate accumulated after activation of lipid peroxidation. The activity of brain SDH was normalized by directed modification of the function of the central nervous system via administration of phenamine (amphetamine) into the injured animals.

  9. Lipid peroxidation: pathophysiological and pharmacological implications in the eye

    PubMed Central

    Njie-Mbye, Ya Fatou; Kulkarni-Chitnis, Madhura; Opere, Catherine A.; Barrett, Aaron; Ohia, Sunny E.

    2013-01-01

    Oxygen-derived free radicals such as hydroxyl and hydroperoxyl species have been shown to oxidize phospholipids and other membrane lipid components leading to lipid peroxidation. In the eye, lipid peroxidation has been reported to play an important role in degenerative ocular diseases (age-related macular degeneration, cataract, glaucoma, diabetic retinopathy). Indeed, ocular tissues are prone to damage from reactive oxygen species due to stress from constant exposure of the eye to sunlight, atmospheric oxygen and environmental chemicals. Furthermore, free radical catalyzed peroxidation of long chain polyunsaturated acids (LCPUFAs) such as arachidonic acid and docosahexaenoic acid leads to generation of LCPUFA metabolites including isoprostanes and neuroprostanes that may further exert pharmacological/toxicological actions in ocular tissues. Evidence from literature supports the presence of endogenous defense mechanisms against reactive oxygen species in the eye, thereby presenting new avenues for the prevention and treatment of ocular degeneration. Hydrogen peroxide (H2O2) and synthetic peroxides can exert pharmacological and toxicological effects on tissues of the anterior uvea of several mammalian species. There is evidence suggesting that the retina, especially retinal ganglion cells can exhibit unique characteristics of antioxidant defense mechanisms. In the posterior segment of the eye, H2O2 and synthetic peroxides produce an inhibitory action on glutamate release (using [3H]-D-aspartate as a marker), in vitro and on the endogenous glutamate and glycine concentrations in vivo. In addition to peroxides, isoprostanes can elicit both excitatory and inhibitory effects on norepinephrine (NE) release from sympathetic nerves in isolated mammalian iris ciliary bodies. Whereas isoprostanes attenuate dopamine release from mammalian neural retina, in vitro, these novel arachidonic acid metabolites exhibit a biphasic regulatory effect on glutamate release from retina and

  10. Role of Lipid Composition and Lipid Peroxidation in the Sensitivity of Fungal Plant Pathogens to Aluminum Chloride and Sodium Metabisulfite▿

    PubMed Central

    Avis, Tyler J.; Michaud, Mélanie; Tweddell, Russell J.

    2007-01-01

    Aluminum chloride and sodium metabisulfite have shown high efficacy at low doses in controlling postharvest pathogens on potato tubers. Direct effects of these two salts included the loss of cell membrane integrity in exposed pathogens. In this work, four fungal potato pathogens were studied in order to elucidate the role of membrane lipids and lipid peroxidation in the relative sensitivity of microorganisms exposed to these salts. Inhibition of mycelial growth in these fungi varied considerably and revealed sensitivity groups within the tested fungi. Analysis of fatty acids in these fungi demonstrated that sensitivity was related to high intrinsic fatty acid unsaturation. When exposed to the antifungal salts, sensitive fungi demonstrated a loss of fatty acid unsaturation, which was accompanied by an elevation in malondialdehyde content (a biochemical marker of lipid peroxidation). Our data suggest that aluminum chloride and sodium metabisulfite could induce lipid peroxidation in sensitive fungi, which may promote the ensuing loss of integrity in the plasma membrane. This direct effect on fungal membranes may contribute, at least in part, to the observed antimicrobial effects of these two salts. PMID:17337539

  11. Effects of oral contraceptive norethindrone on blood-lipid and lipid peroxidation parameters.

    PubMed

    Saha, A; Roy, K; De, K; Sengupta, C

    2000-01-01

    Considering importance of the lipophilicity of norethindrone (log P=2.97), a significant contributor to its mechanism of action, interaction of the drug with total lipids of goat whole blood have been investigated using phospholipid binding, fatty acid composition and peroxidation phenomena as the parameters under investigation. The objective was to derive an insight into the pharmacodynamic behavior of the drug by correlating biological activity with drug induced changes in lipid constituents. Significant loss in phospholipid along with changes in fatty acid cotmposition was observed after incubation of whole blood with norethindrone at 56 ng/ml (effective contraceptive concentration in blood) in varying periods of time. This may be ascribed to binding affinity of norethindrone with lipid constituents in blood. Lipid binding potential of the drug may have a role in its therapeutic effect. Lipid peroxidation induction potential of norethindrone was quantitatively measured in the context of its toxicity. The results reveal that northindrone caused significant extent of lipid peroxidation. Ascorbic acid, a promising antioxidant, at equivalent human dose levels of 250 mg and 500 mg could significantly reduce norethindrone induced lipid peroxidation.

  12. Lipid peroxidation, hemolysis and antioxidant enzymes of erythrocytes in stroke.

    PubMed

    Sudha, K; Rao, Ashalatha V; Rao, Suryanarayana; Rao, Anjali

    2004-04-01

    Erythrocyte membrane lipid peroxidation and consequent percentage hemolysis and related antioxidant enzymes viz., superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase were determined in 16 cases of hemorrhagic stroke and 30 cases of thrombotic stroke. The results obtained were compared with 50 age and sex matched controls. 12 thrombotic stroke patients who showed symptomatic recovery after medication were considered for follow up. Lipid peroxidation and percentage hemolysis in patients with thrombotic stroke and hemorrhagic stroke was significantly elevated when compared to controls. Glutathione reductase and superoxide dismutase levels were found to be significantly reduced in thrombotic stroke and hemorrhagic stroke respectively, when compared to healthy subjects. There was no significant difference in the other parameters when compared to controls. In post treatment thrombotic stoke, catalase and glutathione reductase levels increased significantly and oxidative hemolysis decreased compared to their pretreatment values. Thus, our results indicate considerable oxidative stress in stroke.

  13. Lipid peroxidation and antioxidant enzymes activity in avian semen.

    PubMed

    Partyka, Agnieszka; Lukaszewicz, Ewa; Niżański, Wojciech

    2012-10-01

    The present study compared the antioxidant system and lipid peroxidation in semen of two avian species: chicken and goose. The experiment was conducted on Greenleg Partridge roosters and White Koluda(®) ganders, each represented by 10 mature males. Malondialdehyde (MDA) concentration, catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were determined in sperm cells and seminal plasma. In gander spermatozoa, the amount of MDA was 10 times greater (P<0.01) than in rooster spermatozoa. Each of the investigated antioxidant enzymes had greater (P<0.01) activity in goose than chicken sperm. Catalase activity was detected in seminal plasma and spermatozoa from both studied species for the first time. In seminal plasma, the activity of GPx was two times greater (P<0.01) in the White Koluda(®) than in chickens, whereas SOD activity was less (P<0.01) than in chickens. This is the first study describing the presence of CAT in avian semen and the occurrence of indicator of lipid peroxidation (LPO) in geese. Data from the present study clearly show the species-specific differences in the activity of antioxidant defense and LPO. The greater amount of lipid peroxidation and greater activity of antioxidant enzymes in goose semen might suggest that spermatozoa were under greater oxidative stress and the enzymes were not utilized for the protection of functionally and structurally impaired cells. In turn, in fresh chicken semen a lesser activity of antioxidant enzymes accompanied with a lesser lipid peroxidation amount and good semen quality could indicate that fowl spermatozoa were under oxidative stress, but the enzymes were employed to protect and maintain sperm quality. Copyright © 2012 Elsevier B.V. All rights reserved.

  14. Chromosome aberration and lipid peroxidation in chromium-exposed workers.

    PubMed

    Maeng, S H; Chung, H W; Kim, K J; Lee, B M; Shin, Y C; Kim, S J; Yu, I J

    2004-01-01

    Chromosome aberration frequency and lipid peroxidation levels were analyzed to investigate their efficacy as biological markers for monitoring the genotoxicity and oxidative damage in Korean chromium (Cr)-exposed workers. Fifty-one Cr-exposed workers and 31 age-matched controls in ten chrome-plating plants were sampled. The Cr level was measured in the workers' blood and urine, and in the ambient air at the workplaces. The conventional Giemsa staining method and fluorescence in situ hybridization (FISH) technique were used for chromosome aberration analysis. Spectrum green whole chromosome paint specific for chromosome 4 was used in the FISH procedure. As for lipid peroxidation, malondialdehyde (MDA) was measured in the blood plasma as thiobarbituric acid-reactive substances (TBARS). The blood Cr concentration was statistically correlated with both the frequency of chromatid exchange and the total frequency of chromosome/chromatid breaks and exchanges, as detected by the Giemsa staining. Meanwhile, the frequency of translocation, as detected by the FISH technique, was significantly higher in the Cr-exposed workers than in the controls and it correlated with the blood Cr concentration. Although the concentration of MDA, the metabolite of lipid peroxidation, in the exposed workers was higher than that of the controls, no statistically significant correlation between the MDA level and the blood or urine Cr levels was observed. Accordingly, the genotoxicity and oxidative damage (plasma lipid peroxidation) in the Korean Cr-exposed workers were consequential at quite low exposure levels, plus chromosome rearrangement, especially translocation, was clearly evident as a biological response marker for Cr exposure based on a significant positive correlation between the translocations detected by FISH and the Cr in the blood.

  15. The effect of ghee (clarified butter) on serum lipid levels and microsomal lipid peroxidation

    PubMed Central

    Sharma, Hari; Zhang, Xiaoying; Dwivedi, Chandradhar

    2010-01-01

    Ghee, also known as clarified butter, has been utilized for thousands of years in Ayurveda as a therapeutic agent. In ancient India, ghee was the preferred cooking oil. In the last several decades, ghee has been implicated in the increased prevalence of coronary artery disease (CAD) in Asian Indians due to its content of saturated fatty acids and cholesterol and, in heated ghee, cholesterol oxidation products. Our previous research on Sprague-Dawley outbred rats, which serve as a model for the general population, showed no effect of 5 and 10% ghee-supplemented diets on serum cholesterol and triglycerides. However, in Fischer inbred rats, which serve as a model for genetic predisposition to diseases, results of our previous research showed an increase in serum total cholesterol and triglyceride levels when fed a 10% ghee-supplemented diet. In the present study, we investigated the effect of 10% dietary ghee on microsomal lipid peroxidation, as well as serum lipid levels in Fischer inbred rats to assess the effect of ghee on free radical mediated processes that are implicated in many chronic diseases including cardiovascular disease. Results showed that 10% dietary ghee fed for 4 weeks did not have any significant effect on levels of serum total cholesterol, but did increase triglyceride levels in Fischer inbred rats. Ghee at a level of 10% in the diet did not increase liver microsomal lipid peroxidation or liver microsomal lipid peroxide levels. Animal studies have demonstrated many beneficial effects of ghee, including dose-dependent decreases in serum total cholesterol, low density lipoprotein (LDL), very low density lipoprotein (VLDL), and triglycerides; decreased liver total cholesterol, triglycerides, and cholesterol esters; and a lower level of nonenzymatic-induced lipid peroxidation in liver homogenate. Similar results were seen with heated (oxidized) ghee which contains cholesterol oxidation products. A preliminary clinical study showed that high doses of

  16. Analysis of the kinetics of lipid peroxidation in terms of characteristic time-points.

    PubMed

    Pinchuk, Ilya; Lichtenberg, Dov

    2014-02-01

    Measuring peroxidation of aggregated lipids in model systems (liposomes, micelles, emulsions or microemulsions) as well as in samples of biological origin ex vivo (isolated lipoproteins, blood sera or plasma) is widely used in medical and biological investigations, to evaluate the oxidative stress, antioxidants' efficiency and lipid oxidizability in different pathophysiological states. To avoid possible artifacts, such investigations must be based on the time course of peroxidation (i.e. on kinetic studies). To be able to compare complex kinetic profiles, it is important to characterize them in terms of mechanistically meaningful and experimentally unequivocal parameters. In this review, we characterize the typically observed continuous kinetic profiles in terms of a limited number of characteristic time-points (both commonly used and additional time-points and their combinations) that can be derived from experimental time-dependencies. The meaning of each of the experimentally observed characteristic parameters is presented in terms of rate constants and concentrations, derived on the basis of mechanistic considerations. Theoretical expressions for these characteristic parameters are based on a model that includes both the inhibited peroxidation and the uninhibited peroxidation occurring after consumption of the antioxidant(s). Comparison between theoretically predicted dependencies and experimental data support our treatment considered with special emphasis on transition metals-induced peroxidation of lipoproteins.

  17. Measuring oxidative stress: the confounding effect of lipid concentration in measures of lipid peroxidation.

    PubMed

    Pérez-Rodríguez, Lorenzo; Romero-Haro, Ana A; Sternalski, Audrey; Muriel, Jaime; Mougeot, Francois; Gil, Diego; Alonso-Alvarez, Carlos

    2015-01-01

    Lipid peroxidation products are widely used as markers of oxidative damage in the organism. To properly interpret the information provided by these markers, it is necessary to know potential sources of bias and control confounding factors. Here, we investigated the relationship between two indicators of lipid mobilization (circulating levels of triglycerides and cholesterol) and two common markers of oxidative damage (plasma levels of malondialdehyde and hydroperoxides; the latter estimated from the d-ROMs assay kit). The following five avian species were studied: red-legged partridge (Alectoris rufa), zebra finch (Taeniopygia guttata), spotless starling (Sturnus unicolor), marsh harrier (Circus aeroginosus), and Montagu's harrier (Circus pygargus). In all cases, plasma triglyceride levels positively and significantly correlated with lipid peroxidation markers, explaining between 8% and 34% of their variability. Plasma cholesterol, in contrast, showed a significant positive relationship only among spotless starling nestlings and a marginally significant association in zebra finches. These results indicate that lipid peroxidation marker levels covary with circulating lipid levels. We discuss the potential causes and implications of this covariation and recommend that future studies that measure oxidative damage using lipid peroxidation markers report both raw and relative levels (i.e., corrected for circulating triglycerides). Whether the observed pattern also holds for other tissues and in other taxa would deserve further research.

  18. Effects of various compounds on lipid peroxidation mediated by detergent-solubilized rat liver NADPH-cytochrome C reductase.

    PubMed

    Kamataki, T; Sugita, O; Naminohira, S; Kitagawa, H

    1978-12-01

    A reconstituted lipid peroxidation system containing NADPH-cytochrome c reductase isolated from detergent-solubilized rat liver microsomes was used to determine the effects of several compounds, including drugs, on the lipid peroxidation activity. EDTA and ferrous ion were essential requirements for reconstitution of the activity. The addition of 1,10-phenanthroline to the system containing both EDTA and ferrous ion further enhanced the activity. Pyrocatecol, thymol, p-aminophenol, imipramine, p-chloromercuribenzoate (PCMB) and alpha-tocopherol exhibited strong inhibition, aniline, N-monomethylaniline, aminopyrine, benzphetamine, SKF 525-A and NADP exhibited moderate inhibition, and phenol, benzoic acid, acetanilide and nicotinamide exhibited less or no inhibition at the concentrations lower than 1000 micron M. Metal ions such as Hg+, Hg2+, Co2+, Cu2+, Mn2+ and U6+ inhibited lipid peroxidation strongly. In addition, Cd2+, St2+ and Ca2+ exhibited less potent to moderate inhibition, and Ba2+ and Mg2+ were without effects on the activity. Among sulfhydryl compounds tested, dithiothreitol inhibited lipid peroxidation to a greater extent than did the other three compounds, glutathione, cysteine and mercaptoethanol.

  19. An in vitro model to test relative antioxidant potential: Ultraviolet-induced lipid peroxidation in liposomes

    SciTech Connect

    Pelle, E.; Maes, D.; Padulo, G.A.; Kim, E.K.; Smith, W.P. )

    1990-12-01

    Since antioxidants have been shown to play a major role in preventing some of the effects of aging and photoaging in skin, it is important to study this phenomenon in a controlled manner. This was accomplished by developing a simple and reliable in vitro technique to assay antioxidant efficacy. Inhibition of peroxidation by antioxidants was used as a measure of relative antioxidant potential. Liposomes, high in polyunsaturated fatty acids (PUFA), were dispersed in buffer and irradiated with ultraviolet (UV) light. Irradiated liposomes exhibited a significantly higher amount of hydroperoxides than liposomes containing antioxidants in a dose- and concentration-dependent manner. Lipid peroxidation was determined spectrophotometrically by an increase in thiobarbituric acid reacting substances. To further substantiate the production of lipid peroxides, gas chromatography was used to measure a decrease in PUFA substrate. In order of decreasing antioxidant effectiveness, the following results were found among lipophilic antioxidants: BHA greater than catechin greater than BHT greater than alpha-tocopherol greater than chlorogenic acid. Among hydrophilic antioxidants, ascorbic acid and dithiothreitol were effective while glutathione was ineffective. In addition, ascorbic acid was observed to act synergistically with alpha-tocopherol, which is in agreement with other published reports on the interaction of these two antioxidants. Although peroxyl radical scavengers seem to be at a selective advantage in this liposomal/UV system, these results demonstrate the validity of this technique as an assay for measuring an antioxidant's potential to inhibit UV-induced peroxidation.

  20. Prolongation of the lag time preceding peroxidation of serum lipids: a measure of antioxidant capacity.

    PubMed

    Pinchuk, Ilya; Lichtenberg, Dov

    2015-01-01

    Antioxidants inhibit oxidation processes and by this affect many biological processes. This, in turn, promotes continuing efforts to synthesize new efficient antioxidants and discover compounds of natural origin capable of preventing peroxidation. Although many assays have been developed to evaluate antioxidants, the search for improved protocols is still actual. The presented protocol is based on the effect of antioxidant on the kinetics of peroxidation of lipids in human blood serum. Specifically, we evaluate the capacity of antioxidant by the relative prolongation of lag phase (delay) of copper-induced peroxidation of lipids in unfractionated serum. The main advantage of the assay is that it implements inhibition of peroxidation in physiologically relevant system. We propose expressing the results of the assay either in terms of the relative prolongation of the lag per 1 μM of antioxidant or as the concentration of antioxidant required to double the lag. To allow for comparing the results with those of other assays, these results may be normalized and expressed in terms of the unitless "TROLOX equivalents."

  1. Photolysis and membrane lipid peroxidation of human erythrocytes by m-chloroperbenzoic acid.

    PubMed

    Abou-Seif, M A; Elgendy, E M

    1998-09-14

    The aim of the present work was to investigate the biological hazard of photooxidation products of m-chloroperbenzoic acid (mCPBA), as a novel photo-sensitizer, on lysis and membrane lipid peroxidation of human red blood cells (RBC). The photohemolysis activity of mCPBA oxidative products was concentration- and exposure time-dependent. Ten minutes photoexposure time and 100 micromol/L of mCPBA concentration were optimum to study the effect of generated superoxide (O2.-) and hydroxyl (.OH) radicals on RBC. The hemolytic effect of mCPBA was highly significantly inhibited by formate (as an .OH radical scavenger) compared with the partial inhibition effect of SOD-like Cu(II) complex (as O2.- radical Scavenger). The MDA value (an end product of membrane lipid peroxidation of RBC) induced by mCPBA was highly significantly decreased by formate. The generation of O2.- radicals by mCPBA was also confirmed by the partial hemolytic effect of phenazine methosulfate (PMS., O2.- radical generation). The data suggest the molecular mechanism of the oxygen radical species (O2.- and .OH through the photosensitization reaction of mCPBA and explain that hydroxyl radicals (.OH) play an active role in the photohemolysis process and peroxidation of membrane lipids of human erythrocytes.

  2. Sesame lignans enhance antioxidant activity of vitamin E in lipid peroxidation systems.

    PubMed

    Ghafoorunissa; Hemalatha, S; Rao, M Vishnu Vardhana

    2004-07-01

    The antioxidant properties of sesame lignans (sesamol, sesamin and sesamolin) were evaluated in comparison to tocols (alpha- and gamma-tocopherols and alpha-tocotrienol) and butylated hydroxytoluene (BHT) using the following in vitro lipid peroxidation systems: (i) rat liver microsomes and cumene hydroperoxide (CumOOH)/Fe2+-ADP-NADPH (enzymatic) or (ii) rat liver mitochondria and Fe2+-ascorbate (nonenzymatic) systems. Sesamol containing a free phenolic group inhibited lipid peroxidation in both the systems whereas sesamin and sesamolin having methylenedioxy groups were effective only in the microsomal system. Since detoxifying enzymes are localized in microsomes, the inhibitory effects of sesamin and sesamolin observed in the microsomal system may be attributed to their metabolites. However, the inhibitory effects of lignans were lower than tocols and BHT. Combination of individual lignans and tocopherols (alpha, gamma) or alpha-tocotrienol showed higher inhibitory effects than the sum of individual inhibitions in CumOOH and Fe2+-ascorbate systems suggesting synergistic interactions. The time course of CumOOH-mediated lipid peroxidation showed a lag period and a decreased rate of thiobarbituric acid reactive product formation in the presence of individual lignans in combination with alpha-tocopherol suggesting recycling of alpha-tocopherol.

  3. Lipid peroxides as endogenous oxidants forming 8-oxo-guanosine and lipid-soluble antioxidants as suppressing agents.

    PubMed

    Kanazawa, Kazuki; Sakamoto, Miku; Kanazawa, Ko; Ishigaki, Yoriko; Aihara, Yoshiko; Hashimoto, Takashi; Mizuno, Masashi

    2016-07-01

    The oxidation of guanosine to 8-oxo-2'-deoxyguanosine (8-oxo-dG) in DNA is closely associated with induction of various diseases, but the endogenous oxidant species involved remains unclear. Hydrogen peroxides (H2O2) have been considered to be the oxidant, while lipid peroxides are another possible oxidant because generated easily in bio-membranes surrounding DNA. The oxidant potency was compared between lipid peroxides and H2O2. Linoleic acid hydroperoxides (LOOH) formed 8-oxo-dG at a higher level than H2O2 in guanosine or double-stranded DNA. In the presence of a physiological concentration of Fe(2+) to produce hydroxyl radicals, LOOH was also a stronger oxidant. In a lipid micelle, LOOH markedly produced 8-oxo-dG at a concentration one-tenth of that of H2O2. Upon adding to rat hepatic mitochondria, phosphatidylcholine hydroperoxides produced 8-oxo-dG abundantly. Employing HepG2 cells after pretreated with glutathione peroxidase inhibitor, LOOH formed 8-oxo-dG more abundantly than H2O2. Then, antioxidants to suppress the 8-oxo-dG formation were examined, when the nuclei of pre-incubated HepG2 with antioxidants were exposed to LOOH. Water-soluble ascorbic acid, trolox, and N-acetyl cysteine showed no or weak antioxidant potency, while lipid-soluble 2,6-dipalmitoyl ascorbic acid, α-tocopherol, and lipid-soluble phytochemicals exhibited stronger potency. The present study shows preferential formation of 8-oxo-dG upon LOOH and the inhibition by lipid-soluble antioxidants.

  4. Lipid peroxides as endogenous oxidants forming 8-oxo-guanosine and lipid-soluble antioxidants as suppressing agents

    PubMed Central

    Kanazawa, Kazuki; Sakamoto, Miku; Kanazawa, Ko; Ishigaki, Yoriko; Aihara, Yoshiko; Hashimoto, Takashi; Mizuno, Masashi

    2016-01-01

    The oxidation of guanosine to 8-oxo-2'-deoxyguanosine (8-oxo-dG) in DNA is closely associated with induction of various diseases, but the endogenous oxidant species involved remains unclear. Hydrogen peroxides (H2O2) have been considered to be the oxidant, while lipid peroxides are another possible oxidant because generated easily in bio-membranes surrounding DNA. The oxidant potency was compared between lipid peroxides and H2O2. Linoleic acid hydroperoxides (LOOH) formed 8-oxo-dG at a higher level than H2O2 in guanosine or double-stranded DNA. In the presence of a physiological concentration of Fe2+ to produce hydroxyl radicals, LOOH was also a stronger oxidant. In a lipid micelle, LOOH markedly produced 8-oxo-dG at a concentration one-tenth of that of H2O2. Upon adding to rat hepatic mitochondria, phosphatidylcholine hydroperoxides produced 8-oxo-dG abundantly. Employing HepG2 cells after pretreated with glutathione peroxidase inhibitor, LOOH formed 8-oxo-dG more abundantly than H2O2. Then, antioxidants to suppress the 8-oxo-dG formation were examined, when the nuclei of pre-incubated HepG2 with antioxidants were exposed to LOOH. Water-soluble ascorbic acid, trolox, and N-acetyl cysteine showed no or weak antioxidant potency, while lipid-soluble 2,6-dipalmitoyl ascorbic acid, α-tocopherol, and lipid-soluble phytochemicals exhibited stronger potency. The present study shows preferential formation of 8-oxo-dG upon LOOH and the inhibition by lipid-soluble antioxidants. PMID:27499574

  5. Nonthermal dielectric-barrier discharge plasma-induced inactivation involves oxidative DNA damage and membrane lipid peroxidation in Escherichia coli.

    PubMed

    Joshi, Suresh G; Cooper, Moogega; Yost, Adam; Paff, Michelle; Ercan, Utku K; Fridman, Gregory; Friedman, Gary; Fridman, Alexander; Brooks, Ari D

    2011-03-01

    Oxidative stress leads to membrane lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves membrane lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for membrane lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.

  6. Reconstitution studies on the involvement of radiation-induced lipid peroxidation in damage to membrane enzymes.

    PubMed

    Yukawa, O; Nagatsuka, S; Nakazawa, T

    1983-04-01

    The effect of radiation on the drug-metabolizing enzyme system of microsomes, reconstituted with liposomes of microsomal phospholipids, NADPH-cytochrome P-450 reductase and cytochrome P-450, was examined to elucidate the role of lipid peroxidation of membranes in radiation-induced damage to membrane-bound enzymes. The reconstituted system of non-irradiated enzymes with irradiated liposomes showed a low activity of hexobarbital hydroxylation, whereas irradiated enzymes combined with non-irradiated liposomes exhibited an activity equal to that of unirradiated controls. Irradiation of liposomes caused a decrease in cytochrome P-450 content by destruction of the haem of cytochrome P-450 and also inhibited the binding capacity of cytochrome P-450 for hexobarbital. The relationship between radiation-induced lipid peroxidation and membrane-bound enzymes is discussed.

  7. Enzyme activity alteration by cadmium administration to rats: the possibility of iron involvement in lipid peroxidation.

    PubMed

    Casalino, E; Sblano, C; Landriscina, C

    1997-10-15

    The specific activities of D-3-hydroxybutyrate dehydrogenase (BDH) and glutamate dehydrogenase (GDH) are reduced in the liver and kidney of rats intoxicated with 2.5 mg Cd/kg body wt and sacrificed after 24 h; conversely ketone-body concentration is strongly increased in both of these organs and blood. In the same animals a great stimulation of antioxidant enzymes glutathione reductase and glutathione peroxidase occurs. The prooxidant state induced by cadmium in liver mitochondria and microsomes is unaffected by superoxide dismutase, catalase, or mannitol, whereas it is completely blocked by vitamin E thus excluding the involvement of reactive oxygen species in this process. The mechanism by which cadmium induces lipid peroxidation has been investigated by measuring the effect of this metal on liposomes. Ninety-minute treatment of liposomes with CdCl2 does not induce any lipid peroxidation. In contrast, Fe2+ ions under the same conditions cause strong liposome peroxidation. It has also been observed that cadmium promotes a time-dependent iron release from biological membranes. When lipid peroxidation is induced by a low concentration (5 microM) of FeCl2, in place of CdCl2, the characteristics of this process and the sensitivity to the various antioxidants used are similar to those observed with Cd. From these results we conclude that the prooxidative effect of cadmium is an indirect one since it is mediated by iron. With regard to the inhibitory effect on BDH and GDH following cadmium intoxication, it does not appear to be imputable to lipid peroxidation since in vitro investigations indicate that the presence of vitamin E does not remove the inhibition at all.

  8. CALCIUM-INDUCED LIPID PEROXIDATION IS MEDIATED BY RHODNIUS HEME-BINDING PROTEIN (RHBP) AND PREVENTED BY VITELLIN.

    PubMed

    Paes, Marcia C; Silveira, Alan B; Ventura-Martins, Guilherme; Luciano, Monalisa; Coelho, Marsen G P; Todeschini, Adriane R; Bianconi, M Lucia; Atella, Georgia C; Silva-Neto, Mário A C

    2015-10-01

    Lipid peroxidation is promoted by the quasi-lipoxygenase (QL) activity of heme proteins and enhanced by the presence of free calcium. Unlike mammalian plasma, the hemolymph of Rhodnius prolixus, a vector of Chagas disease, contains both a free heme-binding protein (RHBP) and circulating lipoproteins. RHBP binds and prevents the heme groups of the proteins from participating in lipid peroxidation reactions. Herein, we show that despite being bound to RHBP, heme groups promote lipid peroxidation through a calcium-dependent QL reaction. This reaction is readily inhibited by the presence of ethylene glycol tetraacetic acid (EGTA), the antioxidant butylated hydroxytoluene or micromolar levels of the main yolk phosphoprotein vitellin (Vt). The inhibition of lipid peroxidation is eliminated by the in vitro dephosphorylation of Vt, indicating that this reaction depends on the interaction of free calcium ions with negatively charged phosphoamino acids. Our results demonstrate that calcium chelation mediated by phosphoproteins occurs via an antioxidant mechanism that protects living organisms from lipid peroxidation.

  9. Lipid peroxidation and cyclooxygenase enzyme inhibitory activities of acidic aqueous extracts of some dietary supplements.

    PubMed

    Raman, Priyadarshini; Dewitt, David L; Nair, Muraleedharan G

    2008-02-01

    The botanical supplement market is growing at a fast pace with more and more people resorting to them for maintaining good health. Echinacea, garlic, ginkgo, ginseng, Siberian ginseng, grape seed extract, kava kava, saw palmetto and St John's wort are some of the popular supplements used for a variety of health benefits. These supplements are associated with various product claims, which suggest that they possess cyclooxygenase (COX) enzyme and lipid s inhibitory activities. COX enzymes are found to be at elevated levels in inflamed and cancerous cells. To test some of the product claims, selected supplements were analysed for their ability to inhibit COX-1 and -2 enzymes and lipid peroxidation in vitro. The supplements were extracted with acidified water (pH 2) at 37 degrees C to simulate the gastric environment. The supplements tested demonstrated varying degrees of COX enzyme inhibition (5-85% for COX-1 and 13-28% for COX-2). Interestingly, extracts of garlic (Meijer), ginkgo (Solaray), ginseng (Nature's Way), Siberian ginseng (GNC, Nutrilite, Solaray, Natrol), kava kava (GNC, Sundown, Solaray) and St John's wort (Nutrilite) selectively inhibited COX-2 enzyme. These supplements also inhibited lipid peroxidation in vitro (5-99%). The results indicated that the consumption of these botanical supplements studied possess health benefits.

  10. Ultraviolet- and sunlight-induced lipid peroxidation in liposomal membrane

    SciTech Connect

    Mandal, T.K.; Chatterjee, S.N.

    1980-08-01

    Ultraviolet radiation and sunlight caused lipid peroxidation in the liposomal membrane (as detected by measurement of the oxidation index, A/sub 233//A/sub 215/, and the amount of malondialdehyde formed) and made the membrane leaky (as revealed by the release of the trapped chromate anions). The oxidation index and the formation of malondialdehyde increased linearly with increasing dose of radiation and depended significantly on the dose rate. The effects were smaller in liposomes derived from Vibrio cholerae phospholipid than in those derived from egg lecithin. The effects of the radiation dose and dose rate on hemolysis and peroxidation (MDA formation) of the erythrocyte membrane followed a similar pattern. A direct correlation between the percentage leakage of chromate (Y) and the oxidation index (X) of the liposomal system was obtained as Y = 236.5 x X.

  11. Lycopene control of benzophenone-sensitized lipid peroxidation

    NASA Astrophysics Data System (ADS)

    Cvetković, Dragan; Marković, Dejan

    2012-05-01

    Lycopene antioxidant activity in the presence of two different mixtures of phospholipids in hexane solution, under continuous regime of UV-irradiation from three different ranges (UV-A, UV-B, and UV-C) has been evaluated in this work. Lycopene expected role was to control lipid peroxidation, by scavenging free radicals generated by UV-irradiation, in the presence and in the absence of selected photosensitizer, benzophenone. This work shows that lycopene undergoes to UV-induced destruction (bleaching), highly dependent on the incident photons energy input, more expressed in the presence than in the absence of benzophenone. The further increase ("excess") of its bleaching is undoubtedly related to the further increase of its antioxidant activity in the presence of benzophenone, having the same cause: increase of (phospholipids peroxidation) chain-breaking activities.

  12. Lipid peroxidation is increased in tears from the elderly.

    PubMed

    Benlloch-Navarro, Soledad; Franco, Ilenia; Sánchez-Vallejo, Violeta; Silvestre, Dolores; Romero, Francisco Javier; Miranda, María

    2013-10-01

    We describe a procedure in which tears, obtained from Schirmer strips, are used to measure a marker of lipid peroxidation, malondialdehyde (MDA). We also compared the levels of proteins and MDA in tears from two groups of people: young adults (18-30 years old) and elderly adults (65-85 years old), because the data related to total protein concentration of human tears vary widely and because the majority of people over the age of 65 experience some symptoms of dry eyes and this condition has been recognized as an oxidative stress-induced disease. Our results show a significant difference in the protein concentration of the tears taken from the two age categories, younger adults (18-30 years old) and older adults (65-85 years old). Herein, we report for the first time an increase in MDA concentrations determined by HPLC in human tears based on age. It is possible that alterations in the tear lipid layer may lead to an increase in lipid peroxidation. Further studies are needed to understand the nature and function of tear film and stability in order to obtain new methods to analyze tears in patients with different diseases. In this sense, it would be interesting to compare MDA concentration in tears from control subjects and from people with meibomian gland dysfunction. Copyright © 2013 Elsevier Ltd. All rights reserved.

  13. Comparison between in vitro lipid peroxidation in fresh sheep platelets and peroxidative processes during sheep platelet ageing under storage at 4 degrees C.

    PubMed

    Martín-Valmaseda, E M; Sánchez-Yagüe, J; Rodríguez, M C; Gómez, F P; Llanillo, M

    1999-07-15

    Incubation of sheep platelet crude membranes with xanthine oxidase (XO)/hypoxanthine/Fe(2+)-ADP revealed: (i) a fast peroxidative response - with a maximal linear rate of 14 nmol malondialdehyde (MDA) equivalents/mg protein, as evidenced by the thiobarbituric acid test - and a decrease in the polyunsaturated fatty acid (PUFA) content of the platelet crude membranes; (ii) a decrease in the lipid fluidity in the deep lipid core of the membranes but not at the membrane surface; (iii) a dramatic inhibitory effect on glucose 6-phosphatase (Glc-6-Pase) but not on acetylcholinesterase activity. Platelets were also aged by storage at 4 degrees C in their own plasma or in Seto additive solution. In these media, platelet aggregates were visible and the effects on platelet phospholipids, PUFA, lipid extract fluorescence, crude membrane fluidity and membrane-bound enzyme activities were assessed for comparison with those observed in in vitro lipid peroxidation. The sensitivity of membranes from stored platelets to lipid peroxidation was also assessed. Storage of platelets in plasma for 5 days was associated with different changes in their crude membranes such as decreases in arachidonic acid contents, the decrease not being avoided by the presence of phospholipase A(2) inhibitors, increases in MDA equivalents, conjugated dienes and lipid extract fluorescence, decreases in the amounts of MDA equivalents formed by platelet crude membranes treated with the oxidizing agents, changes in membrane fluidity and inhibition of Glc-6-Pase. All these alterations were less pronounced or even abolished after platelet storage in Seto. These findings suggest that platelet lipid peroxidation due to XO/hypoxanthine/Fe(2+)-ADP and platelet membrane alterations observed after platelet ageing under storage at 4 degrees C share common features. Also, as regards the prevention of peroxidative processes, Seto solution permits better storage of sheep platelets than plasma.

  14. Tyrosyl radical generated by myeloperoxidase is a physiological catalyst for the initiation of lipid peroxidation in low density lipoprotein.

    PubMed

    Savenkova, M L; Mueller, D M; Heinecke, J W

    1994-08-12

    Myeloperoxidase, a heme protein secreted by activated phagocytes, is expressed in human atherosclerotic lesions. The enzyme uses H2O2 generated by the cells to oxidize L-tyrosine to tyrosyl radical, a catalyst for protein dityrosine synthesis. We have explored the possibility that tyrosyl radical initiates lipid peroxidation, which may be of pivotal importance in transforming low density lipoprotein (LDL) into atherogenic particles. Exposure of LDL to L-tyrosine and activated human neutrophils caused peroxidation of LDL lipids. LDL oxidation required L-tyrosine but was independent of free metal ions; catalase and heme poisons were inhibitory. Incubation of LDL with L-tyrosine, myeloperoxidase, and H2O2 likewise caused lipid peroxidation, and this reaction was inhibited by heme poisons and catalase. Replacement of L-tyrosine with O-methyltyrosine, which cannot form tyrosyl radical, inhibited LDL oxidation by both activated neutrophils and myeloperoxidase. The antioxidants ascorbate and probucol, but not vitamin E, inhibited LDL oxidation by myeloperoxidase, H2O2, and L-tyrosine. Ascorbate blocked dityrosine synthesis, while probucol scavenged chain-propagating peroxyl radicals in the lipid phase of LDL. These results indicate that tyrosyl radical stimulates LDL lipid peroxidation. In striking contrast to other cell-mediated mechanisms for LDL oxidation, the myeloperoxidase-catalyzed reaction is independent of free metal ions. This raises the possibility that tyrosyl radical generated by myeloperoxidase is of physiological importance in making LDL atherogenic.

  15. Lipid peroxidation induced by cercosporin as a possible determinant of its toxicity.

    PubMed

    Cavallini, L; Bindoli, A; Macrì, F; Vianello, A

    1979-12-01

    The photodynamic action of cercosporin was assayed in various kinds of natural and artificial membranes. Cerosporin induces lipoperoxidation of liposomes, rat liver and pea internode mitochondria and microsomes, estimated both as malondialdehyde (MDA) formation and O2 consumption. Cercosporin-induced lipoperoxidation is inhibited by either singlet oxygen quenchers, free radical trapping agents or EDTA. Superoxide anion (O2-), hydrogen peroxide and hydroxyl radicals (.OH) are not involved in the activity of cercosporin. In addition cercosporin, by chelating iron, lowers the lipoperoxidation induced by such a metal. Therefore cercosporin stimulates, through singlet oxygen production, the hydroperoxide formation but, at the same time, it inhibits the continuation of the iron-mediated free radical chain. The present results suggest that cellular lipid peroxidation has a certain relevance to toxic activity of cercosporin.

  16. Methods to create thermally oxidized lipids and comparison of analytical procedures to characterize peroxidation.

    PubMed

    Liu, P; Kerr, B J; Chen, C; Weber, T E; Johnston, L J; Shurson, G C

    2014-07-01

    The objective of this experiment was to evaluate peroxidation in 4 lipids, each with 3 levels of peroxidation. Lipid sources were corn oil (CN), canola oil (CA), poultry fat, and tallow. Peroxidation levels were original lipids (OL), slow-oxidized lipids (SO), and rapid-oxidized lipids (RO). To produce peroxidized lipids, OL were either heated at 95°C for 72 h to produce SO or heated at 185°C for 7 h to produce RO. Five indicative measurements (peroxide value [PV], p-anisidine value [AnV], thiobarbituric acid reactive substances [TBARS] concentration, hexanal concentration, 4-hydroxynonenal [HNE] concentration, and 2,4-decadienal [DDE]) and 2 predictive tests (active oxygen method [AOM] stability and oxidative stability index [OSI]) were performed to quantify the level of oxidation of the subsequent 12 lipids with varying levels of peroxidation. Analysis showed that a high PV accurately indicated the high level of lipid peroxidation, but a moderate or low PV may be misleading due to the unstable characteristics of hydroperoxides as indicated by the unchanged PV of rapidly oxidized CN and CA compared to their original state (OL). However, additional tests, which measure secondary peroxidation products such as AnV, TBARS, hexanal, HNE, and DDE, may provide a better indication of lipid peroxidation than PV for lipids subjected to a high level of peroxidation. Similar to PV analysis, these tests may also not provide irrefutable information regarding the extent of peroxidation because of the volatile characteristics of secondary peroxidation products and the changing stage of lipid peroxidation. For the predictive tests, AOM accurately reflected the increased lipid peroxidation caused by SO and RO as indicated by the increased AOM value in CN and CA but not in poultry fat and tallow, which indicated a potential disadvantage of the AOM test. Oxidative stability index successfully showed the increased lipid peroxidation caused by SO and RO in all lipids, but it too may

  17. Lipid peroxidation of plants under microgravity and its simulation.

    PubMed

    Zhadko, S I; Polulyakh YuA; Vorobyeva, T V; Baraboy, V A

    1994-01-01

    In series of space experiments aboard the biosatellites "Cosmos 1887", "Bion 9", the orbital stations "Salut", "Mir" and under clinostating, changes of lipid peroxidation (LPO) and antioxidation activity (AOA) of Chlorella, Haplopappus tissue culture, wheat and pea roots were determined. The changes had a complex fluctuation character; three steps of response were established: LPO decreasing accompanied by AOA increase; stabilization LPO <==> AOA balance; secondary LPO activation. Most early and highly amplitude decreasing of LPO were fixed in mitochondria. The rate of response have been increased on multicellular level of plants organization.

  18. Lipid peroxidation of plants under microgravity and its simulation

    NASA Astrophysics Data System (ADS)

    Zhadko, S. I.; Polulyakh, Yu. A.; Vorobyeva, T. V.; Baraboy, V. A.

    1994-08-01

    In series of space experiments a board the biosatellites ``Cosmos 1887'', ``Bion 9'', the orbital stations ``Salut'', ``Mir'' and under clinostating, changes of lipid peroxidation (LPO) and antioxidation activity (AOA) of Chlorella, Haplopappus tissue culture, wheat and pea roots were determined. The changes had a complex fluctuation character three steps of response were established; LPO decreasing accompanied by AOA increase; stabilization LPO⇄AOA balance; secondary LPO activation. Most early and highly amplitude decreasing of LPO were fixed in mitochondria. The rate of response have been increased on multicellular level of plants organization.

  19. 4-Hydroxy-nonenal—A Bioactive Lipid Peroxidation Product †

    PubMed Central

    Schaur, Rudolf J.; Siems, Werner; Bresgen, Nikolaus; Eckl, Peter M.

    2015-01-01

    This review on recent research advances of the lipid peroxidation product 4-hydroxy-nonenal (HNE) has four major topics: I. the formation of HNE in various organs and tissues, II. the diverse biochemical reactions with Michael adduct formation as the most prominent one, III. the endogenous targets of HNE, primarily peptides and proteins (here the mechanisms of covalent adduct formation are described and the (patho-) physiological consequences discussed), and IV. the metabolism of HNE leading to a great number of degradation products, some of which are excreted in urine and may serve as non-invasive biomarkers of oxidative stress. PMID:26437435

  20. Effect of acylethanolamides on lipid peroxidation and paraoxonase activity.

    PubMed

    Zolese, Giovanna; Bacchetti, Tiziana; Masciangelo, Simona; Ragni, Letizia; Ambrosi, Simona; Ambrosini, Annarina; Marini, Milvia; Ferretti, Gianna

    2008-01-01

    N-acylethanolamides (NAEs) are hydrophobic molecules synthesized in many tissues. An increase in the plasma levels of NAEs has been observed in human diseases. Previous studies have suggested that NAEs could exert a protective effect against oxidative stress. Aim of the study was to investigate whether NAEs (oleoylethanolamide, palmitoylethanolamide and anandamide), differing for acyl chain length and unsaturation, exert a protective role against plasma lipid peroxidation triggered by incubation with Cu2+2 or AAPH (2,2'-azobis(2-amidinopropane) dihydrochloride). Moreover, we investigated the effect of NAEs on the activity of HDL-associated paraoxonase (PON1), an enzyme involved in the antioxidant end anti-inflammatory role of human high density lipoproteins (HDL). The results demonstrated that the NAEs protect plasma lipids and PON1 activity against AAPH and/or copper-induced oxidation.

  1. Glutathione delays varies as-tocopherol oxidation and subsequent lipid peroxidation in rat liver microsomes

    SciTech Connect

    Robey, S.; Mavis, R.

    1986-05-01

    A method has been developed for in vitro trace radiolabeling of rat liver microsomes with /sup 3/H-..cap alpha..-tocopherol (..cap alpha..T*) which allows virtually complete oxidation of the ..cap alpha..T* under oxidizing conditions. The supernatant of a 16,000 xg centrifugation of homogenized rat liver, containing the cytosolic rat liver vitamin E (VE) transfer protein, was incubated with an ethanolic solution of ..cap alpha..T* for 10 minutes at 37/sup 0/C. Labeled microsomes were collected in the washed 100,000 xg pellet. Microsomes were then incubated with 30 ..mu..M Fe/sup 2 +/ in an NADPH-generating system, and both production of malondialdehyde (MDA) (a product of lipid peroxidation) and oxidation of ..cap alpha..T* were monitored over a time course in the presence and absence of glutathione (GSH). The results indicate virtually complete oxidation of ..cap alpha..T* precedes significant membrane lipid peroxidation, and that addition of 5 mM GSH delays both ..cap alpha..T* oxidation and subsequent MDA production. This suggests that the previously observed VE-dependent heat labile inhibition of microsomal lipid peroxidation by GSH involves maintaining membrane levels of ..cap alpha..-tocopherol.

  2. In vitro effects of alloxan/copper combinations on lipid peroxidation, protein oxidation and antioxidant enzymes.

    PubMed

    Alexandrova, Albena; Petrov, L; Kessiova, Mila; Kirkova, Margarita

    2007-12-01

    The in vitro effects of alloxan and the product of its reduction dialuric acid (alone or in combination with copper ions) on lipid peroxidation, carbonyl content, GSH level and antioxidant enzyme activities in rat liver and kidney have been studied. The effects of Cu2+/alloxan and Cu2+/dialuric acid were compared with those of Fe3+/alloxan and Fe3+/dialuric acid. Unlike alloxan, dialuric acid increased liver and kidney lipid peroxidation; similar effects were registered in the presence of Fe3+. In the presence of Cu2+/dialuric acid, the lipid peroxidation was strongly inhibited and vice versa--the liver protein oxidation was increased. Alloxan and dialuric acid, as well as their combinations with Fe3+ had no effect on the total GSH level. Both substances did not affect the Cu2+-induced changes in GSH level, glucose-6-phosphate dehydrogenase and gluthatione reductase activities. In contrast, Cu2+ had no effect on dialuric-acid induced changes in gluthatione peroxidase and superoxide dismutase activities. The present in vitro results, concerning the metal dependence of the effects of alloxan and dialuric acid, are a premise for in vivo study of alloxan effects in metal-loaded animals.

  3. Effects of metal ions on lipid peroxidation in cultured rat hepatocytes loaded with alpha-linolenic acid.

    PubMed

    Furono, K; Suetsuga, T; Sugihara, N

    1996-06-07

    We investigated the ability of various redox-active metal ions to induce lipid peroxidation in normal and alpha-linolenic acid-loaded (LNA-loaded) cultured rat hepatocytes. Lipid peroxidation was estimated by the accumulation of malondialdehyde (MDA) in the culture medium. At low concentrations induction was highest with ferrous ions (Fe), whereas at high concentrations, vanadium (V) and copper ions (Cu) had the greatest effect on both groups of hepatocytes. With any one of the three metal ions, the extent of lipid peroxidation in LNA-loaded hepatocytes was several times greater compared to normal cells. In addition, upon the addition of Fe or V, LNA-loaded hepatocytes were injured whereas normal cells were not. The addition of Cu caused substantial cell injury in normal hepatocytes, and even greater injury in LNA-loaded cells. The prevention of lipid peroxidation in LNA-loaded hepatocytes by addition of an antioxidant like N,N'-diphenyl-p-phenylene-diamine (DPPD) almost completely prevented Fe- and V-induced cell injury, and reduced Cu-induced cell injury. alpha-Tocopherol behaved in a way similar to but less effective than DPPD. .OH radical scavengers such as mannitol and dimethyl sulfoxide (DMSO) had no effect on lipid peroxidation induced by any metal ions in LNA-loaded hepatocytes. Addition of cadmium ions (Cd), which required the lowest concentration to cause cell injury, induced a slight increase in lipid peroxidation in normal hepatocytes, but did not induce lipid peroxidation to the same extent as seen in LNA-loaded cells treated with any of the three metal ions already mentioned. The inhibition of lipid peroxidation by DPPD scarcely protected LNA-loaded hepatocytes from Cd-induced cell injury. None of the other metal ions including aluminum (Al), chromium (Cr), manganese (Mn), nickel (Ni), lead (Pb), and tin (Sn) ions, effectively induced lipid peroxidation in either group of hepatocytes, except cobalt ions (Co), which had a peroxidative effect in LNA

  4. Antioxidant action of Moringa oleifera Lam. (drumstick) against antitubercular drugs induced lipid peroxidation in rats.

    PubMed

    Ashok Kumar, N; Pari, L

    2003-01-01

    The protective effect of Moringa oleifera Lam. (Moringaceae) on hepatic marker enzymes, lipid peroxidation, and antioxidants was investigated during antitubercular drug (isoniazid, rifampicin, and pyrazinamide)-induced toxicity in rats. Enhanced hepatic marker enzymes and lipid peroxidation of antitubercular drug treatment was accompanied by a significant decrease in the levels of vitamin C, reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase. Administration of Moringa oleifera extract and silymarin significantly decreased hepatic marker enzymes and lipid peroxidation with a simultaneous increase in the level of antioxidants. We speculate that Moringa oleifera extract exerts its protective effects by decreasing liver lipid peroxides and enhancing antioxidants.

  5. Peroxidation of the dried thin film of lipid by high-energy alpha particles from a cyclotron

    SciTech Connect

    Agarwal, S.; Chatterjee, S.N.

    1984-11-01

    High-energy ..cap alpha.. particles produced a dose-dependent linear increase in different lipid peroxidation products (e.g., malondialdehyde (MDA), conjugated dienes, and hydroperoxides) in the dried thin film state. An inverse dose-rate effect was observed when the dose rate was varied by changing either the ..cap alpha..-particle fluence rate or the ..cap alpha..-particle energy. The antioxidants ..cap alpha..-tocopherol and butylated hydroxytoluene (BHT) suppressed the ..cap alpha..-particle-induced lipid peroxidation in the dried thin film state, and in this respect ..cap alpha..-tocopherol was found superior to BHT. It was found that ..cap alpha..-tocopherol was equally efficient in inhibiting lipid peroxidations by ..cap alpha.. particles and ultraviolet light.

  6. Photoirradiation of representative polycyclic aromatic hydrocarbons and twelve isomeric methylbenz[a]anthracene with UVA light: formation of lipid peroxidation.

    PubMed

    Xia, Qingsu; Chou, Ming W; Yin, Jun J; Howard, Paul C; Yu, Hongtao; Fu, Peter P

    2006-05-01

    Polycyclic aromatic hydrocarbons (PAHs) are widespread genotoxic environmental pollutants, which require metabolic activation in order to exert biological activities, including mutagenicity and carcinogenicity. Photoactivation is another activation pathway that can lead to PAH genotoxicity. In this paper, we demonstrate that photoirradiation of a series of representative PAHs, with and without bearing a methyl substituent, with UVA light in the presence of methyl linoleate resulted in the formation of methyl linoleate hydroperoxides (a lipid peroxide). The lipid peroxide formation was inhibited by dithiothreitol (DTT) (free radical scavenger), NaN3 (singlet oxygen and free radical scavenger), and superoxide dismutase (SOD) (superoxide scavenger), but was enhanced by the presence of deuterium oxide (D2O) (extends singlet oxygen lifetime). These results suggest that photoirradiation of PAHs by UVA light generates reactive oxygen species (ROS), which induce lipid peroxidation.

  7. Inhibition of porcine kidney betaine aldehyde dehydrogenase by hydrogen peroxide.

    PubMed

    Rosas-Rodríguez, Jesús A; Figueroa-Soto, Ciria G; Valenzuela-Soto, Elisa M

    2010-01-01

    Renal hyperosmotic conditions may produce reactive oxygen species, which could have a deleterious effect on the enzymes involved in osmoregulation. Hydrogen peroxide was used to provoke oxidative stress in the environment of betaine aldehyde dehydrogenase in vitro. Enzyme activity was reduced as hydrogen peroxide concentration was increased. Over 50% of the enzyme activity was lost at 100 μM hydrogen peroxide at two temperatures tested. At pH 8.0, under physiological ionic strength conditions, peroxide inhibited the enzyme. Initial velocity assays of betaine aldehyde dehydrogenase in the presence of hydrogen peroxide (0-200 μM) showed noncompetitive inhibition with respect to NAD(+) or to betaine aldehyde at saturating concentrations of the other substrate at pH 7.0 or 8.0. Inhibition data showed that apparent V(max) decreased 40% and 26% under betaine aldehyde and NAD(+) saturating concentrations at pH 8.0, while at pH 7.0 V(max) decreased 40% and 29% at betaine aldehyde and NAD(+) saturating concentrations. There was little change in apparent Km(NAD) at either pH, while Km(BA) increased at pH 7.0. K(i) values at pH 8 and 7 were calculated. Our results suggest that porcine kidney betaine aldehyde dehydrogenase could be inhibited by hydrogen peroxide in vivo, thus compromising the synthesis of glycine betaine.

  8. Lipid peroxidation in workers exposed to hexavalent chromium.

    PubMed

    Huang, Y L; Chen, C Y; Sheu, J Y; Chuang, I C; Pan, J H; Lin, T H

    1999-02-26

    The aim of this study was to investigate whether exposure to hexavalent chromium induces lipid peroxidation in human. This study involved 25 chrome-plating factory workers and a reference group of 28 control subjects. The whole-blood and urinary chromium concentrations were determined by graphite furnace atomic absorption spectrophotometry. Malondialdehyde (MDA), the product of lipid peroxidation, was determined by high-performance liquid chromatography, and the activities of protective enzymes were measured by ultraviolet-visible spectrophotometry. In the chrome-plating workers, the mean concentrations of chromium in blood and urine were 5.98 microg/L and 5.25 microg/g creatinine, respectively; the mean concentrations of MDA in blood and urine were 1.7 micromol/L and 2.24 micromol/g creatinine. The concentrations of both chromium and MDA in blood and urine were significantly higher in the chromium-exposed workers. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) were not markedly different between control and exposed workers. Data suggest that MDA may be used as a biomarker for occupational chromium exposure. Antioxidant enzymic activities are not a suitable marker for chromium exposure.

  9. [Study on lipid peroxidation of electrolyzing-aluminum workers].

    PubMed

    Guo, Zhiyong; Zhu, Qixing; Hu, Chuanlai; Yang, Yongjian

    2002-04-01

    In order to study the changes in lipid peroxidation level and anti-oxidase activity in electrolyzing-aluminum workers exposed to both aluminum and fluoride and to find out the sensitive biological monitoring indicators, 65 electrolyzing-aluminum workers are recruited as exposed group and 52 healthy workers as control group. Serum and urine aluminum and fluoride concentration, serum glutathione peroxidase(GSH-Px) activity, serum malonyl dialdehyde (MDA) concentration, whole blood superoxide dismutase(SOD) activity, serum cuprum and zinc concentration, and X-ray of skeleton are detected and taken. The results showed that aluminum and fluoride concentration in serum and urine increase, GSH-Px activity reduces, MDA concentration increases and SOD activity increases, cuprum concentration increases and zinc concentration reduces significantly (P < 0.001) in exposed group compared with those of control group. Both serum aluminum and fluoride concentration are correlated inversely with GSH-Px activity, and correlated with MDA concentration and SOD activity. It is suggested that serum aluminum and fluoride concentration can clearly reflect the loading capacity of body aluminum and fluoride. Occupational exposure to both aluminum and fluoride lead to rising of lipid peroxidation and abnormal metabolism of cuprum and zinc before changes in skeleton occurred. Serum MDA concentration and GSH-Px activity might be the potential early-stage indicators of biological surveillance for electrolyzing-aluminum workers' health. The increase of SOD activity may be a kind of body compensations.

  10. Oxidative and reductive metabolism of lipid-peroxidation derived carbonyls

    PubMed Central

    Singh, Mahavir; Kapoor, Aniruddh; Bhatnagar, Aruni

    2015-01-01

    Extensive research has shown that increased production of reactive oxygen species (ROS) results in tissue injury under a variety of pathological conditions and chronic degenerative diseases. While ROS are highly reactive and can incite significant injury, polyunsaturated lipids in membranes and lipoproteins are their main targets. ROS-triggered lipid peroxidation reactions generate a range of reactive carbonyl species (RCS), and these RCS spread and amplify ROS-related injury. Several RCS generated in oxidizing lipids, such as 4-hydroxy trans-2-nonenal (HNE), 4-oxo-2-(E)-nonenal (ONE), acrolein, malondialdehyde (MDA) and phospholipid aldehydes have been shown to be produced under conditions of oxidative stress and contribute to tissue injury and dysfunction by depleting glutathione and other reductants leading to the modification of proteins, lipids, and DNA. To prevent tissue injury, these RCS are metabolized by several oxidoreductases, including members of the aldo-keto reductase (AKR) superfamily, aldehyde dehydrogenases (ALDHs), and alcohol dehydrogenases (ADHs). Metabolism via these enzymes results in RCS inactivation and detoxification, although under some conditions, it can also lead to the generation of signaling molecules that trigger adaptive responses. Metabolic transformation and detoxification of RCS by oxidoreductases prevent indiscriminate ROS toxicity, while at the same time, preserving ROS signaling. A better understanding of RCS metabolism by oxidoreductases could lead to the development of novel therapeutic interventions to decrease oxidative injury in several disease states and to enhance resistance to ROS-induced toxicity. PMID:25559856

  11. Effect of N-acetylcysteine on blood and tissue lipid peroxidation in lipopolysaccharide-induced obstructive jaundice.

    PubMed

    Caglikulekci, Mehmet; Dirlik, Musa; Pata, Cengiz; Plasse, Marylene; Tamer, Lulufer; Ogetman, Zekai; Ercan, Bahadir

    2006-01-01

    In obstructive jaundice, free radical production is increased and antioxidative activity is reduced. N-Acetylcysteine (NAC) has a beneficial effect with anti-inflammatory and antioxidant activity, acting as a free radical scavenger. NAC inhibits inducible nitric oxide synthase, suppresses cytokine expression/release, and inhibits adhesion molecule expression and nuclear factor kappa B. The aim of this study was to investigate the effects of NAC on liver/renal tissue and serum lipid peroxidation in lipopolysaccharide (LPS)-induced obstructive jaundice. We randomized 60 rats into 6 groups: group 1, Sham; group 2, obstructive jaundice (OJ) induced after bile-duct ligation; group 3, OJ + NAC (100 mg kg- 1 subcutaneously); group 4, OJ + LPS (10 mg kg-1); group 5, OJ + NAC + LPS; and group 6, OJ + LPS + NAC. For each group, the biochemical markers of lipid peroxidation and the antioxidant products were measured in serum and liver/renal tissue after sacrifice. Almost all lipid peroxidation products levels were increased and antioxidant products levels were decreased in groups who received LPS (groups 4, 5, and 6), but the effect was less remarkable when NAC was administered before LPS (group 5). The same trend was seen for groups with OJ +/- LPS who did not received NAC or received it after induced toxemia (groups 2, 4, and 6) as compared to groups 1 and 3. Moreover, in the case of OJ + LPS, rats treated with NAC before LPS (group 5) had lower lipid peroxidation products levels and higher antioxidant products levels as compared to those who did not received NAC (group 4). This phenomenon was not reproducible with NAC administered after LPS (group 6). Thus, results of this study showed that NAC prevents the deleterious effects of LPS in obstructive jaundice by reducing lipid peroxidation in serum and liver/renal tissue if administered before LPS. Nonetheless, NAC failed to prevent the lipid peroxidation in the case of established endotoxemia in obstructive jaundice.

  12. Does mercury promote lipid peroxidation? An in vitro study concerning mercury, copper, and iron in peroxidation of low-density lipoprotein.

    PubMed

    Seppänen, Kari; Soininen, Pasi; Salonen, Jukka T; Lötjönen, Simo; Laatikainen, Reino

    2004-11-01

    In order to explore the observed association among mercury, atherosclerosis, and coronary heart disease, the effects of mercury, copper, and iron on the peroxidation of low-density lipoprotein (LDL) and on the enzymatic activities of glutathione peroxidase and myeloperoxidase were investigated in vitro. On the basis of our nuclear magnetic resonance (NMR) experiments, we conclude that mercury does not promote the direct nonenzymatic peroxidation of LDL, like copper and iron. In our enzyme measurements, mercury inhibited slightly myeloperoxidase, although not significantly in presence of LDL. Instead, inorganic mercury, but not methylmercury chloride, inhibited glutathione peroxidase effectively and copper even at 10 micromol/L, below physiological concentrations, doubled the inhibition rate. Copper and iron had no direct effect on glutathione peroxidase, but they both seem to activate production of HOCl by myeloperoxidase. We conclude here that, first, mercury and methylmercury do not promote direct lipid peroxidation, but that, second, a simultaneous exposure to high inorganic mercury, copper, and iron and low selenium concentrations can lead to a condition in which mercury promotes lipid peroxidations. This mechanism provides a plausible molecular-level explanation for the observed association between high body mercury content and atherosclerosis.

  13. Vanadate-induced toxicity towards isolated perfused rat livers: the role of lipid peroxidation.

    PubMed

    Younes, M; Strubelt, O

    1991-02-11

    The toxic potential of sodium orthovanadate towards isolated perfused rat livers was investigated at a dose of 2 mmol/l. In livers from fasted rats, vanadate led to a release of cytosolic (glutamate-pyruvate-transaminase (GPT) and lactate dehydrogenase (LDH] and mitochondrial (glutamate dehydrogenase (GLDH] enzymes, an accumulation of calcium in the liver, a marked depletion of hepatic glutathione and an enhanced release of it into the perfusate, as well as an augmented formation and release of thiobarbituric acid-reactive material by the liver. Furthermore, a marked inhibition of oxygen consumption was observed. Vanadate-induced vasoconstriction resulted in a progressive decrease in perfusate flow rate. Control experiments with similarly reduced flow rates led to a comparable reduction in oxygen consumption. GPT and LDH release and hepatic glutathione depletion were also evident, though to a lesser extent than in the presence of vanadate, but no increase in GLDH release, in tissue calcium content or TBA-reactive material in the liver or the perfusate were observed. Thus, indirect toxic effects due to a reduced flow rate contribute only partly to vanadate hepatotoxicity and do not affect mitochondrial integrity. Omission of calcium from the perfusate did not prevent hepatotoxic responses to vanadate, although less calcium was present in the treated livers than in the control organs, indicating that calcium influx is not involved in vanadate-induced hepatotoxicity in the intact organ, in contrast to isolated hepatocytes. Feeding the animals, resulting in an activation of anaerobic energy conservation reactions, strongly attenuated vanadate hepatotoxicity indicating that the energetic status of the liver is the main target of vanadate. Superoxide dismutase did not affect the hepatotoxic responses of livers from fasted rats towards vanadate, while allopurinol and deferrioxamine inhibited lipid peroxidation and hepatotoxicity due to vanadate. The strong correlation

  14. Tyrosine oxidation and nitration in transmembrane peptides is connected to lipid peroxidation.

    PubMed

    Bartesaghi, Silvina; Herrera, Daniel; Martinez, Débora M; Petruk, Ariel; Demicheli, Verónica; Trujillo, Madia; Martí, Marcelo A; Estrín, Darío A; Radi, Rafael

    2017-05-15

    Tyrosine nitration is an oxidative post-translational modification that can occur in proteins associated to hydrophobic bio-structures such as membranes and lipoproteins. In this work, we have studied tyrosine nitration in membranes using a model system consisting of phosphatidylcholine liposomes with pre-incorporated tyrosine-containing 23 amino acid transmembrane peptides. Tyrosine residues were located at positions 4, 8 or 12 of the amino terminal, resulting in different depths in the bilayer. Tyrosine nitration was accomplished by exposure to peroxynitrite and a peroxyl radical donor or hemin in the presence of nitrite. In egg yolk phosphatidylcholine liposomes, nitration was highest for the peptide with tyrosine at position 8 and dramatically increased as a function of oxygen levels. Molecular dynamics studies support that the proximity of the tyrosine phenolic ring to the linoleic acid peroxyl radicals contributes to the efficiency of tyrosine oxidation. In turn, α-tocopherol inhibited both lipid peroxidation and tyrosine nitration. The mechanism of tyrosine nitration involves a "connecting reaction" by which lipid peroxyl radicals oxidize tyrosine to tyrosyl radical and was fully recapitulated by computer-assisted kinetic simulations. Altogether, this work underscores unique characteristics of the tyrosine oxidation and nitration process in lipid-rich milieu that is fueled via the lipid peroxidation process. Copyright © 2017 Elsevier Inc. All rights reserved.

  15. Rat liver microsomal lipid peroxidation produced during the oxidative metabolism of ethacrynic acid.

    PubMed

    Yamamoto, K; Masubuchi, Y; Narimatsu, S; Kobayashi, S; Horie, T

    2001-04-01

    Thiobarbituric acid reactive substances (TBARS) were produced in rat liver microsomal suspension incubated with ethacrynic acid (loop diuretic drug) and NADPH. Two oxidative metabolites of ethacrynic acid with dicarboxylic acid and hydroxylated ethyl group, respectively, were formed in the reaction mixture. The oxidative metabolism of ethacrynic acid was inhibited by cytochrome P450 inhibitors. The formation of TBARS was remarkably depressed by inhibitors like diethyldithiocarbamate and disulfiram. These results indicate that lipid peroxidation occurred in rat liver microsomes through the oxidative metabolism of ethacrynic acid.

  16. The mechanism of Fe(2+)-initiated lipid peroxidation in liposomes: the dual function of ferrous ions, the roles of the pre-existing lipid peroxides and the lipid peroxyl radical.

    PubMed Central

    Tang, L; Zhang, Y; Qian, Z; Shen, X

    2000-01-01

    The mechanism of Fe(2+)-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe(2+) whenever the second dose of Fe(2+) was added, which indicates that Fe(2+) has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe(2+) could no longer initiate lipid peroxidation and the acceleration of Fe(2+) oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOO(.)), N,N'-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe(2+) oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOO(.) are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe(2+) and can be scavenged by its reaction with Fe(2+). Only when Fe(2+) is oxidized to such a degree that LOO(.) is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe(2+) with LOOH and LOO(.) into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe(2+)-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe(2+) to lipid and the required oxidation of Fe(2+). PMID:11062055

  17. The role of aldehyde oxidase in ethanol-induced hepatic lipid peroxidation in the rat.

    PubMed Central

    Shaw, S; Jayatilleke, E

    1990-01-01

    Hepatic lipid peroxidation has been implicated in the pathogenesis of alcohol-induced liver injury, but the mechanism(s) by which ethanol metabolism or resultant free radicals initiate lipid peroxidation is not fully defined. The role of the molybdenum-containing enzymes aldehyde oxidase and xanthine oxidase in the generation of such free radicals was investigated by measuring alkane production (lipoperoxidation products) in isolated rat hepatocytes during ethanol metabolism. Inhibition of aldehyde oxidase and xanthine oxidase (by feeding tungstate at 100 mg/day per kg) decreased alkane production (80-95%), whereas allopurinol (20 mg/kg by mouth), a marked inhibitor of xanthine oxidase, inhibited alkane production by only 35-50%. Addition of acetaldehyde (0-100 microM) (in the presence of 50 microM-4-methylpyrazole) increased alkane production in a dose-dependent manner (Km of aldehyde oxidase for acetaldehyde 1 mM); menadione, an inhibitor of aldehyde oxidase, virtually inhibited alkane production. Desferrioxamine (5-10 microM) completely abolished alkane production induced by both ethanol and acetaldehyde, indicating the importance of catalytic iron. Thus free radicals generated during the metabolism of acetaldehyde by aldehyde oxidase may be a fundamental mechanism in the initiation of alcohol-induced liver injury. PMID:2363695

  18. Lipid peroxidation by "free" iron ions and myoglobin as affected by dietary antioxidants in simulated gastric fluids.

    PubMed

    Lapidot, Tair; Granit, Rina; Kanner, Joseph

    2005-05-04

    Grilled red turkey muscle (Doner Kabab) is a real "fast food" containing approximately 200 microM hydroperoxides, homogenized in simulated gastric fluid and oxidized more rapidly at pH 3.0 than at pH 5.0, after 180 min, producing 1200 and 600 microM hydroperoxides, respectively. The effects of "free" iron ions and metmyoglobin, two potential catalyzers of lipid peroxidation in muscle foods, were evaluated for linoleic acid peroxidation at pH 3.0 of simulated gastric fluid. The prooxidant effects of free iron ions on linoleic acid peroxidation in simulated gastric fluid was evaluated in the presence of ascorbic acid. At low concentrations of ascorbic acid, the effects were prooxidative, which was reversed at high concentrations. In the presence of metmyoglobin, ascorbic acid with or without free iron enhanced the antioxidative effect. Lipid peroxidation by an iron-ascorbic acid system was inhibited totally by 250-500 microM catechin at pH 3.0. The catechin antioxidant effect was determined also in the iron-ascorbic acid system containing metmyoglobin. In this system, catechin totally inhibited lipid peroxidation at a concentration 20-fold lower than without metmyoglobin. The ability of catechin to inhibit lipid peroxidation was also determined at a low pH with beta-carotene as a sensitive target molecule for oxidation. The results show that a significant protection was achieved only with almost 100-fold higher antioxidant concentration. Polyphenols from different groups were determined for the antioxidant activity at pH 3.0. The results show a high antioxidant activity of polyphenols with orthodihydroxylated groups at the B ring, unsaturation, and the presence of a 4-oxo group in the heterocyclic ring, as demonstrated by quercetin.

  19. [Lipid peroxidation in microalgae cells under simulated microgravity].

    PubMed

    Li, Gen-bao; Wang, Gao-hong; Song, Li-rong; Liu, Yong-ding

    2002-08-01

    Objective. To provide direct evidences for effects of microgravity on structure and function of plasma membrane. Method. Malondialdehyde (MDA) content was examined on the basis of quantitative reaction of both MDA and thiobarbituric acid (TBA), and electrolyte leaking was determined with conductometer model DDS-11A. Result. Experiments showed that under simulated microgravity, lipid peroxidation and the content of MDA increased. Meanwhile, the membrane permeability increased in cells of two microalgae: Anabaena sp PCC7120 and Synechococcus 7942. Conclusion. Our results suggest that there is some commonness between microgravity stress and certain other environmental stresses. And cellular membrane might be the site of perception of gravity in unicells without special gravity sensitive structure, such as alga cells.

  20. Biomarkers of lipid peroxidation in Alzheimer disease (AD): an update.

    PubMed

    Bradley-Whitman, Melissa A; Lovell, Mark A

    2015-07-01

    Increasing evidence suggests that free radical-mediated oxidation of biological substrates is a key feature of Alzheimer's disease (AD) pathogenesis. While it has long been established that biomarkers of lipid peroxidation (LPO) are elevated in AD brain as well as ventricular CSF postmortem, more recent studies have demonstrated increased LPO biomarkers in postmortem brain from subjects with mild cognitive impairment, the earliest clinically detectable phase of dementia and preclinical AD, the earliest detectable pathological phase. Furthermore, multiple LPO biomarkers are elevated in readily accessible biological fluids throughout disease progression. Collectively, these studies demonstrate that LPO is an early feature during disease progression and may be considered a key pathway for targeted therapeutics as well as an enhancer of diagnostic accuracy for early detection of subjects during the prodromal phase.

  1. Biomarkers of lipid peroxidation in Alzheimer disease (AD): an update

    PubMed Central

    Bradley-Whitman, Melissa A.; Lovell, Mark A.

    2015-01-01

    Increasing evidence suggests free radical mediated oxidation of biological substrates is a key feature of Alzheimer’s disease (AD) pathogenesis. While it has long been established that biomarkers of lipid peroxidation (LPO) are elevated in AD brain as well as ventricular CSF postmortem, more recent studies have demonstrated increased LPO biomarkers in postmortem brain from subjects with mild cognitive impairment (MCI), the earliest clinically detectable phase of dementia and preclinical AD (PCAD), the earliest detectable pathological phase. Furthermore, multiple LPO biomarkers are elevated in readily accessible biological fluids throughout disease progression. Collectively these studies demonstrate that LPO is an early feature during disease progression and may be considered a key pathway for targeted therapeutics as well as an enhancer of diagnostic accuracy for early detection of subjects during the prodromal phase. PMID:25895140

  2. Reaction conditions affecting the relationship between thiobarbituric acid reactivity and lipid peroxides in human plasma.

    PubMed

    Lapenna, D; Ciofani, G; Pierdomenico, S D; Giamberardino, M A; Cuccurullo, F

    2001-08-01

    The thiobarbituric acid (TBA) reactivity of human plasma was studied to evaluate its adequacy in quantifying lipid peroxidation as an index of systemic oxidative stress. Two spectrophotometric TBA tests based on the use of either phosphoric acid (pH 2.0, method A) or trichloroacetic plus hydrochloric acid (pH 0.9, method B) were employed with and without sodium sulfate (SS) to inhibit sialic acid (SA) reactivity with TBA. To correct for background absorption, the absorbance values at 572 nm were subtracted from those at 532 nm, which represent the absorption maximum of the TBA:MDA adduct. Method B gave values of TBA-reactive substances (TBARS) 2-fold higher than those detected with method A. SS lowered TBARS by about 50% with both methods, indicating a significant involvement of SA in plasma TBA reactivity. Standard SA, at a physiologically relevant concentration of 1.5 mM, reacted with TBA, creating interference problems, which were substantially eliminated by SS plus correction for background absorbance. When method B was carried out in the lipid and protein fraction of plasma, SS inhibited by 65% TBARS formation only in the latter. Protein TBARS may be largely ascribed to SA-containing glycoproteins and, to a minor extent, protein-bound MDA. Indeed, EDTA did not affect protein TBARS assessed in the presence of SS. TBA reactivity of whole plasma and of its lipid fraction was instead inhibited by EDTA, suggesting that lipoperoxides (and possibly monofunctional lipoperoxidation aldehydes) are involved as MDA precursors in the TBA test. Pretreatment of plasma with KI, a specific reductant of hydroperoxides, decreased TBARS by about 27%. Moreover, aspirin administration to humans to inhibit prostaglandin endoperoxide generation reduced plasma TBARS by 40%. In conclusion, reaction conditions affect the relationship between TBA reactivity and lipid peroxidation in human plasma. After correction for the interfering effects of SA in the TBA test, 40% of plasma TBARS

  3. Visible Light-Induced Lipid Peroxidation of Unsaturated Fatty Acids in the Retina and the Inhibitory Effects of Blueberry Polyphenols.

    PubMed

    Liu, Yixiang; Zhang, Di; Hu, Jimei; Liu, Guangming; Chen, Jun; Sun, Lechang; Jiang, Zedong; Zhang, Xichun; Chen, Qingchou; Ji, Baoping

    2015-10-28

    The lipid peroxidation of unsaturated fatty acids (UFAs) in the retina not only threatens visual cells but also affects the physiological health of the retina. In this work, the potential damages caused by daily visible light exposure on retinal UFAs were evaluated via a simulated in vitro model. At the same time, the benefits of dietary supplementation of blueberries to the eyes were also assessed. After prolonged light exposure, lipid peroxidation occurred for both docosahexaenoic and arachidonic acids (DHA and AA, respectively). The oxidized UFAs presented obvious cytotoxicity and significantly inhibited cell growth in retinal pigment epithelium cells. Among the different blueberry polyphenol fractions, the flavonoid-rich fraction, in which quercetin was discovered as the main component, was considerably better in preventing visible light-induced DHA lipid peroxidation than the anthocyanin- and phenolic acid-rich fractions. Then the retinal protective activity of blueberry polyphenols against light-induced retinal injury was confirmed in vivo. On the basis of the above results, inhibiting lipid peroxidation of UFAs in the retina is proposed to be another important function mechanism for antioxidants to nourish eyes.

  4. Singlet oxygen in copper-catalyzed lipid peroxidation in erythrocyte membranes

    SciTech Connect

    Ding, A.H.; Chan, P.C.

    1984-04-01

    Lipid hydroperoxide was generated in human erythrocyte membranes by irradiation with near ultraviolet (UV) light in the presence of a photosensitizer, hematoporphyrin, but no production of 2-thiobarbituric acid-reactive materials (malonaldehyde and its precursors) was detected. Incubation of the irradiated membranes with CuSO4 led to increased levels of hydroperoxide and formation of malonaldehyde. Hydroperoxides were essential for initiating the Cu(II)-catalyzed peroxidation as no significant activity was observed with nonirradiated membranes and Cu(II) unless an organic peroxide, either t-butyl hydroperoxide or cumene hydroperoxide, was added. Catalytic activity was also found with Fe(II), but not with other metal ions tested. The peroxidation catalyzed with Cu(II) was partially inhibited by several singlet oxygen quenchers but was not affected by superoxide dismutase, catalase or OH radical scavengers. The possible involvement of singlet oxygen in the Cu(II)-catalyzed peroxidation reaction was further supported by a 3-fold enhancement of malonaldehyde production in D/sub 2/O.

  5. Targeting lipid peroxidation and mitochondrial imbalance in Friedreich's ataxia.

    PubMed

    Abeti, Rosella; Uzun, Ebru; Renganathan, Indhushri; Honda, Tadashi; Pook, Mark A; Giunti, Paola

    2015-09-01

    Friedreich's ataxia (FRDA) is an autosomal recessive disorder, caused by reduced levels of the protein frataxin. This protein is located in the mitochondria, where it functions in the biogenesis of iron-sulphur clusters (ISCs), which are important for the function of the mitochondrial respiratory chain complexes. Moreover, disruption in iron biogenesis may lead to oxidative stress. Oxidative stress can be the cause and/or the consequence of mitochondrial energy imbalance, leading to cell death. Fibroblasts from two FRDA mouse models, YG8R and KIKO, were used to analyse two different categories of protective compounds: deuterised poly-unsaturated fatty acids (dPUFAs) and Nrf2-inducers. The former have been shown to protect the cell from damage induced by lipid peroxidation and the latter trigger the well-known Nrf2 antioxidant pathway. Our results show that the sensitivity to oxidative stress of YG8R and KIKO mouse fibroblasts, resulting in cell death and lipid peroxidation, can be prevented by d4-PUFA and Nrf2-inducers (SFN and TBE-31). The mitochondrial membrane potential (ΔΨm) of YG8R and KIKO fibroblasts revealed a difference in their mitochondrial pathophysiology, which may be due to the different genetic basis of the two models. This suggests that variable levels of reduced frataxin may act differently on mitochondrial pathophysiology and that these two cell models could be useful in recapitulating the observed differences in the FRDA phenotype. This may reflect a different modulatory effect towards cell death that will need to be investigated further.

  6. Structure-dependent lipid peroxidation by photoirradiation of pyrene and its mono-substituted derivatives

    PubMed Central

    Fullove, Tracie Perkins; Johnson, Britney; Yu, Hongtao

    2014-01-01

    Pyrene, one of the most studied polycyclic aromatic hydrocarbons can damage biological macromolecules and cause toxicity when irradiated by light. The effect of substituents, 1-amino, 1-hydroxy, 1-nitro, and 1-bromo, on light-induced lipid peroxidation is studied. Degradation kinetics and photoproduct analyses were conducted to test how these substituents affect the photoreaction. All five compounds have different photodegradation rates, and these rates parallel their light absorptivity. Four out of the five compounds induce lipid peroxidation when irradiated with UVA light; whereas, 1-aminopyrene causes minimum or no lipid peroxidation. The relative amount of lipid peroxidation caused is: 1-Bromopyrene > Pyrene > 1-Nitropyrene ≈ 1-Hydroxypyrene > 1-Aminopyrene. This relative lipid peroxidation is dependent on structure due to the following factors: light absorptivity, relative rates of the competing processes in the excited states, nature of the photoreaction, and nature of the photoproducts. PMID:23245298

  7. 'Mitochondrial energy imbalance and lipid peroxidation cause cell death in Friedreich's ataxia'

    PubMed Central

    Abeti, R; Parkinson, M H; Hargreaves, I P; Angelova, P R; Sandi, C; Pook, M A; Giunti, P; Abramov, A Y

    2016-01-01

    Friedreich's ataxia (FRDA) is an inherited neurodegenerative disease. The mutation consists of a GAA repeat expansion within the FXN gene, which downregulates frataxin, leading to abnormal mitochondrial iron accumulation, which may in turn cause changes in mitochondrial function. Although, many studies of FRDA patients and mouse models have been conducted in the past two decades, the role of frataxin in mitochondrial pathophysiology remains elusive. Are the mitochondrial abnormalities only a side effect of the increased accumulation of reactive iron, generating oxidative stress? Or does the progressive lack of iron-sulphur clusters (ISCs), induced by reduced frataxin, cause an inhibition of the electron transport chain complexes (CI, II and III) leading to reactive oxygen species escaping from oxidative phosphorylation reactions? To answer these crucial questions, we have characterised the mitochondrial pathophysiology of a group of disease-relevant and readily accessible neurons, cerebellar granule cells, from a validated FRDA mouse model. By using live cell imaging and biochemical techniques we were able to demonstrate that mitochondria are deregulated in neurons from the YG8R FRDA mouse model, causing a decrease in mitochondrial membrane potential (▵Ψm) due to an inhibition of Complex I, which is partially compensated by an overactivation of Complex II. This complex activity imbalance leads to ROS generation in both mitochondrial matrix and cytosol, which results in glutathione depletion and increased lipid peroxidation. Preventing this increase in lipid peroxidation, in neurons, protects against in cell death. This work describes the pathophysiological properties of the mitochondria in neurons from a FRDA mouse model and shows that lipid peroxidation could be an important target for novel therapeutic strategies in FRDA, which still lacks a cure. PMID:27228352

  8. The generation of oxidation products of benzo(a)pyrene by lipid peroxidation: a study using gamma-irradiation

    SciTech Connect

    Gower, J.D.; Wills, E.D.

    1984-09-01

    The role which active oxygen and radicals generated by the peroxidation of unsaturated fatty acids could play in the oxidation of benzo(a)pyrene has been studied using gamma-irradiation. Irradiation of benzo(a)pyrene resulted in the formation of benzo(a)pyrene 1,6-, 3,6- and 6,12-quinones and other more polar products which were analysed by h.p.l.c. OH. radicals are believed to be involved in this oxidation. The presence of polyunsaturated fatty acids and polyunsaturated lipids stimulated the formation of benzo(a)pyrene products following gamma-irradiation. Oxidation of benzo(a)pyrene also occurred over a period of days in the presence of autoxidising mackerel oil. The rate of benzo(a)pyrene oxidation was related to the extent of lipid peroxidation as determined by malonaldehyde formation. Malonaldehyde production as a result of peroxidising lipids was inhibited by benzo(a)pyrene which suggested that benzo(a)pyrene reacted directly with lipid peroxy radicals or hydroperoxides generated in the process of lipid peroxidation. These results demonstrate that oxidation products of the peroxidation of lipids and fatty acids are able to react directly with benzo(a)pyrene to form products including benzo(a)pyrene quinones without the presence of enzymes such as the cytochrome P-450 mixed function oxidase system and prostaglandin synthetase. It is possible that benzo(a)pyrene may be activated by these types of reactions in vivo or in vitro when benzo(a)pyrene is in contact with polyunsaturated lipids in foodstuffs or the intestinal lumen and peroxidation of unsaturated fats may play an important role in human carcinogenesis.

  9. LDL in patients with subclinical hypothyroidism shows increased lipid peroxidation.

    PubMed

    Zha, Kexi; Zuo, Changting; Wang, Aihong; Zhang, Bingchang; Zhang, Yan; Wang, Bei; Wang, Yunjia; Zhao, Jiajun; Gao, Ling; Xu, Chao

    2015-08-25

    Population-based studies have demonstrated that subclinical hypothyroidism (SCH) is an independent risk factor for atherosclerosis (OR = 1.9). However, this connection cannot be entirely explained by dyslipidemia accompanied by SCH. Lipid peroxidation also plays an important role in the development of atherosclerosis. In this study, we aimed to evaluate oxidative stress in SCH patients, as measured according to concentrations of hydroxy-octadecadienoic acids (HODEs) and hydroxy-eicosatetraenoic acids (HETEs) in both plasma and low density lipoproteins (LDL). The concentrations of HODEs and HETEs in both LDL and plasma were examined in euthyroid (n = 10), mild SCH (4.5 ≤ TSH < 10 mU/L, n = 10), and significant SCH (TSH ≥ 10 mU/L, n = 10) subjects, using a liquid chromatograph-electrospray ionization- mass spectrometer. Then, we explored the relationship among LDL oxidation, TSH levels, and carotid intima-media thickness (IMT), a biomarker of subclinical atherosclerosis. Serum LDL-C levels and mean-IMT in the significant SCH group were higher than in the euthyroid group (p < 0.05). The HODE and HETE concentrations clearly increased in the significant SCH patients compared with the euthyroid subjects, but there was no difference between the mild SCH and euthyroid groups. Among all subjects, linear and significant positive correlations were identified between TSH and mean-IMT after adjustment for confounding factors (r = 0.480, p = 0.018). Both 9-HODE (r = 0.376, p = 0.041) and 13-HODE (r = 0.447, p = 0.013) in LDL were linearly and positively correlated with TSH. The concentrations of HODEs (both 9-HODE and 13-HODE) in LDL were much higher in the thickened IMT group than in the normal IMT group (p =  .017 and 0.015, respectively). HODEs in LDL were also positively associated with mean-IMT. Our findings showed that lipid peroxidation was higher in the significant SCH patients than in the euthyroid subjects, which suggested that qualitative as well as quantitative

  10. Sensitivity of plant mitochondrial terminal oxidases to the lipid peroxidation product 4-hydroxy-2-nonenal (HNE)

    PubMed Central

    2005-01-01

    We have investigated the effect of the lipid peroxidation product, HNE (4-hydroxy-2-nonenal), on plant mitochondrial electron transport. In mitochondria isolated from Arabidopsis thaliana cell cultures, HNE inhibited succinate-dependent oxygen consumption via the Aox (alternative oxidase), but had minimal effect on respiration via Cox (cytochrome c oxidase). Maximal Cox activity, measured with reduced cytochrome c as substrate, was only slightly inhibited by high concentrations of HNE, at which Aox was completely inhibited. Incubation with HNE prevented dimerization of the Aox protein, suggesting that one site of modification was the conserved cysteine residue involved in dimerization and activation of this enzyme (CysI). However, a naturally occurring isoform of Aox lacking CysI and unable to be dimerized, LeAox1b from tomato (Lycopersicon esculentum), was equally sensitive to HNE inhibition, showing that other amino acid residues in Aox also interact with HNE. The presence of HNE in vivo in Arabidopsis cell cultures was also investigated. Induction of oxidative stress in the cell cultures by the addition of hydrogen peroxide, antimycin A or menadione, caused a significant increase in hydroxyalkenals (of which HNE is the most prominent). Western blotting of mitochondrial proteins with antibodies against HNE adducts, demonstrated significant modification of proteins during these treatments. The implications of these results for the response of plants to reactive oxygen species are discussed. PMID:15689186

  11. PADMA-28, a traditional tibetan herbal preparation inhibits the respiratory burst in human neutrophils, the killing of epithelial cells by mixtures of oxidants and pro-inflammatory agonists and peroxidation of lipids.

    PubMed

    Ginsburg, I; Sadovnik, M; Sallon, S; Milo-Goldzweig, I; Mechoulam, R; Breuer, A; Gibbs, D; Varani, J; Roberts, S; Cleator, E; Singh, N

    1999-01-01

    Both aqueous and methanolic fractions derived from the Tibetan preparation PADMA-28 (a mixture of 22 plants) used as an anti-atherosclerotic agent, and which is non-cytolytic to a variety of mammalian cells, were found to strongly inhibit (1) the killing of epithelial cells in culture induced by 'cocktails' comprising oxidants, membrane perforating agents and proteinases; (2) the generation of luminol-dependent chemiluminescence in human neutrophils stimulated by opsonized bacteria; (3) the peroxidation of intralipid (a preparation rich in phopholipids) induced in the presence of copper; and (4) the activity of neutrophil elastase. It is proposed that PADMA-28 might prove beneficial for the prevention of cell damage induced by synergism among pro-inflammatory agonists which is central in the initiation of tissue destruction in inflammatory and infectious conditions.

  12. Lipid Peroxidation-Dependent Cell Death Regulated by GPx4 and Ferroptosis.

    PubMed

    Imai, Hirotaka; Matsuoka, Masaki; Kumagai, Takeshi; Sakamoto, Taro; Koumura, Tomoko

    2017-01-01

    Glutathione peroxidase 4 (Phospholipid hydroperoxide glutathione peroxidase, PHGPx) can directly reduce phospholipid hydroperoxide. Depletion of GPx4 induces lipid peroxidation-dependent cell death in embryo, testis, brain, liver, heart, and photoreceptor cells of mice. Administration of vitamin E in tissue specific GPx4 KO mice restored tissue damage in testis, liver, and heart. These results indicate that suppression of phospholipid peroxidation is essential for cell survival in normal tissues in mice. Ferroptosis is an iron-dependent non-apoptotic cell death that can elicited by pharmacological inhibiting the cystine/glutamate antiporter, system Xc(-) (type I) or directly binding and loss of activity of GPx4 (Type II) in cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression, but not in normal cells. Ferroptosis by Erastin (Type I) and RSL3 (RAS-selective lethal 3, Type II) treatment was suppressed by an iron chelator, vitamin E and Ferrostatin-1, antioxidant compound. GPx4 can regulate ferroptosis by suppression of phospholipid peroxidation in erastin and RSL3-induced ferroptosis. Recent works have identified several regulatory factors of erastin and RSL3-induced ferroptosis. In our established GPx4-deficient MEF cells, depletion of GPx4 induce iron and 15LOX-independent lipid peroxidation at 26 h and caspase-independent cell death at 72 h, whereas erastin and RSL3 treatment resulted in iron-dependent ferroptosis by 12 h. These results indicated the possibility that the mechanism of GPx4-depleted cell death might be different from that of ferroptosis induced by erastin and RSL3.

  13. Carbon Monoxide Modulates Connexin Function through a Lipid Peroxidation-Dependent Process: A Hypothesis

    PubMed Central

    Retamal, Mauricio A.

    2016-01-01

    Hemichannels are ion channels composed of six connexins (Cxs), and they have the peculiarity to be permeable not only to ions, but also to molecules such as ATP and glutamate. Under physiological conditions they present a low open probability, which is sufficient to enable them to participate in several physiological functions. However, massive and/or prolonged hemichannel opening induces or accelerates cell death. Therefore, the study of the molecular mechanisms that control hemichannel activity appears to be essential for understanding several physiological and pathological processes. Carbon monoxide (CO) is a gaseous transmitter that modulates many cellular processes, some of them through modulation of ion channel activity. CO exerts its biological actions through the activation of guanylate cyclase and/or inducing direct carbonylation of proline, threonine, lysine, and arginine. It is well accepted that guanylate cyclase dependent pathway and direct carbonylation, are not sensitive to reducing agents. However, it is important to point out that CO—through a lipid peroxide dependent process—can also induce a secondary carbonylation in cysteine groups, which is sensitive to reducing agents. Recently, in our laboratory we demonstrated that the application of CO donors to the bath solution inhibited Cx46 hemichannel currents in Xenopus laevis oocytes, a phenomenon that was fully reverted by reducing agents. Therefore, a plausible mechanism of CO-induced Cx46 hemichannel inhibition is through Cx46-lipid oxidation. In this work, I will present current evidence and some preliminary results that support the following hypothesis: Carbon monoxide inhibits Cx46 HCs through a lipid peroxidation-dependent process. The main goal of this paper is to broaden the scientific community interest in studying the relationship between CO-Fatty acids and hemichannels, which will pave the way to more research directed to the understanding of the molecular mechanism(s) that control

  14. Date seed oil inhibits hydrogen peroxide-induced oxidative stress in human epidermal keratinocytes.

    PubMed

    Ines, Dammak; Sonia, Boudaya; Fatma, Ben Abdallah; Souhail, Besbes; Hamadi, Attia; Hamida, Turki; Basma, Hentati

    2010-03-01

    Oxidative stress has been implicated in various skin diseases through the generation of reactive oxygen species and the depletion of endogenous antioxidant systems. The administration of antioxidants is reportedly helpful, notably to enhance the healing process. To protect the skin against oxidative damages, we have studied the effect of new oil: "date seed oil" (DSO). This oil, may serve as a potential source of natural antioxidants such as phenols and tocopherols. Here, we report the protective effect of DSO against hydrogen peroxide (H(2)O(2))-induced oxidative stress in terms of lipid peroxidation, depletion of endogenous antioxidant defense enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) using normal human epidermal keratinocytes (NHEK). In the investigated model system, DSO has significant chemoprotective effect, by inhibition of damage caused by H(2)O(2) compared with cells without such addition endowing with a radical scavenging ability. Treatment of NHEK with DSO inhibited H(2)O(2)-induced lipid peroxidation. In addition, this oil inhibited H(2)O(2)-induced depletion of antioxidant defense components, such as SOD, CAT and GPx. Our findings demonstrate that DSO is an efficient extract that is able to prevent keratinocytes oxidative damage induced by H(2)O(2) exposure and may thus be a potential promising candidate, as a chemopreventive agent, in the development of keratinocytes-related pathologies.

  15. Arsenic increased lipid peroxidation in rat tissues by a mechanism independent of glutathione levels.

    PubMed Central

    Ramos, O; Carrizales, L; Yáñez, L; Mejía, J; Batres, L; Ortíz, D; Díaz-Barriga, F

    1995-01-01

    The role of lipid peroxidation in the mechanism of arsenic toxicity was investigated in female rats pretreated with N-acetylcysteine (NAC, a glutathione [GSH] inducer) or with buthionine sulfoximine (BSO, a GSH depletor). Rats were challenged with sodium arsenite, and sacrificed 1 hr after this treatment. Results showed that arsenic decreased GSH levels and increased lipid peroxidation in liver, kidney, and heart, with a larger effect at 18.2 mg/kg than at 14.8 mg/kg for lipid peroxidation induction. In the liver of rats treated with arsenic, pretreatment with NAC increased the levels of GSH and decreased lipid peroxidation. In kidney and heart, NAC pretreatment protected the tissues against arsenic-induced depletion of GSH levels, but the same degree of protection was not found for lipid peroxidation induction. In its turn, BSO had an additive effect with arsenic in lowering the levels of GSH in the liver and kidney, but an inverse correlation between GSH levels and lipid peroxidation was found only in liver. Arsenic content in tissues of rats pretreated with NAC was lower than in rats treated only with arsenic. In rats with depleted levels of GSH (BSO-pretreated rats), a shift in arsenic tissue distribution was found, with higher levels in skin and lower levels in kidney. A clear tendency for a positive correlation between arsenic concentration and lipid peroxidation levels was found in liver, kidney, and heart. PMID:7621808

  16. Positive influence of Centchroman on cardiovascular system and tissue lipid peroxidation in rats.

    PubMed

    Jatwa, Rameshwar; Kar, Anand

    2007-11-01

    Centchroman, a nonsteroidal oral contraceptive, was evaluated for its hitherto unstudied effect on cardiovascular system, thyroid function and tissue lipid peroxidation in rats. Wistar sperm-positive female rats were treated with Centchroman (1.5 mg/kg per day, po) for 10 days and the alterations in serum concentration of thyroid hormones [triiodothyronine (T(3)) and thyroxine (T(4))], insulin, glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phospahatase (ALP) activity, hepatic type-1 iodothyronine 5'-monodeiodinase (5'D) enzyme activity and hepatic, renal, cardiac and serum lipid peroxidation (LPO) were studied. Simultaneously, alterations in endogenous antioxidants [superoxide dismutase (SOD); catalase (CAT) and reduced glutathione (GSH)], relative risk ratio (RR), atherogenic index (AI) and daily rate of food and water consumption were also investigated as supportive parameters. Centchroman administration resulted in the complete inhibition of pregnancy. It increased serum T(4) marginally and HDL-C levels, hepatic SOD, CAT and GSH; cardiac SOD and GSH and renal SOD and CAT activity significantly. However, it reduced LPO in all tissues; concentrations of other serum lipids; AI; RR and activity of ALP. As Centchroman administration did not alter the concentrations of most active thyroid hormone, T(3), serum insulin and glucose, it appears that the drug has no side effect on thyroid function and glucose metabolism. Rather, it possesses cardiovascular and anti-peroxidative benefits.

  17. Effect of coenzyme Q10 on the survival time and lipid peroxidation of adriamycin (doxorubicin) treated mice.

    PubMed

    Shinozawa, S; Etowo, K; Araki, Y; Oda, T

    1984-02-01

    The effect of coenzyme Q10 (Co Q10) was examined on the survival time and lipid peroxidation of adriamycin (ADM)-treated ICR mice. Co Q10 showed a protective effect against a subacute toxicity in mice induced by two intraperitoneal administrations of ADM (15 mg/kg). The group treated orally with 10 mg/kg of Co Q10 showed the longest survival time of all the groups studied (16.81 +/- 10.29 days, mean +/- S.D.) and a significantly longer survival time (p less than 0.001) than the ADM-alone group (7.48 +/- 1.99 days). The inhibitory effect of Co Q10 on the plasma and tissue lipid peroxidation levels did not correlate with the effect of prolonging the survival time of mice. Co Q10 tended to inhibit rises in plasma and liver lipid peroxidation levels induced by ADM administration, but there was no statistically significant difference between treatments. There was a statistically significant different inhibitory effect in the kidney lipid peroxidation levels, but was not in those of the heart.

  18. Linoleic Acid-Induced Ultra-Weak Photon Emission from Chlamydomonas reinhardtii as a Tool for Monitoring of Lipid Peroxidation in the Cell Membranes

    PubMed Central

    Prasad, Ankush; Pospíšil, Pavel

    2011-01-01

    Reactive oxygen species formed as a response to various abiotic and biotic stresses cause an oxidative damage of cellular component such are lipids, proteins and nucleic acids. Lipid peroxidation is considered as one of the major processes responsible for the oxidative damage of the polyunsaturated fatty acid in the cell membranes. Various methods such as a loss of polyunsaturated fatty acids, amount of the primary and the secondary products are used to monitor the level of lipid peroxidation. To investigate the use of ultra-weak photon emission as a non-invasive tool for monitoring of lipid peroxidation, the involvement of lipid peroxidation in ultra-weak photon emission was studied in the unicellular green alga Chlamydomonas reinhardtii. Lipid peroxidation initiated by addition of exogenous linoleic acid to the cells was monitored by ultra-weak photon emission measured with the employment of highly sensitive charged couple device camera and photomultiplier tube. It was found that the addition of linoleic acid to the cells significantly increased the ultra-weak photon emission that correlates with the accumulation of lipid peroxidation product as measured using thiobarbituric acid assay. Scavenging of hydroxyl radical by mannitol, inhibition of intrinsic lipoxygenase by catechol and removal of molecular oxygen considerably suppressed ultra-weak photon emission measured after the addition of linoleic acid. The photon emission dominated at the red region of the spectrum with emission maximum at 680 nm. These observations reveal that the oxidation of linoleic acid by hydroxyl radical and intrinsic lipoxygenase results in the ultra-weak photon emission. Electronically excited species such as excited triplet carbonyls are the likely candidates for the primary excited species formed during the lipid peroxidation, whereas chlorophylls are the final emitters of photons. We propose here that the ultra-weak photon emission can be used as a non-invasive tool for the

  19. Palm olein oil produces less lipid peroxidation products than soya bean oil.

    PubMed

    Zaiton, Z; Merican, Z; Khalid, B A; Mohamed, J B; Baharom, S

    1997-06-01

    The soleus muscles of hyperthyroid rats were used to investigate the effect of palm olein oil and soya bean oil on the production of lipid peroxidation products. It was found that palm olein oil but not soya bean oil significantly decreased malonaldehyde and conjugated diene levels of the soleus muscles of hyperthyroid rats. These findings suggest that palm olein per se produces less lipid peroxidation products than soya bean oil. Such an assay method gives a composite net picture of the propensity of an oil to produce lipid peroxidation products.

  20. Effect of thiamine hydrochloride on lead induced lipid peroxidation in rat liver and kidney.

    PubMed

    Senapati, S K; Dey, S; Dwivedi, S K; Patra, R C; Swarup, D

    2000-08-01

    Thiamine hydrochloride was studied on lead-induced endogenous lipid peroxidation in rat hepatic and renal tissues following po doses of 2.73 mg lead/kg bw for 6 w. Simultaneous use of 25 mg thiamine hydrochloride/kg bw po reduced lead accumulation in liver and kidneys. There were significant decreases in endogenous lipid peroxide in liver and kidney from thiamine hydrochloride-treated rats. Histopathological lesions in thiamine-treated livers and kidneys were milder in comparison to lesions in untreated Pb-exposed animals. This indicates the prophylactic potential of thiamine for lead-induced lipid peroxidation.

  1. Mammographic density, blood telomere length and lipid peroxidation.

    PubMed

    Erdmann, Natalie J; Harrington, Lea A; Martin, Lisa J

    2017-07-19

    Extensive mammographic density is a strong risk factor for breast cancer, but may also be an indicator of biological age. In this study we examined whether mammographic density is related to blood telomere length, a potential marker of susceptibility to age-related disease. We measured mammographic density by a computer assisted method and blood telomere length using a validated PCR method. Urinary malondialdehyde (MDA), a marker of lipid peroxidation, was measured in 24 hour urine collections. In the 342 women examined telomere length was negatively correlated with age, was lower in postmenopausal compared to premenopausal women and in smokers compared to non-smokers, and was positively correlated with urinary MDA. Telomere length was not associated with percent mammographic density or dense area, before or after adjustment for risk factors and MDA. However, there was a significant interaction between telomere length and MDA in their association with mammographic density. At lower levels of MDA, mammographic density and telomere length were inversely associated; while at high levels of MDA, there was evidence of a J-shaped association between mammographic density and telomere length. Further work is need to replicate these results and to examine the association of mammographic density with age-related chronic disease and mortality.

  2. Theoretical modeling of hydroxyl-radical-induced lipid peroxidation reactions.

    PubMed

    Tejero, Ismael; Gonzalez-Lafont, Angels; Lluch, José M; Eriksson, Leif A

    2007-05-24

    The OH-radical-induced mechanism of lipid peroxidation, involving hydrogen abstraction followed by O2 addition, is explored using the kinetically corrected hybrid density functional MPWB1K in conjunction with the MG3S basis set and a polarized continuum model to mimic the membrane interior. Using a small nonadiene model of linoleic acid, it is found that hydrogen abstraction preferentially occurs at the mono-allylic methylene groups at the ends of the conjugated segment rather than at the central bis-allylic carbon, in disagreement with experimental data. Using a full linoleic acid, however, abstraction is correctly predicted to occur at the central carbon, giving a pentadienyl radical. The Gibbs free energy for abstraction at the central C11 is approximately 8 kcal/mol, compared to 9 kcal/mol at the end points (giving an allyl radical). Subsequent oxygen addition will occur at one of the terminal atoms of the pentadienyl radical fragment, giving a localized peroxy radical and a conjugated butadiene fragment, but is associated with rather high free energy barriers and low exergonicity at the CPCM-MPWB1K/MG3S level. The ZPE-corrected potential energy surfaces obtained without solvent effects, on the other hand, display considerably lower barriers and more exergonic reactions.

  3. Loss of PLA2G6 leads to elevated mitochondrial lipid peroxidation and mitochondrial dysfunction

    PubMed Central

    Castillo-Quan, Jorge Iván; Bartolome, Fernando; Angelova, Plamena R.; Li, Li; Pope, Simon; Cochemé, Helena M.; Khan, Shabana; Asghari, Shabnam; Bhatia, Kailash P.; Hardy, John; Abramov, Andrey Y.; Partridge, Linda

    2015-01-01

    The PLA2G6 gene encodes a group VIA calcium-independent phospholipase A2 beta enzyme that selectively hydrolyses glycerophospholipids to release free fatty acids. Mutations in PLA2G6 have been associated with disorders such as infantile neuroaxonal dystrophy, neurodegeneration with brain iron accumulation type II and Karak syndrome. More recently, PLA2G6 was identified as the causative gene in a subgroup of patients with autosomal recessive early-onset dystonia-parkinsonism. Neuropathological examination revealed widespread Lewy body pathology and the accumulation of hyperphosphorylated tau, supporting a link between PLA2G6 mutations and parkinsonian disorders. Here we show that knockout of the Drosophila homologue of the PLA2G6 gene, iPLA2-VIA, results in reduced survival, locomotor deficits and organismal hypersensitivity to oxidative stress. Furthermore, we demonstrate that loss of iPLA2-VIA function leads to a number of mitochondrial abnormalities, including mitochondrial respiratory chain dysfunction, reduced ATP synthesis and abnormal mitochondrial morphology. Moreover, we show that loss of iPLA2-VIA is strongly associated with increased lipid peroxidation levels. We confirmed our findings using cultured fibroblasts taken from two patients with mutations in the PLA2G6 gene. Similar abnormalities were seen including elevated mitochondrial lipid peroxidation and mitochondrial membrane defects, as well as raised levels of cytoplasmic and mitochondrial reactive oxygen species. Finally, we demonstrated that deuterated polyunsaturated fatty acids, which inhibit lipid peroxidation, were able to partially rescue the locomotor abnormalities seen in aged flies lacking iPLA2-VIA gene function, and restore mitochondrial membrane potential in fibroblasts from patients with PLA2G6 mutations. Taken together, our findings demonstrate that loss of normal PLA2G6 gene activity leads to lipid peroxidation, mitochondrial dysfunction and subsequent mitochondrial membrane

  4. Tenoxicam modulates antioxidant redox system and lipid peroxidation in rat brain.

    PubMed

    Naziroğlu, Mustafa; Uğuz, Abdulhadi Cihangir; Gokçimen, Alpaslan; Bülbül, Metin; Karatopuk, Dilek Ulusoy; Türker, Yasin; Cerçi, Celal

    2008-09-01

    We investigated effects of two doses of Tenoxicam, a type 2 cyclooxygenase inhibitor, administration on lipid peroxidation and antioxidant redox system in cortex of the brain in rats. Twenty-two male Wistar rats were randomly divided into three groups. First group was used as control. 10 and 20 mg/kg body weight Tenoxicam were intramuscularly administrated to rats constituting the second and third groups for 10 days, respectively. Both dose of Tenoxicam administration resulted in significant increase in the glutathione peroxidase activity, reduced glutathione and vitamins C and E of cortex of the brain. The lipid peroxidation levels in the cortex of the brain were significantly decreased by the administration. Vitamin A and beta-carotene concentration was not affected by the administration. There was no statistical difference in all values between 10 and 20 mg Tenoxicam administrated groups. In conclusion, treatment of brain with 10 and 20 mg Tenoxicam has protective effects on the oxidative stress by inhibiting free radical and supporting antioxidant redox system.

  5. Protective effect of resveratrol on ethanol-induced lipid peroxidation in rats.

    PubMed

    Kasdallah-Grissa, A; Mornagui, B; Aouani, E; Hammami, M; Gharbi, N; Kamoun, A; El-Fazaa, S

    2006-01-01

    Chronic ethanol treatment induces an increase in oxidative stress. As polyphenolic compounds are potent antioxidants, we aimed to examine whether dietary supplementation of resveratrol may attenuate lipid peroxidation, the major end-point of oxidative damage resulting from chronic ethanol administration. Three groups of male Wistar rats were used. The first group served as control and received a daily intraperitoneal injection of 0.9% saline. The second group of rats was daily injected with 35% ethanol at 3 g/kg body weight. The third group was given the same dose of ethanol and supplemented with resveratrol (5 g/kg) in the standard diet. Malondialdehyde (MDA), an indicator of oxidative stress, was measured in the liver, heart, brain, and testis. At the end of a 6 weeks treatment period, MDA levels were significantly increased by 51.5, 53.7, 72.7, and 40.5% in the liver, heart, brain, and testis, respectively. However, when ethanol treated rats were given resveratrol the increase in MDA levels was significantly reduced in all organs to nearly those of control rats. Resveratrol is able to inhibit the ethanol-induced lipid peroxidation and have protective effect against oxidative injury.

  6. Relationship between Active Oxygen Species, Lipid Peroxidation, Necrosis, and Phytoalexin Production Induced by Elicitins in Nicotiana.

    PubMed Central

    Rusterucci, C.; Stallaert, V.; Milat, M. L.; Pugin, A.; Ricci, P.; Blein, J. P.

    1996-01-01

    Excised leaves of Nicotiana tabacum var Xanthi and Nicotiana rustica were treated with cryptogein and capsicein, basic and acidic elicitins, respectively. Both compounds induced leaf necrosis, the intensity of which depended on concentration and duration of treatment. N. tabacum var Xanthi was the most sensitive species and cryptogein was the most active elicitin. Lipid peroxidation in elicitin-treated Nicotiana leaves was closely correlated with the appearance of necrosis. Elicitin treatments induced a rapid and transient burst of active oxygen species (AOS) in cell cultures of both Nicotiana species, with the production by Xanthi cells being 6-fold greater than that by N. rustica. Similar maximum AOS production levels were observed with both elicitins, but capsicein required 10-fold higher concentrations than those of cryptogein. Phytoalexin production was lower in response to both elicitins in N. tabacum var Xanthi cells than in N. rustica cells, and capsicein was the most efficient elicitor of this response. In cryptogein-treated cell suspensions, phytoalexin synthesis was unaffected by diphenyleneiodonium, which inhibited AOS generation, nor was it affected by tiron or catalase, which suppressed AOS accumulation in the extracellular medium. These results suggest that AOS production, lipid peroxidation, and necrosis are directly related, whereas phytoalexin production depends on neither the presence nor the intensity of these responses. PMID:12226334

  7. Studies on the in vitro interaction of mitomycin C, nitrofurantoin and paraquat with pulmonary microsomes. Stimulation of reactive oxygen-dependent lipid peroxidation.

    PubMed

    Trush, M A; Mimnaugh, E G; Ginsburg, E; Gram, T E

    1982-03-01

    In vitro experiments were performed to evaluate the capacity of the redox cycling compounds mitomycin C (MC), nitrofurantoin (NF) and paraquat (PQ) to stimulate pulmonary microsomal lipid peroxidation. It was observed that the interaction of MC, NF or PQ with rat or mouse lung microsomes in the presence of an NADPH-generating system and an O2 atmosphere resulted in significant lipid peroxidation. All three compounds demonstrated similar concentration dependency, similar time courses and the ability to generate lipid peroxidation-associated chemiluminescence. The stimulation of lipid peroxidation by MC, NF or PQ was inhibited significantly by superoxide dismutase, glutathione, ascorbic acid, catalase and EDTA, agents which either scavenge reactive oxygen and/or prevent the generation of secondary reactive oxygen metabolites. In addition, the ability of MC or NF, but not PQ, to stimulate lipid peroxidation was reduced significantly following preincubation with microsomes and NADPH under N2 (15-20 min) prior to incubation under O2. During this period under N2. MC and NF underwent reductive metabolism of their quinone and nitro moieties respectively. Thus, it appears that under aerobic conditions the pulmonary microsomal-mediated redox cycling of MC, NF and PQ is accompanied by the stimulation of reactive oxygen-dependent lipid peroxidation.

  8. [Peroxidation of lipids in mitochondrial membranes, induced by enzymatic deamination of biogenic amines].

    PubMed

    Kagan, V E; Smirnov, A V; Savov, V M; Gorkin, V Z

    1984-01-01

    In presence of ferrous cations and ascorbate lipid peroxidation in mitochondrial membranes has been induced by incubation of fragments of the membrane devoid of catalase activity with amines which are substrates of monoamine oxidases of the B type (2-phenyl ethylamine, benzylamine) or transformed monoamine oxidases of type A (cadaverine). In the samples containing both cadaverine and benzylamine the highest stimulation of lipid peroxidation was noted. To the contrary, a substrate of the monoamine oxidases of the type A (serotonin) caused under the same conditions an antioxidative effect. The following conditions are obligatory to induce lipid peroxidation in mitochondria by incubation with amines: I. absence of catalase activity in the biomembranes; 2. presence of physiological concentrations of Fe2+. Physiological concentrations of ascorbate or alterations of pH in the samples caused additional stimulation of the lipid peroxidation.

  9. Lipid peroxidation in mitochondrial membranes induced by enzymatic deamination of biogenic amines.

    PubMed

    Kagan, V E; Smirnov, A V; Savov, V M; Prilipko, L L; Gorkin, V Z

    1983-01-01

    In the presence of Fe2+ and ascorbate lipid peroxidation in mitochondrial membranes is induced by incubation of membrane fragments devoid of catalase activity with amines which are the substrates of monoamine oxidases of the type B (2-phenylethylamine, benzylamine) or transformed monoamine oxidases of the type A (cadaverine). The highest stimulation of lipid peroxidation is observed in the samples containing both cadaverine and benzylamine. On the contrary, the substrate of the monoamine oxidases of the type A, serotonin, causes an antioxidative effect under these conditions. The necessary prerequisites for lipid peroxidation induction in mitochondria during their incubation with amines are i) the absence of catalase activity in the biomembranes and, ii) the presence of physiological concentrations of Fe2+. Physiological concentrations of ascorbate or pH shifts cause additional stimulation of lipid peroxidation.

  10. "In vitro" effect of lipid peroxidation metabolites on elongation factor-2.

    PubMed

    Argüelles, Sandro; Machado, Alberto; Ayala, Antonio

    2006-03-01

    Elongation Factor-2 (eEF-2) is the protein that catalyzes the translocation of the ribosome through mRNA. Not all oxidants affect eEF-2, which is extremely sensitive to oxidative stress caused mainly by lipid peroxidant compounds such as cumene hydroperoxide and t-butyl hydroperoxide. Lipid peroxides constitute a potential hazard to living organisms because of their direct reactivity with a variety of biomolecules and the ability to decompose into free radicals and reactive aldehydes. In this "in vitro" study, we show the effect of three of these aldehydes on the levels of hepatic eEF-2. The results suggest that the toxicity associated with prooxidant-mediated hepatic lipid peroxidation on protein synthesis can originate from the interaction of the aldehydic end products of lipid peroxidation with eEF-2.

  11. [The effect of microwaves on lipid peroxidation and on lipid and mineral metabolism in warm-blooded animals (experimental research)].

    PubMed

    Guliaev, V Iu; Tereshin, S Iu; Oranskiĭ, I E

    1990-01-01

    The experiments on 50 white mature male rats have provided evidence on the effect produced by microwave therapy on lipid peroxidation, lipid and mineral metabolism and weight of the animals. The effect varied with frequency, wavelength and the site of the exposure (abdominal or cervical zones).

  12. The effectiveness of a lipid peroxide in oxidizing protein and non-protein thiols

    PubMed Central

    Little, C.; O'Brien, P. J.

    1968-01-01

    1. Thiol oxidation by a lipid peroxide or hydrogen peroxide was as efficient in denatured non-haem proteins as in small thiols. Both peroxides were relatively ineffective in oxidizing haemoprotein thiols, especially at low pH. Increased amounts of haematin decreased greatly the efficiency of GSH oxidation by peroxides especially at low pH. 2. Other than the haematin ring, the thiol group was found to be probably the group in proteins most sensitive to modification by peroxides. 3. At low concentrations, the fatty acid moiety of a lipid peroxide appeared to impede thiol oxidation in proteins, probably by hydrophobic bonding to the protein, rather than to stimulate thiol oxidation by denaturing the protein and thereby increasing the exposure and reactivity of the thiol group. 4. The relative rates of thiol oxidation by peroxides in the different thiols were: haemoprotein thiols>small thiols>other protein thiols. In all cases, thiol oxidation was much more rapid by the lipid peroxide than by hydrogen peroxide. PMID:5637351

  13. Inhibitory effects of aromatic herbs on lipid peroxidation and protein oxidative modification by copper.

    PubMed

    Toda, Shizuo

    2003-05-01

    Aromatic herbs have been used as carminatives. Oxygen free radicals are generated in ischaemia/reperfusion injury in the stomach, and induce lipid peroxidation or protein oxidative modification. Several aromatic herbs were shown to have inhibitory effects on the generation of oxygen free radicals. It was shown that several aromatic herbs, Caryophylli Flos, Cinnamomi Cortex, Foeniculi Fructus and Zedoariae Rhizoma, have inhibitory effects on lipid peroxidation or protein oxidative modification by copper.

  14. Effect of ethanol and the catalase inhibitor aminotriazole on lipid peroxidation in the rat myocardium

    SciTech Connect

    Panchenko, L.F.; Pirozhkov, S.V.; Popova, S.V.; Antonenkov, V.D.

    1987-09-01

    The authors study the effect of chronic administration of ethanol and aminotriazole on the level of lipid peroxidation in the ray myocardium. The action of natural and artificial antioxidants on alcohol-induced lipid peroxidation also was studied. To determine the level of chemiluminescence, 1 ml of a sample of nuclear free homogenate or of the total fraction of particles was introduced for radioactivity measurement. After incubation the spontaneous weak luminescence was measured.

  15. Relationship between parameters of lipid peroxidation during obstructive jaundice and after bile flow restoration.

    PubMed

    Dudnik, L B; Tsupko, A N; Shupik, M A; Akhaladze, G G; Galperin, E I; Latonova, L V; Pantaz, E A; Alessenko, A V

    2008-01-01

    Restoration of bile flow after 9-day cholestasis in rat liver normalized the content of lipid peroxidation products. The removal of the cholestatic factor after 12-day cholestasis was not followed by recovery of these parameters. We showed that measurement of serum concentration of lipid peroxidation products in patients with cholelithiasis during the preoperative period holds promise for selection of the optimum time for surgical treatment and prediction of the risk of postoperative complications.

  16. Effects of soyasaponins on lipid peroxidation through the secretion of thyroid hormones.

    PubMed

    Ishii, Yasuko; Tanizawa, Hisayuki

    2006-08-01

    We investigated how soyasaponins (SS), which had been isolated from soybeans (Glycine max Merrill, seeds), influenced lipid peroxidation. The in vivo reduction in hepatic lipid peroxidation in mice intraperitoneally injected with total soyasaponins (TSS) was comparable to that which has been observed for alpha-tocopherol (VE). However, TSS and its five main constituent saponins (I, II, III, A1, and A2) had a much weaker in vitro inhibitory effect on lipid peroxidation induced by NADPH in mouse liver microsomes than VE. Therefore, we were not able to explain the in vivo effect of SS on lipid peroxidation level through direct antioxidative effects. We also demonstrated that TSS increased the levels of serum thyroid hormones. The effect of serum thyroid hormones on in vitro lipid peroxidation was much stronger than that observed for VE. Furthermore, the effects of TSS on levels of serum thyroid hormones and LPO were markedly decreased by propylthiouracil, an antithyroid drug. These results indicate that the effects of SS on lipid peroxidation levels appear to be mediated through the secretion of thyroid hormones.

  17. Lipid peroxidation is an early event in necrosis of wheat hybrid.

    PubMed

    Dalal, M; Khanna-Chopra, R

    1999-08-19

    We previously reported enhanced superoxide anion generation in an F1 necrotic hybrid produced from normal parents (Khanna-Chopra et al., Biochem. Biophys. Res. Commun. (1998) 248, 712-715). Further investigation of the mechanism of necrosis shows the possibility of lipid peroxidation as an early event in the death of necrotic leaves. Lipid peroxidation resulting from the inability of free radical scavenging is often associated with cell death. In this study the accumulation of malondialdehyde, an end product of lipid peroxidation, was measured in hybrid leaves and those of the parents. Lipid peroxidation was higher in the hybrid leaves through out the leaf ontogeny. This was accompanied by increased membrane permeability. Cell viability measured by a TTC reduction test showed a significant correlation with conductivity. There was no apparent effect on photosynthetic pigments and maximum efficiency of PSII (Fv/Fm) until the appearance of necrotic lesions on the hybrid leaf. There seems to be a close relationship among lipid peroxidation, membrane permeability, and cell viability in the leaves undergoing necrosis. This suggests the possibility of a genetic mechanism whereby the scavenging of free radical is impaired, leading to enhanced lipid peroxidation and membrane permeability, resulting in necrosis and death of the hybrid leaves in wheat.

  18. Lipid peroxidation and antioxidative vitamins under extreme endurance stress.

    PubMed

    Rokitzki, L; Logemann, E; Sagredos, A N; Murphy, M; Wetzel-Roth, W; Keul, J

    1994-06-01

    The aim of this study was to examine whether extreme endurance stress of trained athletes can influence lipid peroxidation and muscle enzymes. A randomized and placebo-controlled study was carried out on 24 trained long-distance runners who were substituted with alpha-tocopherol (400 I.U. d-1) and ascorbic acid (200 mg d-1) during 4.5 weeks prior to a marathon race. The serum concentrations of retinol, ascorbic acid, beta-carotene, alpha-tocopherol, malondialdehyde (TBARS) and uric acid as well as glutathione peroxidase (GSH Px) and catalase were measured 4.5 weeks before (A), immediately before (B), immediately after (C) and 24 h after (D) the course. After competition (C) TBARS serum concentrations of the athletes (n = 22) decreased in both groups (P < 0.0001). The ascorbic acid serum concentration increased significantly in the supplemented group from (A) to (B) (P < 0.01), from (B) to (C) (P < 0.001) and in the placebo group a significant increase from (B) to (C) (P < 0.01) was observed. The alpha-tocopherol serum concentration increased significantly in the supplemented group from (A) to (B) (P < 0.001) and from (B) to (C) (P < 0.05). The enzymes glutathione peroxidase (GSH Px) and catalase measured in erythrocytes as well as the serum selenium levels did not show significant differences at any time. A significant increase of CK concentration was observed from (C) to (D) in the supplemented group (P < 0.01) and in the placebo group (P < 0.001). The increase of CK serum concentration is remarkably lower in the supplemented group compared with the placebo group (P < 0.01). It is concluded that endurance training coupled with antioxidant vitamin supplementation reduces blood CK increase under exercise stress.

  19. Almonds reduce biomarkers of lipid peroxidation in older hyperlipidemic subjects.

    PubMed

    Jenkins, David J A; Kendall, Cyril W C; Marchie, Augustine; Josse, Andrea R; Nguyen, Tri H; Faulkner, Dorothea A; Lapsley, Karen G; Blumberg, Jeffrey

    2008-05-01

    Nut consumption has been associated with reduced coronary heart disease (CHD) risk. In addition to cholesterol-lowering properties, almonds have been shown to lower oxidized LDL concentrations. However, little is known regarding their effects on other markers of oxidative stress. The dose-response effects of whole almonds, taken as snacks, were compared with low-saturated fat (<5% energy) whole-wheat muffins (control) in the therapeutic diets of hyperlipidemic subjects. In a randomized crossover study, 27 hyperlipidemic men and women consumed 3 isoenergetic (mean 423 kcal/d or 1770 kJ/d) supplements each for 1 mo. Supplements consisted of full-dose almonds (73 +/- 3 g/d), half-dose almonds plus half-dose muffins (half-dose almonds), and full-dose muffins (control). Subjects were assessed at wk 0, 2 and 4. Mean body weights differed < or = 300 g between treatments, although the weight loss on the half-dose almond treatment was greater than on the control (P < 0.01). At 4 wk, the full-dose almonds reduced serum concentrations of malondialdehyde (MDA) (P = 0.040) and creatinine-adjusted urinary isoprostane output (P = 0.026) compared with the control. Serum concentrations of alpha- or gamma-tocopherol, adjusted or unadjusted for total cholesterol, were not affected by the treatments. Almond antioxidant activity was demonstrated by their effect on 2 biomarkers of lipid peroxidation, serum MDA and urinary isoprostanes, and supports the previous finding that almonds reduced oxidation of LDL-C. Antioxidant activity provides an additional possible mechanism, in addition to lowering cholesterol, that may account for the reduction in CHD risk with nut consumption.

  20. Isoleukotrienes are biologically active free radical products of lipid peroxidation.

    PubMed

    Harrison, K A; Murphy, R C

    1995-07-21

    The free radical oxidation of arachidonic acid esterified to glycerophospholipids is known to generate complex metabolites, termed isoprostanes, that share structural features of prostaglandins derived from prostaglandin H2 synthase. Furthermore, certain isoprostanes have been found to exert biological activity through endogenous receptors on cell surfaces. Using mass spectrometry and ancillary techniques, the free radical oxidation of 1-hexadecanoyl-2-arachidonoyl-glycerophosphocholine was studied in the search for products of arachidonic acid isomeric to the leukotrienes that are derived from 5-lipoxygenase-catalyzed metabolism of arachidonic acid. Several conjugated triene metabolites were chromatographically separated from known 5-lipoxygenase products and structures characterized as 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid esterified to the glycerophosphocholine backbone. We have termed these products as B4-isoleukotrienes. Following saponification some, but not all, B4-isoleukotrienes were found to exert biological activity in elevating intracellular calcium in Indo-1-loaded human polymorphonuclear leukocytes. This activity could be blocked by a leukotriene B4 receptor antagonist. An EC50 of approximately 30 nM was determined for one unique B4-isoleukotriene with a relative retention index of 2.54. We have shown that free radical processes can lead to the formation of biologically active isoleukotrienes in glycerophosphocholine liposomes, and we propose that B4-isoleukotrienes may also be formed in membrane glycerophospholipids as a result of lipid peroxidation during tissue injury. Such B4-isoleukotrienes could then mediate events of tissue damage through activation of leukotriene B4 receptors on target cells.

  1. Lipid Peroxidation in a Stomach Medium Is Affected by Dietary Oils (Olive/Fish) and Antioxidants: The Mediterranean versus Western Diet.

    PubMed

    Tirosh, Oren; Shpaizer, Adi; Kanner, Joseph

    2015-08-12

    Red meat is an integral part of the Western diet, and high consumption is associated with an increased risk of chronic diseases. Using a system that simulated the human stomach, red meat was interacted with different oils (olive/fish) and lipid peroxidation was determined by measuring accumulation of malondialdehyde (MDA) and lipid peroxides (LOOH). Olive oil decreased meat lipid peroxidation from 121.7 ± 3.1 to 48.2 ± 1.3 μM and from 327.1 ± 9.5 to 77.3 ± 6.0 μM as assessed by MDA and ROOH, respectively. The inhibitory effect of olive oil was attributed to oleic acid rather than its polyphenol content. In contrast, fish oils from tuna or an ω-3 supplement dramatically increased meat lipid peroxidation from 96.2 ± 3.6 to 514.2 ± 6.7 μM MDA. Vitamin E inhibited meat lipid peroxidation in the presence of olive oil but paradoxically increased peroxidation in the presence of fish oil. The inhibitory properties of oleic acid may play a key role in the health benefits of the Mediterranean diet.

  2. Fatty acid composition and lipid peroxidation of soft-shelled turtle, Pelodiscus sinensis, fed different dietary lipid sources.

    PubMed

    Lin, Way-Yee; Huang, Chen-Huei

    2007-01-01

    Juvenile soft-shelled turtles (Pelodiscus sinensis) were fed 7 diets containing 8% of lard, soybean oil, olive oil, menhaden fish oil, or mixtures of 1 to 1 ratio of fish oil and lard, soybean oil, olive oil for 10 weeks. Growth and muscle proximate compositions of the turtles were not affected by different dietary treatments (p>0.05). Fatty acid profiles in muscle polar lipids, muscle non-polar lipids, and liver polar lipids reflected the fatty acid composition of dietary lipid source. Turtles fed diets containing fish oil generally contained significantly higher (p<0.05) proportion of highly unsaturated fatty acids (HUFA) in both polar and non-polar lipids of muscle and polar fraction of liver lipids than those fed other oils. Non-polar fraction of liver lipids from all groups of turtles contained less than 1% of HUFA. All turtles contained relatively high proportions of oleic acid in their lipids regardless of the dietary lipid source. Further, lipid peroxidation in both muscle tissue and liver microsomes of turtles fed fish oil as the sole lipid source was greater (p<0.05) than those fed fish oil-free diets. Turtles fed olive oil as the sole lipid source had the lowest lipid peroxidation rate among all dietary groups. The results indicate that dietary n-3 HUFA may not be crucial for optimal growth of soft-shelled turtles although they may be used for metabolic purpose. Further, high level of dietary HUFA not only increases the HUFA content in turtle tissues, but also enhances the susceptibility of these tissues to lipid peroxidation.

  3. Effect of lipid peroxidation on membrane-bound Ca2+-ATPase activity of the intestinal brush-border membranes.

    PubMed

    Ohta, A; Mohri, T; Ohyashiki, T

    1989-09-04

    We have studied lipid peroxidation and Ca2+-ATPase activity of the porcine intestinal brush-border membranes using a oxygen-radical-generating system consisting of dithiothreitol (DTT)/Fe2+ and tert-butyl hydroperoxide (t-BuOOH). The rates of lipid peroxidation were measured by formation of thiobarbituric acid-reactive substances (TBAR) and conjugated diene. Incubation of the membranes with DTT/Fe2+ in the absence and presence of t-BuOOH resulted in a slight (about 20%) and a marked (about 50%) inhibition of Ca2+-ATPase activity, respectively. The degree of inhibition was dependent on the hydroperoxide concentration. Addition of thiourea effectively protected Ca2+-ATPase activity but catalase and superoxide dismutase showed a slight and no effect on protection of the ATPase activity, respectively. Results of kinetic studies on the ATPase activity with varying ATP and Ca2+ concentrations revealed that the decrease in the enzyme activity by treatment with these oxidizing agents is mainly due to decrease of the Vmax value. Modification of SH groups in the membrane proteins by thiol group reagents such as N-ethylmaleimide, monoiodoacetate and monoiodacetamide did not induce the inhibition of Ca2+-ATPase activity. From these results, it is suggested that inhibition of the ATPase activity of the membranes by treatment with DTT/Fe2+ in the presence and absence of t-BuOOH is dependent on lipid peroxidation and that oxidative modification of SH groups may not be directly involved to the loss of the ATPase activity. In addition, results of the fluorescence anisotropy measurements of pyrene-labeled membranes suggested that change in the Ca2+-ATPase activity is partly related to a decrease in the membrane lipid fluidity.

  4. Effect of human Apo AIV against lipid peroxidation of very low density lipoproteins.

    PubMed

    Ferretti, G; Bacchetti, T; Bicchiega, V; Curatola, G

    2002-01-01

    Recent studies have demonstrated that Apo AIV exerts a protective effect against atherosclerosis. Moreover, Qin et al. (Am. J. Physiol. 274 (1998) H1836) have demonstrated that Apo AIV, isolated from rat plasma, exerts an inhibitory effect against Cu(2+)-induced lipid peroxidation of intestinal lymph and LDL. The aim of the study was to investigate whether human Apo AIV exerts a protective effect against Cu(2+)-induced lipid peroxidation. Our results demonstrated that human Apo AIV exerted an inhibitory effect against Cu(2+) and AAPH induced lipid peroxidation of VLDL, as shown by the lower increase in the levels of TBARS and conjugated dienes in lipoproteins preincubated with Apo AIV. In addition, the tryptophan (Trp) and probe 2-(dimethylamino)-6-lauroylnaphthalene (Laurdan) fluorescence studies demonstrated that the modifications of spectral properties in both lipoproteins preincubated with Apo AIV were lower with respect to ox-lipoproteins, suggesting that Apo AIV prevents the modification of physico-chemical properties due to peroxidation.

  5. Interrelationship of antioxidative status, lipid peroxidation, and lipid profile in insulin-dependent and non-insulin-dependent diabetic patients.

    PubMed

    Cimbaljević, Branko; Vasilijević, Ana; Cimbaljević, Slavica; Buzadzić, Biljana; Korać, Aleksandra; Petrović, Vesna; Janković, Aleksandra; Korać, Bato

    2007-10-01

    This study aimed to investigate the interrelationship of plasma lipid profile, lipid peroxidation, and erythrocyte antioxidative defense in patients with insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. Plasma levels of total cholesterol, triglycerides, and lipid peroxides and the activities of copper, zinc superoxide dismutase (CuZnSOD), catalase, glutathione peroxidase (GSH-Px), as well as the amount of glutathione in erythrocytes, were determined in IDDM, NIDDM, and nondiabetic control subjects. Additionally, morphology of erythrocytes in all subjects was examined. Plasma levels of total cholesterol and triglycerides were significantly increased in NIDDM compared with controls. Also, the lipid peroxide level was higher in NIDDM than in either control or IDDM subjects. CuZnSOD activity in erythrocytes was elevated in NIDDM patients compared with the control. In NIDDM patients, more extensive erythrocyte spherocytosis and echinocytosis compared with both control and IDDM subjects were observed. In contrast with the IDDM group, the observed abnormality in lipid metabolism in NIDDM patients is closely associated with increased lipid peroxidation, changes in antioxidative defense, and erythrocyte morphology.

  6. Protective role of arzanol against lipid peroxidation in biological systems.

    PubMed

    Rosa, Antonella; Pollastro, Federica; Atzeri, Angela; Appendino, Giovanni; Melis, M Paola; Deiana, Monica; Incani, Alessandra; Loru, Debora; Dessì, M Assunta

    2011-01-01

    This study examines the protective effect of arzanol, a pyrone-phloroglucinol etherodimer from Helichrysum italicum subsp. microphyllum, against the oxidative modification of lipid components induced by Cu(2+) ions in human low density lipoprotein (LDL) and by tert-butyl hydroperoxide (TBH) in cell membranes. LDL pre-treatment with arzanol significantly preserved lipoproteins from oxidative damage at 2h of oxidation, and showed a remarkable protective effect on the reduction of polyunsaturated fatty acids and cholesterol levels, inhibiting the increase of oxidative products (conjugated dienes fatty acids hydroperoxides, 7β-hydroxycholesterol, and 7-ketocholesterol). Arzanol, at non-cytotoxic concentrations, exerted a noteworthy protection on TBH-induced oxidative damage in a line of fibroblasts derived from monkey kidney (Vero cells) and in human intestinal epithelial cells (Caco-2), decreasing, in both cell lines, the formation of oxidative products (hydroperoxides and 7-ketocholesterol) from the degradation of unsaturated fatty acids and cholesterol. The cellular uptake and transepithelial transport of the compound were also investigated in Caco-2 cell monolayers. Arzanol appeared to accumulate in Caco-2 epithelial cells. This phenol was able to pass through the intestinal Caco-2 monolayers, the apparent permeability coefficients (P(app)) in the apical-to-basolateral and basolateral-to-apical direction at 2h were 1.93±0.36×10(-5) and 2.20±0.004×10(-5)cm/s, respectively, suggesting a passive diffusion pathway. The results of the work qualify arzanol as a potent natural antioxidant with a protective effect against lipid oxidation in biological systems.

  7. Dietary lipid level influences fatty acid profiles, tissue composition, and lipid peroxidation of soft-shelled turtle, Pelodiscus sinensis.

    PubMed

    Huang, Chen-Huei; Lin, Way-Yee; Chu, Jen-Hong

    2005-11-01

    Dietary lipids containing equal portions of soybean oil and fish oil were fed to juvenile Chinese soft-shelled turtle, Pelodiscus sinensis, at supplementation level of 0 to 15% for 8 weeks. Tissue fat contents of turtles increased when dietary lipid concentration increased. Fatty acid profiles for turtles fed diets supplemented with 6% or higher levels of lipids were similar to those in dietary lipids. On absolute value basis, fatty acids of 14-, 16-, and 18-carbons in muscle of turtles fed diet without lipid supplementation were higher than those in the initial turtle muscle. Among them, C16:1 and C18:1 was approximately 4 and 2 fold higher, respectively, than that of the initial turtles. By contrast, absolute amounts of C20:5 and C22:6 in muscle of turtles fed diet without lipid supplementation were slightly less than those in the initial turtles. For turtles fed lipid supplemented diets, tissue C20:5 and C22:6, however, increased when dietary lipid level increased. These results suggest that soft-shelled turtles are capable of synthesizing fatty acids up to 18 carbons from other nutrients and that they may have limited or no ability to synthesize highly unsaturated fatty acids. Lipid peroxidation measured by thiobarbituric acid-reactive substances in tissues of turtles fed 12% and 15% lipids was greater (p<0.05) than that in turtles fed 3% to 9% lipids. This could be due to high lipid and unsaturated fatty acid content in these tissues. On lipid basis, lipid peroxidation in turtles fed diet without lipid supplementation was the highest among all groups suggesting the existence of antioxidant factors in the dietary lipids.

  8. Induced lipid peroxidation in ram sperm: semen profile, DNA fragmentation and antioxidant status.

    PubMed

    Hamilton, Thais Rose dos Santos; de Castro, Letícia Signori; Delgado, Juliana de Carvalho; de Assis, Patrícia Monken; Siqueira, Adriano Felipe Perez; Mendes, Camilla Mota; Goissis, Marcelo Demarchi; Muiño-Blanco, Teresa; Cebrián-Pérez, José Álvaro; Nichi, Marcílio; Visintin, José Antonio; D'Ávila Assumpção, Mayra Elena Ortiz

    2016-04-01

    Action of reactive oxygen species, protamination failures and apoptosis are considered the most important etiologies of sperm DNA fragmentation. This study evaluated the effects of induced lipid peroxidation susceptibility on native semen profile and identified the mechanisms involved in sperm DNA fragmentation and testicular antioxidant defense on Santa Ines ram sperm samples. Semen was collected from 12 adult rams (Ovis aries) performed weekly over a 9-week period. Sperm analysis (motility, mass motility, abnormalities, membrane and acrosome status, mitochondrial potential, DNA fragmentation, lipid peroxidation and intracellular free radicals production); protamine deficiency; PRM1, TNP1 and TNP2 gene expression; and determination of glutathione peroxidase (GPx), glutathione reductase, catalase (CAT) and superoxide dismutase activity and immunodetection in seminal plasma were performed. Samples were distributed into four groups according to the sperm susceptibility to lipid peroxidation after induction with ascorbate and ferrous sulfate (low, medium, high and very high). The results were analyzed by GLM test and post hoc least significant difference. We observed an increase in native GPx activity and CAT immunodetection in groups with high susceptibility to induced lipid peroxidation. We also found an increase in total sperm defects, acrosome and membrane damages in the group with the highest susceptibility to induced lipid peroxidation. Additionally, the low mitochondrial membrane potential, susceptible to chromatin fragmentation and the PRM1 mRNA were increased in the group showing higher susceptibility to lipid peroxidation. Ram sperm susceptibility to lipid peroxidation may compromise sperm quality and interfere with the oxidative homeostasis by oxidative stress, which may be the main cause of chromatin damage in ram sperm. © 2016 Society for Reproduction and Fertility.

  9. Effects of diffusible products of peroxidation of rat liver microsomal lipids

    PubMed Central

    Benedetti, Angelo; Casini, Alessandro F.; Ferrali, Marco; Comporti, Mario

    1979-01-01

    The effects on cellular structures of products of peroxidation of rat liver microsomal lipids were investigated. A system containing actively peroxidizing liver microsomal fraction was separated from a revealing or target system by a dialysis membrane. The target system, contained in the dialysis tube, consisted of either intact cells (erythrocytes) or subcellular fractions (liver microsomal fraction). When liver microsomal fractions were incubated with NADPH (or an NADPH-generating system), lipid peroxidation, as measured by the amount of malonaldehyde formed, occurred very rapidly. The malon-aldehyde concentration tended to equilibrate across the dialysis membrane. When the target system consisted of erythrocytes, haemolysis occurred abruptly after a lag phase. The lysis was greatly accelerated when erythrocytes from vitamin E-deficient rats were used, but no haemolysis was observed when erythrocytes from vitamin E-treated rats were used. When, in the same system, freshly prepared liver microsomal fractions were exposed to diffusible factors produced by lipid peroxidation, the glucose 6-phosphatase activity markedly decreased. A similar decrease in glucose 6-phosphatase activity, as well as a smaller but significant decrease in cytochrome P-450, was observed when the target microsomal fractions were exposed to diffusible factors derived from the peroxidation of liver microsomal lipids in a separate preincubation step. These and additional experiments indicated that the toxicological activity is relatively stable. Experiments in which the hepatic microsomal fractions destined for lipid peroxidation contained radioactively labelled arachidonic acid, previously incorporated into the membranes, showed that part of the radioactivity released from the microsomal fraction into the incubation medium entered the dialysis tube and was recovered bound to the constituents of the microsomal fractions of the target system. These results indicate that during the course of the

  10. Vitamin E-supplemented diets reduce lipid peroxidation but do not alter either pituitary-adrenal, glucose, and lactate responses to immobilization stress or gastric ulceration.

    PubMed

    Armario, A; Campmany, L; Borras, M; Hidalgo, J

    1990-01-01

    It has been suggested that antioxidant administration to rats would reduce the physiological response to stress. In the present experiment adult male rats were given diets supplemented with vitamin E for one or seven days before they were subjected to immobilization stress. Vitamin E administration reduced hepatic and gastric lipid peroxidation in unstressed rats but did not modify the pituitary-adrenal, glucose and lactose responses to 1 or 18 h immobilization. Similarly, gastric ulceration caused by 18 h immobilization was unaffected by the diets. These results indicate that the inhibition of lipid peroxidation does not modify the response of several, well-known, stress-markers in the rat.

  11. Measurement of lipid peroxidation products in rabbit brain and organs (response to aluminum exposure).

    PubMed

    Bertholf, R L; Nicholson, J R; Wills, M R; Savory, J

    1987-01-01

    A method was developed for measuring the concentration of lipid peroxidation products in rabbit brain, heart, lung, liver, and kidney tissue. Specimens were homogenized in cold buffer, acidified, and heated to near boiling in the presence of thiobarbituric acid in order to form the malondialdehyde-thiobarbiturate adduct. After centrifugation, the supernatant was injected onto a reversed-phase high pressure liquid chromatography (HPLC) column, and the effluent was monitored for absorbance at 532 nm. Absorbances were compared to a standard curve constructed from absorbance data for tetraethoxypropane standards, which yield stoichiometric amounts of the malondialdehyde-thiobarbiturate adduct. Results were expressed as nmol of adduct per gram (dry weight) of tissue. Hippocampus had significantly greater concentrations of lipid peroxidation products (79.0 +/- 15.7 nmol per g) than did brainstem (52.1 +/- 13.8 nmol per g), but there was no significant increase in lipid peroxidation in aluminum treated rabbit brains when compared with controls. Aluminum intoxication appeared, however, to stimulate lipid peroxidation in heart, lung, liver, and kidney. Aluminum accumulation in brain and organ tissue of treated rabbits was confirmed by atomic absorption spectrophotometry of an acid digest of the homogenate. These results are in contrast to previous studies which demonstrated an increase in lipid peroxidation products in rat brains following oral administration of aluminum hydroxide.

  12. Correlation among lung damage after radiation, amount of lipid peroxides, and antioxidant enzyme activities

    SciTech Connect

    Nozue, M.; Ogata, T.

    1989-04-01

    The correlation between lipid peroxidation and morphologic changes was examined in Sprague-Dawley rat lungs after 30 Gy single thoracic radiation. The rats were sacrificed every week until the end of the fifth week after radiation. The left lungs were used for the measurement of lipid peroxides and antioxidant enzymes activities. The right lungs were examined by light and electron microscopy. Amounts of lung lipid peroxides were within normal limits, and no cellular degenerative changes were observed in the lungs except for subendothelial and interstitial edema 2 weeks after radiation. Lipid peroxides drastically increased and marked degenerative cellular changes such as edematous swelling, vacuolation, and destruction of cell membranes occurred in the alveolar septa following the third week after radiation. The activities of catalase were significantly higher during the period from the second to the fifth week and those of superoxide dismutase and glutathione peroxidase increased at the end of the fifth week. Our results demonstrated that the acceleration of lipid peroxidation was well correlated with the morphologic expression of cell injury in the irradiated lungs.

  13. Induction of antioxidant enzyme activity and lipid peroxidation level in ion-beam-bombarded rice seeds

    NASA Astrophysics Data System (ADS)

    Semsang, Nuananong; Yu, LiangDeng

    2013-07-01

    Low-energy ion beam bombardment has been used to mutate a wide variety of plant species. To explore the indirect effects of low-energy ion beam on biological damage due to the free radical production in plant cells, the increase in antioxidant enzyme activities and lipid peroxidation level was investigated in ion-bombarded rice seeds. Local rice seeds were bombarded with nitrogen or argon ion beams at energies of 29-60 keV and ion fluences of 1 × 1016 ions cm-2. The activities of the antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione S-transferase (GST) and lipid peroxidation level were assayed in the germinated rice seeds after ion bombardment. The results showed most of the enzyme activities and lipid peroxidation levels in both the argon and nitrogen bombarded samples were higher than those in the natural control. N-ion bombardment could induce higher levels of antioxidant enzyme activities in the rice samples than the Ar-ion bombardment. Additional effects due to the vacuum condition were found to affect activities of some antioxidant enzymes and lipid peroxidation level. This study demonstrates that ion beam bombardment and vacuum condition could induce the antioxidant enzyme activity and lipid peroxidation level which might be due to free radical production in the bombarded rice seeds.

  14. Comparison of the effects of metals on cellular injury and lipid peroxidation in isolated rat hepatocytes

    SciTech Connect

    Stacey, N.H.; Klaassen, C.D.

    1981-01-01

    Various mechanisms, including increases in lipid peroxidation, have been proposed to account for metal-induced cellular injury. By comparing several metals in the same cell population, it is possible to determine whether a correlation exists between ability to produce cell injury and ability to alter parameters pertaining to a particular mechanism. Of particular interest in this study was the relation between metal-induced cytotoxicity and increases in lipid peroxidation. The effects of Cr, Mn, Zn, Ni, Pb, Se, V, Fe, Cd, Hg, and Cu, at final concentrations of 1 to 1000 ..mu..M, on the viability of isolated hepatocytes were therefore examined by assessing the loss of intracellular K/sup +/ and aspartate aminotransferase (AST). Simultaneously, the ability of the metals to induce lipid peroxidation, as measured by an increase in thiobarbituric acid (TBA) reactants, was assessed. Hg and Cu required the lowest concentration to produce cellular injury, while Cd produced less dramatic changes in cell viability and Fe at 1000 ..mu..M produced only a small decrease in intracellular K/sup +/. The largest absolute increases in lipid peroxidation were found in the presence of V, followed by Fe and Hg, with Cd and Se causing the smallest increase in TBA reactants. These observations suggest that the lipid peroxidation associated with Cd and Hg is not necessarily responsible for the loss of cell viability induced by these two metals.

  15. Effect of genistein against copper-induced lipid peroxidation of human high density lipoproteins (HDL).

    PubMed

    Ferretti, G; Bacchetti, T; Menanno, F; Curatola, G

    2004-01-01

    Several studies have demonstrated that the isoflavone genistein exerts a protective effect against lipid peroxidation of low density lipoproteins (LDL). Aim of our study was to investigate whether genistein protects high density lipoproteins (HDL), isolated from normolipemic subjects, against Cu(++)-induced lipid peroxidation. Our results demonstrated that genistein exerts an inhibitory effect against Cu(++)-induced lipid peroxidation of HDL, as shown by the lower increase in the levels of conjugated dienes in lipoproteins oxidized after preincubation with different concentrations of genistein (0.5-2.5microM). Moreover the analysis of fluorescence emission spectra of tryptophan (Trp) and Laurdan (6-dodecanoyl-2-dimethyl-aminonaphthalene) demonstrated that genistein prevents the alterations of apoprotein structure and physico-chemical properties, associated with Cu(++)-triggered lipid peroxidation of lipoproteins. The protective effect exerted by genistein against oxidative damage of lipoproteins was realized at concentrations similar to those observed in plasma of human subjects consuming a traditional soy diet or receiving a soy supplement. Therefore, we suggested that antioxidant activity exerted by genistein against lipid peroxidation of HDL in vitro could be of physiological relevance.

  16. Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors

    PubMed Central

    Negre-Salvayre, A; Coatrieux, C; Ingueneau, C; Salvayre, R

    2007-01-01

    Reactive carbonyl compounds (RCCs) formed during lipid peroxidation and sugar glycoxidation, namely Advanced lipid peroxidation end products (ALEs) and Advanced Glycation end products (AGEs), accumulate with ageing and oxidative stress-related diseases, such as atherosclerosis, diabetes or neurodegenerative diseases. RCCs induce the ‘carbonyl stress' characterized by the formation of adducts and cross-links on proteins, which progressively leads to impaired protein function and damages in all tissues, and pathological consequences including cell dysfunction, inflammatory response and apoptosis. The prevention of carbonyl stress involves the use of free radical scavengers and antioxidants that prevent the generation of lipid peroxidation products, but are inefficient on pre-formed RCCs. Conversely, carbonyl scavengers prevent carbonyl stress by inhibiting the formation of protein cross-links. While a large variety of AGE inhibitors has been developed, only few carbonyl scavengers have been tested on ALE-mediated effects. This review summarizes the signalling properties of ALEs and ALE-precursors, their role in the pathogenesis of oxidative stress-associated diseases, and the different agents efficient in neutralizing ALEs effects in vitro and in vivo. The generation of drugs sharing both antioxidant and carbonyl scavenger properties represents a new therapeutic challenge in the treatment of carbonyl stress-associated diseases. PMID:17643134

  17. Antioxidant properties of aqueous extracts of unripe Musa paradisiaca on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro.

    PubMed

    Shodehinde, Sidiqat Adamson; Oboh, Ganiyu

    2013-06-01

    To evaluate and compare antioxidant activities of the aqueous extracts of unripe plantain (Musa paradisiaca), assess their inhibitory action on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro and to characterize the main phenolic constituents of the plantain products using gas chromatography analysis. Aqueous extracts of plantain products (raw, elastic pastry, roasted and boiled) flour of 0.1 g/mL (each) were used to determine their total phenol, total flavonoid, 1,1 diphenyl-2 picrylhydrazyl (DPPH) and hydroxyl (OH) radical scavenging ability. The inhibitory effect of the extracts on sodium nitroprusside induced lipid peroxidation was also determined. The results revealed that all the aqueous extracts showed antioxidant activity. The boiled flour had highest DPPH and OH radical scavenging ability while raw flour had the highest Fe(2+) chelating ability, sodium nitroprusside inhibitory effect and vitamin C content. The antioxidant results showed that elastic pastry had the highest total phenol and total flavonoid content. Characterization of the unripe plantain products for polyphenol contents using gas chromatography showed varied quantity of apigenin, myricetin, luteolin, capsaicin, isorhaemnetin, caffeic acid, kampferol, quercetin, p-hydroxybenzoic acid, shogaol, glycitein and gingerol per product on the spectra. Considering the antioxidant activities and ability to inhibit lipid peroxidation of unripe plantain, this could justify their traditional use in the management/prevention of diseases related to stress.

  18. Antioxidant properties of aqueous extracts of unripe Musa paradisiaca on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro

    PubMed Central

    Shodehinde, Sidiqat Adamson; Oboh, Ganiyu

    2013-01-01

    Objective To evaluate and compare antioxidant activities of the aqueous extracts of unripe plantain (Musa paradisiaca), assess their inhibitory action on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro and to characterize the main phenolic constituents of the plantain products using gas chromatography analysis. Methods Aqueous extracts of plantain products (raw, elastic pastry, roasted and boiled) flour of 0.1 g/mL (each) were used to determine their total phenol, total flavonoid, 1,1 diphenyl-2 picrylhydrazyl (DPPH) and hydroxyl (OH) radical scavenging ability. The inhibitory effect of the extracts on sodium nitroprusside induced lipid peroxidation was also determined. Results The results revealed that all the aqueous extracts showed antioxidant activity. The boiled flour had highest DPPH and OH radical scavenging ability while raw flour had the highest Fe2+ chelating ability, sodium nitroprusside inhibitory effect and vitamin C content. The antioxidant results showed that elastic pastry had the highest total phenol and total flavonoid content. Characterization of the unripe plantain products for polyphenol contents using gas chromatography showed varied quantity of apigenin, myricetin, luteolin, capsaicin, isorhaemnetin, caffeic acid, kampferol, quercetin, p-hydroxybenzoic acid, shogaol, glycitein and gingerol per product on the spectra. Conclusions Considering the antioxidant activities and ability to inhibit lipid peroxidation of unripe plantain, this could justify their traditional use in the management/prevention of diseases related to stress. PMID:23730557

  19. Chlorophenols induce lipid peroxidation and change antioxidant parameters in the leaves of wheat (Triticum aestivum L.).

    PubMed

    Michałowicz, Jaromir; Posmyk, Małgorzata; Duda, Wirgiliusz

    2009-04-01

    In this work, changes in superoxide dismutase (SOD), catalase (CAT) and guaiacol peroxidase (POD) activity were determined in the leaves of wheat (Triticum aestivum L.) exposed to 2,4-dichlorophenol (2,4-DCP) and pentachlorophenol (PCP). We analyzed the content of free phenols, the level of lipid peroxidation, and also the oxidation of dihydrorhodamine 123 by 2,4-DCP and PCP. Chlorophenols were spiked to soil in concentrations of 0.5 and 5.0 mg kg(-1). Plant seeds were raised in plastic pots containing soil at a temperature of 25 degrees C with a 16-h photoperiod and irradiance of 250 micromol m(-2) s(-1). The leaves were harvested on the third, sixth and twelfth days of the experiment. The inhibition of SOD activity in the leaves of wheat was observed for 2,4-DCP and PCP. 2,4-DCP and PCP induced changes in CAT activity with a stronger effect for PCP. The compounds markedly increased guaiacol POD activity during 12d of the exposition of wheat to their action. The increase in free phenol content was observed both for 2,4-DCP and PCP. Chlorophenols also induced a powerful lipid peroxidation process between the third and sixth days of the experiment. A higher concentration of chlorophenols used in our study induced greater changes in all of the investigated parameters. 2,4-DCP and PCP oxidized the fluorescent probe - dihydrorhodamine 123 - in the concentrations of 5 and 1 ppm, respectively, and the addition of magnesium ions enhanced the oxidative capacity of the examined xenobiotics.

  20. Lipid peroxidation and 4-hydroxy-2-nonenal formation by copper ion bound to amyloid-beta peptide.

    PubMed

    Hayashi, Takaaki; Shishido, Naomi; Nakayama, Kenji; Nunomura, Akihiko; Smith, Mark A; Perry, George; Nakamura, Masao

    2007-12-01

    The lipid peroxidation product 4-hydroxy-2-nonenal (HNE) is proposed to be a toxic factor in the pathogenesis of Alzheimer disease. The primary products of lipid peroxidation are phospholipid hydroperoxides, and degraded reactive aldehydes, such as HNE, are considered secondary peroxidation products. In this study, we investigated the role of amyloid-beta peptide (A beta) in the formation of phospholipid hydroperoxides and HNE by copper ion bound to A beta. The A beta1-42-Cu2+ (1:1 molar ratio) complex showed an activity to form phospholipid hydroperoxides from a phospholipid, 1-palmitoyl-2-linoleoyl phosphatidylcholine, through Cu2+ reduction in the presence of ascorbic acid. The phospholipid hydroperoxides were considered to be a racemic mixture of 9-hydroperoxide and 13-hydroperoxide of the linoleoyl residue. When Cu2+ was bound to 2 molar equivalents of A beta(1-42) (2 A beta1-42-Cu2+), lipid peroxidation was inhibited. HNE was generated from one of the phospholipid hydroperoxides, 1-palmitoyl-2-(13-hydroperoxy-cis-9, trans-11-octadecadienoyl) phosphatidylcholine (PLPC-OOH), by free Cu2+ in the presence of ascorbic acid through Cu2+ reduction and degradation of PLPC-OOH. HNE generation was markedly inhibited by equimolar concentrations of A beta(1-40) (92%) and A beta(1-42) (92%). However, A beta(1-42) binding 2 or 3 molar equivalents of Cu2+ (A beta1-42-2Cu2+, A beta1-42-3Cu2+) acted as a pro-oxidant to form HNE from PLPC-OOH. These findings suggest that, at moderate concentrations of copper, A beta acts primarily as an antioxidant to prevent Cu2+-catalyzed oxidation of biomolecules, but that, in the presence of excess copper, pro-oxidant complexes of A beta with Cu2+ are formed.

  1. Medicinal Mushroom Cracked-Cap Polypore, Phellinus rimosus (Higher Basidiomycetes) Attenuates Acute Ethanol-Induced Lipid Peroxidation in Mice.

    PubMed

    Ajith, Thekkuttuparambil A; Janardhanan, Kainoor K

    2015-01-01

    Alcohol abuse and alcoholism remain one of the major health issues worldwide, especially in developing countries. The protective effect of Phellinus rimosus against acute alcohol-induced lipid peroxidation in the liver, kidney, and brain as well as its effect against antioxidant enzyme activity such as superoxide (SOD) and catalase (CAT) in the liver was evaluated in mice. Ethyl acetate extract of Ph. Rimosus (50 mg/kg body wt, p.o.) 1 h before each administration of alcohol (3 mL/kg, p.o.; total 2 doses at 24-h intervals) protected against lipid peroxidation in all organs and attenuated the decline of SOD and CAT activity in the liver. The fold increase in lipid peroxidation, including conjugated diene and thiobarbituric acid reactive substance (TBARS) levels, was highest in the liver. There were 2.6- and 1.5- fold increases in TBARS levels in the liver of the alcohol alone- and alcohol+Ph. Rimosus-treated groups, compared with that of the normal group. Activity of SOD and CAT in the liver of alcohol- and alcohol+Ph. Rimosus- treated animals was 9.05±1.38, 18.76±1.71, and 11.26±1.02, 31.58±3.35 IU/mg protein, respectively. Extract at 1 mg/mL inhibited 50.6% activity of aniline hydroxylase (CYP2E1) in liver homogenate. From these results, we concluded that the extract significantly protected against the lipid peroxidation. Protection in the liver may be due to the inhibitory effect on CYP2E1 as well as the direct radical scavenging effect of Ph. Rimosus, which warrants further research.

  2. Bioactive potential of Vitis labrusca L. grape juices from the Southern Region of Brazil: phenolic and elemental composition and effect on lipid peroxidation in healthy subjects.

    PubMed

    Toaldo, Isabela Maia; Cruz, Fernanda Alves; Alves, Tatiana de Lima; de Gois, Jefferson Santos; Borges, Daniel L G; Cunha, Heloisa Pamplona; da Silva, Edson Luiz; Bordignon-Luiz, Marilde T

    2015-04-15

    Grapes are rich in polyphenols with biologically active properties. Although the bioactive potential of grape constituents are frequently reported, the effects of Brazilian Vitis labrusca L. grape juices ingestion have not been demonstrated in humans. This study identified the phenolic and elemental composition of red and white grape juices and the effect of organic and conventional red grape juice consumption on lipid peroxidation in healthy individuals. Concentrations of anthocyanins, flavanols and phenolic acids and the in vitro antioxidant activity were significantly higher in the organic juice. The macro-elements K, Ca, Na and Mg were the most abundant minerals in all juices. The acute consumption of red grape juices promoted significant decrease of lipid peroxides in serum and TBARS levels in plasma. It is concluded that red V. labrusca L. grape juices produced in Southern Brazil showed lipid peroxidation inhibition abilities in healthy subjects, regardless of the cultivation system. Copyright © 2014 Elsevier Ltd. All rights reserved.

  3. Lipid peroxidation in the presence of albumin, inhibitory and prooxidative effects.

    PubMed

    Samocha-Bonet, Dorit; Gal, Sigal; Schnitzer, Edit; Lichtenberg, Dov; Pinchuk, Ilya

    2004-11-01

    Oxidative modifications of LDL are involved in atherogenesis. Previously we have developed a simple assay to evaluate the susceptibility of lipids to copper-induced peroxidation in the relatively natural milieu of unfractionated serum in the presence of excess citrate. Based on our previous results we have proposed that the inducer of peroxidation in our optimized assay is a copper-citrate complex. Recent investigations indicate that under certain conditions a copper-albumin complex may induce peroxidation of ascorbate. Two different complexes may be formed in albumin-containing systems (e.g. serum) namely 1:1 and 2:1 copper-albumin complexes. The aim of the present work was to evaluate the possibility that at least one of these complexes may be responsible for the induction of peroxidation of lipids in lipidic systems containing copper and albumin, including our optimized assay. Towards this end, we have investigated the dependence of copper-induced peroxidation on the concentration of added albumin in lipidic systems in the absence and presence of citrate. In all the systems investigated in this study (PLPC liposomes, LDL, HDL and mixtures of HDL and LDL) we found that at low concentrations of free copper (e.g. in the presence of excess citrate) the 2:1 copper-albumin complex is redox-active and that this complex is the major contributor to the initiation of lipid peroxidation in these systems and in our optimized assay. The possible relevance of the induction of peroxidation in vivo by the latter complex has yet to be studied.

  4. Rebamipide attenuates nonsteroidal anti-inflammatory drugs (NSAID) induced lipid peroxidation by the manganese superoxide dismutase (MnSOD) overexpression in gastrointestinal epithelial cells.

    PubMed

    Nagano, Y; Matsui, H; Shimokawa, O; Hirayama, A; Tamura, M; Nakamura, Y; Kaneko, T; Rai, K; Indo, H P; Majima, H J; Hyodo, I

    2012-04-01

    Nonsteroidal anti-inflammatory drugs (NSAIDs) often cause gastrointestinal complications such as gastric ulcers and erosions. Recent studies on the pathogenesis have revealed that NSAIDs induce lipid peroxidation in gastric epithelial cells by generating superoxide anion in mitochondria, independently with cyclooxygenase-inhibition and the subsequent prostaglandin deficiency. Although not clearly elucidated, the impairment of mitochondrial oxidative phosphorylation, or uncoupling, by NSAIDs is associated with the generation of superoxide anion. Physiologically, superoxide is immediately transformed into hydrogen peroxide and diatomic oxygen with manganese superoxide dismutase (MnSOD). Rebamipide is an antiulcer agent that showed protective effects against NSAID-induced lipid peroxidation in gastrointestinal tracts. We hypothesized that rebamipide may attenuate lipid peroxidation by increasing the expression of MnSOD protein in mitochondria and decreasing the leakage of superoxide anion in NSAID-treated gastric and small intestinal epithelial cells. Firstly, to examine rebamipide increases the expression of MnSOD proteins in mitochondria of gastrointestinal epithelial cells, we underwent Western blotting analysis against anti-MnSOD antibody in gastric RGM1 cells and small intestinal IEC6 cells. Secondly, to examine whether the pretreatment of rebamipide decreases NSAID-induced mitochondrial impairment and lipid peroxidation, we treated these cells with NSAIDs with or without rebamipide pretreatment, and examined with specific fluorescent indicators. Finally, to examine whether pretreatment of rebamipide attenuates NSAID-induced superoxide anion leakage from mitochondria, we examined the mitochondria from indomethacin-treated RGM1 cells with electron spin resonance (ESR) spectroscopy using a specific spin-trapping reagent, CYPMPO. Rebamipide increased the expression of MnSOD protein, and attenuated NSAID-induced mitochondrial impairment and lipid peroxidation in RGM1

  5. Effect of stress-induced lipid peroxidation on functions of rat peritoneal macrophages.

    PubMed

    Izgüt-Uysal, V Nimet; Tan, Ruken; Bülbül, Mehmet; Derin, Narin

    2004-01-01

    The aim of the present study was to investigate the effects of stress-induced lipid peroxidation on macrophages' functions. Animals were subjected to 4 h immobilization at 4 degrees C in restraining devices. The peritoneal macrophages obtained from rats exposed to cold and restraint stress exhibited an increase in lipid peroxidation and a decline of chemotaxis and phagocytosis compared with control rats. After supplementation with vitamin E, the increment in thiobarbituric acid reactive substances (TBARS) content as the oxidative stress marker and the decline of chemotaxis and phagocytosis in peritoneal macrophages observed during cold-restraint stress was significantly removed. No significant change in catalase activity of peritoneal macrophages was observed in groups exposed to cold-restraint stress and treated with vitamin E. These findings indicate that phagocytic and chemotactic capacities of peritoneal macrophages are decreased by cold-restraint stress and this effect of stress may be related to lipid peroxidation.

  6. Photoirradiation of polycyclic aromatic hydrocarbon diones by UVA light leading to lipid peroxidation.

    PubMed

    Zhao, Yuewei; Xia, Qingsu; Yin, Jun-Jie; Yu, Hongtao; Fu, Peter P

    2011-09-01

    Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous genotoxic environmental pollutants and potentially pose a health risk to humans. In most if not all cases, PAHs in the environment can be oxidized into their corresponding PAH-diones. This process is considered a detoxification pathway with regard to tumorigenicity. Nevertheless, photo-induced toxicological activity of PAH-diones has not been systematically investigated. In this study, we show that 27 potential environmental PAH-diones induced lipid peroxidation, in a dose (light) response manner, when irradiated with UVA at 7 and 21 J cm(-2). Photoirradiation in the presence of sodium azide, deuterated methanol, or superoxide dismutase revealed that lipid peroxidation is mediated by reactive oxygen species. Electron spin resonance (ESR) spin trapping studies supported this observation. These results suggest that UVA photoirradiation of PAH-diones generates reactive oxygen species and induces lipid peroxidation. Published by Elsevier Ltd.

  7. Increase in plasma lipid peroxide in cats fed a fish diet.

    PubMed

    Momoi, Y; Goto, Y; Tanide, K; Takahashi, N; Watari, T; Yamazo, K; Tsujimoto, H; Kudo, T

    2001-12-01

    Plasma lipid peroxide levels were examined in cats. Plasma lipid peroxide levels in 3 of 4 clinical cases which had been fed raw fish were higher than those in normal cats. When healthy cats were put on a raw fish diet in controlled conditions, a remarkable increase in plasma lipid peroxide was observed. This increase occurred within 1 to 3 weeks in cats without obvious clinical disorders. We also showed that a continuous raw fish diet is necessary to cause the increase, but the increase was transient and restored in spite of a continuous raw fish diet, indicating the development of an unidentified antioxidant process. Our results clearly indicate that intake of foods high in polyunsaturated fatty acid can induce oxidative stress in cats.

  8. Augmentation of macrophage growth-stimulating activity of lipids by their peroxidation

    SciTech Connect

    Yui, S.; Yamazaki, M. )

    1990-02-15

    Previously, we reported that some kinds of lipids (cholesterol esters, triglycerides, and some negatively charged phospholipids) that are constituents of lipoproteins or cell membranes induce growth of peripheral macrophages in vitro. In this paper, we examined the effect of peroxidation of lipids on their macrophage growth-stimulating activity because lipid peroxidation is observed in many pathological states such as inflammation. When phosphatidylserine, one of the phospholipids with growth-stimulating activity, was peroxidized by UV irradiation, its macrophage growth-stimulating activity was augmented in proportion to the extent of its peroxidation. The activity of phosphatidylethanolamine was also increased by UV irradiation. On the other hand, phosphatidylcholine or highly unsaturated free fatty acids, such as arachidonic acid and eicosapentaenoic acid, did not induce macrophage growth irrespective of whether they were peroxidized. The augmented activity of UV-irradiated phosphatidylserine was not affected by the coexistence of an antioxidant, vitamin E or BHT. These results suggest that some phospholipids included in damaged cells or denatured lipoproteins which are scavenged by macrophages in vivo may induce growth of peripheral macrophages more effectively when they are peroxidized by local pathological processes.

  9. Lipid profiling of the Arabidopsis hypersensitive response reveals specific lipid peroxidation and fragmentation processes: biogenesis of pimelic and azelaic acid.

    PubMed

    Zoeller, Maria; Stingl, Nadja; Krischke, Markus; Fekete, Agnes; Waller, Frank; Berger, Susanne; Mueller, Martin J

    2012-09-01

    Lipid peroxidation (LPO) is induced by a variety of abiotic and biotic stresses. Although LPO is involved in diverse signaling processes, little is known about the oxidation mechanisms and major lipid targets. A systematic lipidomics analysis of LPO in the interaction of Arabidopsis (Arabidopsis thaliana) with Pseudomonas syringae revealed that LPO is predominantly confined to plastid lipids comprising galactolipid and triacylglyceride species and precedes programmed cell death. Singlet oxygen was identified as the major cause of lipid oxidation under basal conditions, while a 13-lipoxygenase (LOX2) and free radical-catalyzed lipid oxidation substantially contribute to the increase upon pathogen infection. Analysis of lox2 mutants revealed that LOX2 is essential for enzymatic membrane peroxidation but not for the pathogen-induced free jasmonate production. Despite massive oxidative modification of plastid lipids, levels of nonoxidized lipids dramatically increased after infection. Pathogen infection also induced an accumulation of fragmented lipids. Analysis of mutants defective in 9-lipoxygenases and LOX2 showed that galactolipid fragmentation is independent of LOXs. We provide strong in vivo evidence for a free radical-catalyzed galactolipid fragmentation mechanism responsible for the formation of the essential biotin precursor pimelic acid as well as of azelaic acid, which was previously postulated to prime the immune response of Arabidopsis. Our results suggest that azelaic acid is a general marker for LPO rather than a general immune signal. The proposed fragmentation mechanism rationalizes the pathogen-induced radical amplification and formation of electrophile signals such as phytoprostanes, malondialdehyde, and hexenal in plastids.

  10. Perioperative Intravenous Acetaminophen Attenuates Lipid Peroxidation in Adults Undergoing Cardiopulmonary Bypass: A Randomized Clinical Trial

    PubMed Central

    Billings IV, Frederic T.; Petracek, Michael R.; Roberts II, L. Jackson; Pretorius, Mias

    2015-01-01

    Background Cardiopulmonary bypass (CPB) lyses erythrocytes and induces lipid peroxidation, indicated by increasing plasma concentrations of free hemoglobin, F2-isoprostanes, and isofurans. Acetaminophen attenuates hemeprotein-mediated lipid peroxidation, reduces plasma and urine concentrations of F2-isoprostanes, and preserves kidney function in an animal model of rhabdomyolysis. Acetaminophen also attenuates plasma concentrations of isofurans in children undergoing CPB. The effect of acetaminophen on lipid peroxidation in adults has not been studied. This was a pilot study designed to test the hypothesis that acetaminophen attenuates lipid peroxidation in adults undergoing CPB and to generate data for a clinical trial aimed to reduce acute kidney injury following cardiac surgery. Methods and Results In a prospective double-blind placebo-controlled clinical trial, sixty adult patients were randomized to receive intravenous acetaminophen or placebo starting prior to initiation of CPB and for every 6 hours for 4 doses. Acetaminophen concentrations measured 30 min into CPB and post-CPB were 11.9±0.6 μg/mL (78.9±3.9 μM) and 8.7±0.3 μg/mL (57.6±2.0 μM), respectively. Plasma free hemoglobin increased more than 15-fold during CPB, and haptoglobin decreased 73%, indicating hemolysis. Plasma and urinary markers of lipid peroxidation also increased during CPB but returned to baseline by the first postoperative day. Acetaminophen reduced plasma isofuran concentrations over the duration of the study (P = 0.05), and the intraoperative plasma isofuran concentrations that corresponded to peak hemolysis were attenuated in those subjects randomized to acetaminophen (P = 0.03). Perioperative acetaminophen did not affect plasma concentrations of F2-isoprostanes or urinary markers of lipid peroxidation. Conclusions Intravenous acetaminophen attenuates the increase in intraoperative plasma isofuran concentrations that occurs during CPB, while urinary markers were unaffected

  11. Synthesis and Photoirradiation of Isomeric Ethylchrysenes by UVA Light Leading to Lipid Peroxidation

    PubMed Central

    Chen, Hui-Chan; Xia, Qingsu; Cherng, Shu-Hui; Chen, Shoujun; Lai, Ching-Cheng; Yu, Hongtao; Fu, Peter P.

    2007-01-01

    Polycyclic aromatic hydrocarbons (PAHs) are widespread genotoxic environmental pollutants. We have recently demonstrated that photoirradiation of PAHs leads to cytotoxicity, DNA damage, and induction of lipid peroxidation. In this paper we report the synthesis of all the six isomeric ethylchrysenes and the study of light-induced lipid peroxidation by these ethylchrysenes. 5-Ethylchrysene was synthesized by reaction of 5-keto-5,6,6a,7,8,9,10,10a-octahydrochrysene with CH3CH2MgBr followed by dehydration catalyzed by p-toluenesulfonic acid and dehydrogenation with DDQ in benzene. 1- and 4-Ethylchrysenes were similarly prepared by reaction of 1-keto-1,2,3,4,5,6-hexahydrochrysene and 4-keto-1,2,3,4-tetrahydrochrysenes, respectively with CH3CH2MgBr followed by dehydration and dehydrogenation. Direct acetylation of chrysene followed by Wolff-Kishner or Clemmensen reduction resulted in the formation of 2-, 3-, and 6-ethylchrysenes in 4%, 16%, and 43% yields, respectively. Photoirradiation of these compounds with 7 and 21 J/cm2 UVA light in the presence of methyl linoleate all resulted in lipid peroxidation. For comparison, photoirradiation of 4-methylchrysene and 5-methylchrysene was similarly conducted. For irradiation at a UVA light dose of 21 J/cm2, the level of induced lipid peroxidation is in the order 4-methylchrysene = 5-methylchrysene = 5-ethylchrysene = 4-ethylchrysene = chrysene > 1-ethylchrysene = 2-ethylchrysene > 3-ethylchrysene > 6-ethylchrysene. Compared with chrysene, these results indicate that the ethyl group at C4 or C5 position either slightly enhances or has no effect on the light-induced lipid peroxidation, while at C1-, C2-, C3-, or C6 position reduces light-induced lipid peroxidation. PMID:17617678

  12. Continuous millimeter-wave radiation has no effect on lipid peroxidation in liposomes

    SciTech Connect

    Logani, M.K.; Ziskin, M.C.

    1996-02-01

    The effect of millimeter waves on lipid peroxidation was studied in the presence and absence of melanin. Irradiation of liposomes with continuous millimeter electromagnetic waves at frequencies of 53.6, 61.2 and 78.2 GHz and incident power densities of 10, 1 and 500 mW/cm{sup 2}, respectively, did not show an enhancement in the formation of lipid peroxides compared to unirradiated samples. Liposomes exposed to 254 nm UVC radiation at 0.32 mW/cm{sup 2} and 302 nm UVB radiation at 1.12 mW/cm{sup 2} served as positive controls. No increment in the formation of lipid peroxides was observed when irradiation of liposomes was carried out in the presence of ADP-Fe{sup +3} and EDTA-Fe{sup +3}. Direct irradiation of melanin with millimeter waves did not exhibit an increased formation of superoxide or hydrogen peroxide. The present results indicate that millimeter waves of the above frequencies and intensities do not cause lipid peroxidation in liposomal membranes. 19 refs., 2 figs., 1 tab.

  13. Green tea supplementation affects body weight, lipids, and lipid peroxidation in obese subjects with metabolic syndrome.

    PubMed

    Basu, Arpita; Sanchez, Karah; Leyva, Misti J; Wu, Mingyuan; Betts, Nancy M; Aston, Christopher E; Lyons, Timothy J

    2010-02-01

    To compare the effects of supplementation of green tea beverage or green tea extracts with controls on body weight, glucose and lipid profile, biomarkers of oxidative stress, and safety parameters in obese subjects with metabolic syndrome. Randomized, controlled prospective trial. General Clinical Research Center (GCRC) at University of Oklahoma Health Sciences Center (OUHSC). Thirty-five subjects with obesity and metabolic syndrome were recruited in age- and gender-matched trios and were randomly assigned to the control (4 cups water/d), green tea (4 cups/d), or green tea extract (2 capsules and 4 cups water/d) group for 8 weeks. The tea and extract groups had similar dosing of epiogallocatechin-3-gallate (EGCG), the active compound in green tea. Anthropometrics, blood pressure, fasting glucose and lipids, nuclear magnetic resonance (NMR)-based lipid particle size, safety parameters, biomarkers of oxidative stress (oxidized low-density lipoprotein [LDL], myeloperoxidase [MPO], malondialdehyde and hydroxynonenals [MDA and HNE]), and free catechins were analyzed at screen and at 4 and 8 weeks of the study. Pairwise comparisons showed green tea beverage and green tea extracts caused a significant decrease in body weight and body mass index (BMI) versus controls at 8 weeks (-2.5 +/- 0.7 kg, p < 0.01, and -1.9 +/- 0.6, p < 0.05, respectively). Green tea beverage showed a decreasing trend in LDL-cholesterol and LDL/high-density lipoprotein (HDL) versus controls (p < 0.1). Green tea beverage also significantly decreased MDA and HNE (-0.39 +/- 0.06 microM, p < 0.0001) versus controls. Plasma free catechins were detectable in both beverage and extract groups versus controls at screen and at 8 weeks, indicating compliance and bioavailability of green tea catechins. Green tea beverage consumption (4 cups/d) or extract supplementation (2 capsules/d) for 8 weeks significantly decreased body weight and BMI. Green tea beverage further lowered lipid peroxidation versus age- and

  14. On the role of microsomal aldehyde dehydrogenase in metabolism of aldehydic products of lipid peroxidation.

    PubMed

    Antonenkov, V D; Pirozhkov, S V; Panchenko, L F

    1987-11-30

    To elucidate a possible role of membrane-bound aldehyde dehydrogenase in the detoxication of aldehydic products of lipid peroxidation, the substrate specificity of the highly purified microsomal enzyme was investigated. The aldehyde dehydrogenase was active with different aliphatic aldehydes including 4-hydroxyalkenals, but did not react with malonic dialdehyde. When Fe/ADP-ascorbate-induced lipid peroxidation of arachidonic acid was carried out in an in vitro system, the formation of products which react with microsomal aldehyde dehydrogenase was observed parallel with malonic dialdehyde accumulation.

  15. Ameliorating reactive oxygen species-induced in vitro lipid peroxidation in brain, liver, mitochondria and DNA damage by Zingiber officinale Roscoe.

    PubMed

    Ajith, T A

    2010-01-01

    Iron is an essential nutrient for a number of cellular activities. However, excess cellular iron can be toxic by producing reactive oxygen species (ROS) such as superoxide anion (O(2) (-)) and hydroxyl radical (HO(·)) that damage proteins, lipids and DNA. Mutagenic and genotoxic end products of lipid peroxidation can induce the decline of mitochondrial respiration and are associated with various human ailments including aging, neurodegenerative disorders, cancer etc. Zingiber officinale Roscoe (ginger) is a widely used spice around the world. The protective effect of aqueous ethanol extract of Z. officinale against ROS-induced in vitro lipid peroxidation and DNA damage was evaluated in this study. The lipid peroxidation was induced by hydroxyl radical generated from Fenton's reaction in rat liver and brain homogenates and mitochondrial fraction (isolated from rat liver). The DNA protection was evaluated using H(2)O(2)-induced changes in pBR-322 plasmid and Fenton reaction-induced DNA fragmentation in rat liver. The results indicated that Z. officinale significantly (P<0.001) protected the lipid peroxidation in all the tissue homogenate/mitochondria. The extract at 2 and 0.5 mg/ml could protect 92 % of the lipid peroxidation in brain homogenate and liver mitochondria respectively. The percent inhibition of lipid peroxidation at 1mg/ml of Z. officinale in the liver homogenate was 94 %. However, the extract could partially alleviate the DNA damage. The protective mechanism can be correlated to the radical scavenging property of Z. officinale. The results of the study suggest the possible nutraceutical role of Z. officinale against the oxidative stress induced human ailments.

  16. Involvement of active oxygen in lipid peroxide radical reaction of epidermal homogenate following ultraviolet light exposure

    SciTech Connect

    Nishi, J.; Ogura, R.; Sugiyama, M.; Hidaka, T.; Kohno, M. )

    1991-07-01

    To elucidate the radical mechanism of lipid peroxidation induced by ultraviolet light (UV) irradiation, an electron spin resonance (ESR) study was made on epidermal homogenate prepared from albino rat skin. The exposure of the homogenate to UV light resulted in an increase in lipid peroxide content, which was proportional to the time of UV exposure. Using ESR spin trapping (dimethyl-1-pyrroline-N-oxide, DMPO), the DMPO spin adduct spectrum of lipid radicals (L.) was measured following UV exposure (DMPO-L.:aN = 15.5 G, aH = 22.7 G), as was the spectrum of DMPO-hydroxyl radical (DMPO-OH, aN = aH = 15.5 G). In the presence of superoxide dismutase, the DMPO spin adduct spectrum of lipid radicals was found to be reduced remarkably. Therefore, it was shown that the generation of the lipid radicals partially involves superoxide anion radicals, in addition to hydroxyl radicals. In the ESR free-radical experiment, an ESR signal appeared at g = 2.0064 when the ESR tube filled with homogenate was exposed to UV light at -150 degrees C. The temperature-dependent change in the ESR free radical signal of homogenate exposed to UV light was observed at temperatures varying from -150 degrees C to room temperature. By using degassed samples, it was confirmed that oxygen is involved in the formation of the lipid peroxide radicals (LOO.) from the lipid radicals (L.).

  17. Benefits of blackberry nectar (Rubus spp.) relative to hypercholesterolemia and lipid peroxidation.

    PubMed

    Ferreira de Araujo, P R; da Silva Santos, V; Rodrigues Machado, A; Gevehr Fernandes, C; Silva, J A; da Silva Rodrigues, R

    2011-01-01

    In humans, the normal metabolic activity produces free radicals that constantly, along with other risk factors, including hypercholesterolemia may be responsible for the onset of degenerative diseases. Some bioactive compounds present in blackberry (Rubus spp.) have the ability to act as natural antioxidants can make the food to minimize effects on the body caused by reactive oxygen species. This study verified the benefits of blackberry nectar through the quantification of triglycerides, total and fraction cholesterol HDL (high density lipoprotein) and LDL-cholesterol (low density lipoprotein), blood glucose and lipid peroxidation in hypercholesterolemic hamsters. Two groups were treated with hypercholesterolemic diets (0.1% cholesterol), one of them receiving an additional 5 mL of nectar daily, and a third (control group) treated only with a standard diet. In the blood the quantification of lipids, blood glucose and lipid peroxidation was performed. In the brain, liver and small intestine the lipid peroxidation was determined and in other organs, histopathological evaluations were carried out. The blackberry nectar reduced the triglycerides serum levels, total cholesterol and LDL-cholesterol in hypercholesterolemic hamsters, without influencing the HDL and blood glucose concentrations. A decrease in the initiation of lipid peroxidation reactions in the blood, brain and small intestine was also observed. Only the liver showed histopathological changes (steatosis), due to excess cholesterol, with no positive influence from the nectar.

  18. Acute response of rat liver microsomal lipids, lipid peroxidation, and membrane anisotropy to a single oral dose of polybrominated biphenyls.

    PubMed

    Bernert, J T; Groce, D F

    1984-01-01

    Liver microsomal lipids and lipid peroxidation activities were examined in adult male rats at intervals over a 2-mo period after the administration of a single oral dose of 0 or 500 mg/kg of FireMaster BP-6 in corn oil. Microsomal lipids were markedly altered in the polybrominated biphenyl- (PBB-) dosed animals at the earliest time examined (1 wk), and these changes persisted throughout the remainder of the study. An early decrease in the cholesterol-phospholipid ratio was noted, which probably contributed to the significant decrease in the steady-state fluorescence anisotropy demonstrable in both intact microsomes and in liposomes prepared from microsomal lipid extracts. Significant concentrations of PBBs were present in dosed rat microsomes, but the changes in anisotropy appeared to result from membrane lipid alterations rather than from a direct perturbation by PBBs. Iron ascorbate-induced peroxidation was also greatly enhanced in dosed rat microsomes, even when rats were maintained on a low-iron (25 ppm) diet. These early alterations in membrane fluidity and peroxidative capacity of microsomes may ultimately contribute to the hepatotoxicity of PBBs.

  19. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: Focusing on mitochondria

    PubMed Central

    Zhong, Huiqin; Yin, Huiyong

    2014-01-01

    Oxidative stress-induced lipid peroxidation has been associated with human physiology and diseases including cancer. Overwhelming data suggest that reactive lipid mediators generated from this process, such as 4-hydroxynonenal (4-HNE), are biomarkers for oxidative stress and important players for mediating a number of signaling pathways. The biological effects of 4-HNE are primarily due to covalent modification of important biomolecules including proteins, DNA, and phospholipids containing amino group. In this review, we summarize recent progress on the role of 4-HNE in pathogenesis of cancer and focus on the involvement of mitochondria: generation of 4-HNE from oxidation of mitochondria-specific phospholipid cardiolipin; covalent modification of mitochondrial proteins, lipids, and DNA; potential therapeutic strategies for targeting mitochondrial ROS generation, lipid peroxidation, and 4-HNE. PMID:25598486

  20. Anthocyanin content, lipid peroxidation and cyclooxygenase enzyme inhibitory activities of sweet and sour cherries.

    PubMed

    Mulabagal, Vanisree; Lang, Gregory A; DeWitt, David L; Dalavoy, Sanjeev S; Nair, Muraleedharan G

    2009-02-25

    Cherries contain bioactive anthocyanins that are reported to possess antioxidant, anti-inflammatory, anticancer, antidiabetic and antiobese properties. The present study revealed that red sweet cherries contained cyanidin-3-O-rutinoside as major anthocyanin (>95%). The sweet cherry cultivar "Kordia" (aka "Attika") showed the highest cyanidin-3-O-rutinoside content, 185 mg/100 g fresh weight. The red sweet cherries "Regina" and "Skeena" were similar to "Kordia", yielding cyanidin-3-O-rutinoside at 159 and 134 mg/100 g fresh weight, respectively. The yields of cyanidin-3-O-glucosylrutinoside and cyanidin-3-O-rutinoside were 57 and 19 mg/100 g fresh weight in "Balaton" and 21 and 6.2 mg/100 g fresh weight in "Montmorency", respectively, in addition to minor quantities of cyanidin-3-O-glucoside. The water extracts of "Kordia", "Regina", "Glacier" and "Skeena" sweet cherries gave 89, 80, 80 and 70% of lipid peroxidation (LPO) inhibition, whereas extracts of "Balaton" and "Montmorency" were in the range of 38 to 58% at 250 microg/mL. Methanol and ethyl acetate extracts of the yellow sweet cherry "Rainier" containing beta-carotene, ursolic, coumaric, ferulic and cafeic acids inhibited LPO by 78 and 79%, respectively, at 250 microg/mL. In the cyclooxygenase (COX) enzyme inhibitory assay, the red sweet cherry water extracts inhibited the enzymes by 80 to 95% at 250 microg/mL. However, the methanol and ethyl acetate extracts of "Rainier" and "Gold" were the most active against COX-1 and -2 enzymes. Water extracts of "Balaton" and "Montmorency" inhibited COX-1 and -2 enzymes by 84, and 91 and 77, and 87%, respectively, at 250 microg/mL.

  1. Alterations in circadian rhythms are associated with increased lipid peroxidation in females with bipolar disorder.

    PubMed

    Cudney, Lauren E; Sassi, Roberto B; Behr, Guilherme A; Streiner, David L; Minuzzi, Luciano; Moreira, Jose C F; Frey, Benicio N

    2014-05-01

    Disturbances in both circadian rhythms and oxidative stress systems have been implicated in the pathophysiology of bipolar disorder (BD), yet no studies have investigated the relationship between these systems in BD. We studied the impact of circadian rhythm disruption on lipid damage in 52 depressed or euthymic BD females, while controlling for age, severity of depressive symptoms and number of psychotropic medications, compared to 30 healthy controls. Circadian rhythm disruption was determined by a self-report measure (Biological Rhythm Interview of Assessment in Neuropsychiatry; BRIAN), which measures behaviours such as sleep, eating patterns, social rhythms and general activity. Malondialdehyde (MDA) levels were measured as a proxy of lipid peroxidation. We also measured the activity of total and extracellular superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST). Multiple linear regressions showed that circadian rhythm disturbance was independently associated with increased lipid peroxidation in females with BD (p < 0.05). We found decreased extracellular SOD (p < 0.05), but no differences in total SOD, CAT or GST activity between bipolar females and controls. Circadian rhythms were not associated with lipid peroxidation in healthy controls, where aging was the only significant predictor. These results suggest an interaction between the circadian system and redox metabolism, in that greater disruption in daily rhythms was associated with increased lipid peroxidation in BD only. Antioxidant enzymes have been shown to follow a circadian pattern of expression, and it is possible that disturbance of sleep and daily rhythms experienced in BD may result in decreased antioxidant defence and therefore increased lipid peroxidation. This study provides a basis for further investigation of the links between oxidative stress and circadian rhythms in the neurobiology of BD.

  2. Role of lipid peroxidation and oxidative stress in 3-methylindole pneumotoxicity

    SciTech Connect

    Cary, M.G.

    1985-01-01

    The cytochrome P-450-catalyzed metabolism of 3-methylindole (3-MI) results in acute lung injury in ruminants and horses. Experiments were conducted to determine the role of lipid peroxidation and oxidative stress in 3-MI pneumotoxicity in goats. Goats were given methylethylketone peroxide (MEKP), a potent peroxidant, 3-MI, indole, or cremophor-EL vehicle. The levels of shortchain hydrocarbons in expired air were measured for 6 hours post-dosing by gas chromatography. Exhaled hydrocarbons increased 20 to 30 fold within 1 hour in goats given MEKP. No significant changes were seen in goats given 3-Mi, indole or cremophor-EL. Levels of thiobarbituric acid-reactive substances, an indicator of lipid peroxidation, were significantly increased in lung tissue from goats given MEKP. In goats given 3-MI, indole or cremophor-EL, the levels were not significantly different from each other. Goats were killed at 6 hours post-dosing and examined post mortem. Bronchiolar epithelial necrosis was seen in goats given 3-MI but there were not lung lesions in other groups. The role of oxygen radicals in 3-MI pneumotoxicity was examined in a goat lung explant system using /sup 51/Cr release as an indicator of cytotoxicity. The results of these studies provide no evidence to support the view that 3-MI pneumotoxicity involves lipid peroxidation or oxidative stress as a result of formation of oxygen or xenobiotic radicals.

  3. Effects of cupric and ferric ions on in vitro lipid peroxidation of human serum

    SciTech Connect

    Dasgupta, A.; Peng, Y.; Zdunek, T. )

    1991-03-15

    Transition metal ions especially ferric ions can catalytically generate free radicals by the Haber-Weiss reaction and initiate lipid peroxidation. Such processes may contribute to the mechanism of acute toxicity by transition metals. Serum pools were prepared from normal blood donors and incubated with 1mM cupric or ferric ions at 37C for 24h. Lipid peroxidation products were subsequently measured by 2-thiobarbituric acid assay as described by Yagi and the values were expressed as {mu}mol/L malonaldehyde equivalents. In another experiment, lipoproteins were coprecipitated with other proteins by 10% phosphotungstic acid/sulfuric acid and precipitates in aqueous suspension were incubated with 1 mM cupric or ferric ions. When sera were incubated, the authors observed higher concentrations of lipid peroxidation products with cupric ions compared to samples supplemented with ferric ions. The mean value for peroxidation products in control group was 2.5 {mu}mol/L. However, the effect was reversed when protein precipitates were incubated in presence of such ions. Ferric ions also caused more peroxidation of linoleic acid and phosphatidylcholine isolated from egg yolk when compared to cupric ions. Such differential behavior may be attributed to different degree of chelation of ferric and cupric ions with serum proteins.

  4. Antioxidant effects of 1,4-dihydropyridine and nitroso aryl derivatives on the Fe+3/ascorbate-stimulated lipid peroxidation in rat brain slices.

    PubMed

    Díaz-Araya, G; Godoy, L; Naranjo, L; Squella, J A; Letelier, M E; Núñez-Vergara, L J

    1998-09-01

    1. Lipid peroxidation in rat brain slices was induced by Fe+3/ascorbate. 2. Brain lipid peroxidation, as measured by malondialdehyde formation, was inhibited by all the tested nitro aryl 1,4-dihydropyridine derivatives over a wide range of concentrations. The time-course antioxidant effects of the most representative agents were assessed. On the basis of both time-course and IC50 experiments the tentative order of antioxidant activity on rat brain slices could be: nicardipine>nisoldipine> (R,S/S,R)-furnidipine > (R,R/S,S)-furnidipine>nitrendipine>nimodipine> nifedipine. 3. 1,4-Dihydropyridine derivatives that lack of a nitro group in the molecule (isradipine, amlodipine) also inhibited lipid peroxidation in rat brain slices but at higher concentrations than that of nitro-substituted derivatives. 4. All the tested nitroso aryl derivatives [2,6-dimethyl-4-(2-nitrosophenyl)-3,5-pyridinedicar. boxylic acid dimethyl ester (NTP), nitrosotoluene, nitrosobenzene] were more potent inhibitors of lipid peroxidation than were the parent nitro compounds. In conclusion, on the basis of the IC50 values determined, the rank order of antioxidant potency for these derivatives can be established as: ortho-nitrosotoluene>NTP>nitrosobenzene.

  5. Oral Consumption of Bitter Gourd and Tomato Prevents Lipid Peroxidation in Liver Associated with DMBA Induced Skin Carcinogenesis in Mice.

    PubMed

    De, Sarmishtha; Chakraborty, Jamuna; Das, Sukta

    2000-01-01

    The protective role of two commonly consumed natural dietary items- bitter gourd and tomato against endogenous as well as 7,12- dimethylbenz(a)anthracene (DMBA) induced lipid peroxidation in the livers of mice was investigated. The rationale for such an approach is that lipid peroxidation has been suggested to play a key role in human cancer development. There was a sharp rise in lipid peroxidation (measured as thiobarbituric acid reactive substances formation) during skin carcinogenesis induced by DMBA in mice. Aqueous extracts of bitter gourd and tomato juice were found to be very potent inhibitors of lipid peroxidation both in normal and DMBA treated mice. Our observations support the hypothesis that natural combinations of phytochemicals present in the fruit juices exert cancer-protective effects via a decrease in lipid peroxidation.

  6. Effect of cold acclimation on GSH, antioxidant enzymes and lipid peroxidation in brown adipose tissue.

    PubMed Central

    Barja de Quiroga, G; López-Torres, M; Pérez-Campo, R; Abelenda, M; Paz Nava, M; Puerta, M L

    1991-01-01

    Cold acclimation increased the activities of superoxide dismutase, catalase, total and selenium (Se)-dependent glutathione peroxidases (GPx) and glutathione reductase by 2-4-fold in the brown adipose tissue (BAT) of cold-acclimated rats. Nevertheless, when expressed per unit protein, the antioxidant enzyme activities were unaltered. Sensitivity to lipid peroxidation and GSH levels both increased by one order of magnitude in the cold on a per weight basis and were still 3-5 times greater in the cold when expressed per mg of protein. We suggest that activation of BAT leads to a large increase in the potential for lipid peroxidation and that the tissue responds to this challenge by increasing practically all of its antioxidant defences. Nevertheless, GSH, and possibly GPx activity, seem to be the principal defences involved in adaptation of the tissue to a higher sensitivity to peroxidative damage after activation. PMID:1854342

  7. In vivo effects of nickel and cadmium in rats on lipid peroxidation and ceruloplasmin activity

    SciTech Connect

    Sole, J.; Huguet, J.; Arola, L.; Romeu, A. )

    1990-05-01

    Before Ni(II) and Cd(II), or any other metallic ion, can interact intracellulary, it must penetrate the cell membrane. The latter, therefore, is a primary target for toxic metals. Damage to cell membranes may allow a greater uptake of metal and thus injury may extend to more critical targets, although loss of plasmatic membrane functionality may be a crucial factor to explain the interactions of these metals with cellular components. In this sense the present study has been carried out. Factors that have been investigated in order to prove the membrane response of nickel and cadmium toxicity include lipid peroxidation, since divalent ions of transition metals can promote lipid peroxidation and this evidently contributes to the toxicity of certain metals and to metal interaction with ceruloplasmin, as its ferroxidase and scavenger of superoxide radicals activities are important protective mechanisms in vivo against peroxidative damage.

  8. Rat colonic lipid peroxidation and antioxidant status: the effects of dietary luteolin on 1,2-dimethylhydrazine challenge.

    PubMed

    Manju, Vaiyapuri; Balasubramaniyan, Vairappan; Nalini, Namasivayam

    2005-01-01

    Colon cancer is the third most common cancer and second leading cause of cancer-related death in the United States. A number of recent articles demonstrate the importance of natural products as cancer chemopreventive agents. In this study, we evaluated the chemopreventive efficacy of luteolin, a flavonoid, on tissue lipid peroxidation and antioxidant status, which are used as biomarkers in DMH-induced experimental colon carcinogenesis. Rats were given a weekly subcutaneous injection of DMH at a dose of 20 mg/kg body weight for 15 weeks. Luteolin (0.2 mg/kg body weight/everyday p.o.) was given to the DMH-treated rats at the initiation and post-initiation stages of carcinogenesis. The animals were killed after 30 weeks. After a total experimental period of 32 weeks (including 2 weeks of acclimatization), tumor incidence was 100% in DMH-treated rats. In those DMH-treated rats that had received luteolin during the initiation or post-initiation stages of colon carcinogenesis, the incidence of cancer and the colon tumor size was significantly reduced as compared to that for DMH-treated rats not receiving luteolin. In the presence of DMH, relative to the results for the control rats, there were decreased levels of lipid peroxidation, as denoted by thiobarbituric acid reactive substances (TBARS), conjugated dienes and lipid hydroperoxides, decreased activities of the enzymic antioxidants superoxide dismutase (SOD) and catalase (CAT), and elevated levels of glutathione and the glutathione-dependent enzymes reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR), and of the non-enzymic antioxidants vitamin C and vitamin E. Our study shows that intragastric administration of luteolin inhibits colon carcinogenesis, not only by modulating lipid peroxidation and antioxidant status, but also by preventing DMH-induced histopathological changes. Our results thus indicate that luteolin could act as a potent

  9. Studies of lipid peroxidation of rat blood after in vivo photodynamic treatment

    NASA Astrophysics Data System (ADS)

    Yanina, Irina Yu.; Navolokin, Nikita A.; Nikitina, Victoria V.; Bucharskaya, Alla B.; Maslyakova, Galina N.; Tuchin, Valery V.

    2011-10-01

    Lipid peroxidation (LP) of blood serum of laboratory animals after in vivo photodynamic treatment was investigated. To determine changes in LP the standard colorimetric test OXYSTAT was used. The results indicate an increase in the intensity of free radical generation in tissues induced by photodynamic treatment.

  10. Studies of lipid peroxidation of rat blood after in vivo photodynamic treatment

    NASA Astrophysics Data System (ADS)

    Yanina, Irina Yu.; Navolokin, Nikita A.; Nikitina, Victoria V.; Bucharskaya, Alla B.; Maslyakova, Galina N.; Tuchin, Valery V.

    2012-03-01

    Lipid peroxidation (LP) of blood serum of laboratory animals after in vivo photodynamic treatment was investigated. To determine changes in LP the standard colorimetric test OXYSTAT was used. The results indicate an increase in the intensity of free radical generation in tissues induced by photodynamic treatment.

  11. [Emoxipin correction of disorders of lipid peroxidation as affected by a slight excess of oxygen pressure].

    PubMed

    Lukash, A I; Vnukov, V V; Prokof'ev, V N; Khodakova, A A; Mogil'nitskaia, L V; Kostenko, E V

    1994-01-01

    The role of the emoxipin (Em.) (2-ethyl-6-methyl-3-oxipyridine) in the correction of the free radical oxidation and allied processes in lung tissues and blood plasma under high-pressure oxygen-prolonged action has been investigated. The studied oxygen exposure (0.3 MPa, 5h) causes the lung stage of oxygen intoxication. It is confirmed by exterior morphological assessment of the lung. The lipid peroxidation increase in lung tissue and blood plasma as well as erythrocyte membranes destabilization result from oxygen exposure. Lipid peroxidation intensity was estimated by determining of content of lipid peroxidation molecular products such as diene conjugates and Shiffs' bases. Erythrocyte membranes stability was evaluated with hemoglobin yield, total iron level and total peroxidase activity in blood plasma. Emoxipin was injected intraperitoneally in a dose 150 mg per 1 kg rats' weight just before the oxygen exposure. Emoxipin is found to improve physiological state of animals and to increase their survival; it normalizes morphology of the lungs and their state; stabilizes erythrocyte membranes injured under oxygen exposure; decreases intensity of lipid peroxidation processes in the lungs and in blood plasma which was previously increased under hyperoxia.

  12. Histochemical detection of lipid peroxidation in the liver of bromobenzene-poisoned mice.

    PubMed Central

    Pompella, A.; Maellaro, E.; Casini, A. F.; Comporti, M.

    1987-01-01

    The possibility of detecting lipid peroxidation histochemically was investigated in liver tissue in vivo, in conditions in which the process has been demonstrated by biochemical methods. The technique was based on the detection of aldehyde functions with the use of the Schiff's reagent. The study was carried out on bromobenzene-intoxicated mice, which generally exhibit levels of lipid peroxidation considerably higher than those observed in the case of other hepatotoxins. Liver sections from control animals were unstainable by the reagent, while sections from bromobenzene-poisoned mice showed a purple stain of various intensity, unhomogeneously distributed, sometimes with a mediolobular localization. Microphotometric measurements were performed at 565 nm by means of a computer-controlled microscope photometer. The ratios of Schiff-positive area relative to total section area, as well as the total extinctions referred to 100 sq mu of the sections, showed a high correlation with the corresponding hepatic contents of malonic dialdehyde, chosen as biochemical index of lipid peroxidation. In vitro studies in which liver sections were incubated in the presence of NADPH-Fe2+, showed a Schiff positivity which increased with the incubation time, confirming the reliability of the histochemical method. Another procedure, based on the use of 2-OH-3-naphtoic acid hydrazide coupled with fast blue B, was also developed and proved to be possibly more sensitive than Schiff's reagent in the detection of lipid peroxidation in liver tissue. Images Figure 1 Figure 2 PMID:3674204

  13. [The relationship of the electrical reactions of the brain to lipid peroxidation processes in pathological aging].

    PubMed

    Fokin, V F; Ponomareva, N V; Orlov, O N; Liderman, R R; Erin, A N

    1989-06-01

    The content of breathing air pentane as in vivo index of lipid peroxidation and electrophysiological parameters (visual evoked potentials and direct current (DC) potential level) of healthy volunteers and patients with senile dementia and Alzheimer's disease following weak stress sound influence were investigated. Unlike healthy subjects correlation between stress-induced changes of pentane level and electrophysiological parameters for patients with psychopathology was shown.

  14. Polyphenols from Berries of Aronia melanocarpa Reduce the Plasma Lipid Peroxidation Induced by Ziprasidone

    PubMed Central

    Dietrich-Muszalska, Anna; Kopka, Justyna

    2014-01-01

    Background. Oxidative stress in schizophrenia may be caused partially by the treatment of patients with antipsychotics. The aim of the study was to establish the effects of polyphenol compounds derived from berries of Aronia melanocarpa (Aronox) on the plasma lipid peroxidation induced by ziprasidone in vitro. Methods. Lipid peroxidation was measured by the level of thiobarbituric acid reactive species (TBARS). The samples of plasma from healthy subjects were incubated with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) alone and with Aronox (5 ug/ml; 50 ug/ml). Results. We observed a statistically significant increase of TBARS level after incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) (after 24 h incubation: P = 7.0 × 10−4, P = 1.6 × 10−3, and P = 2.7 × 10−3, resp.) and Aronox lipid peroxidation caused by ziprasidone was significantly reduced. After 24-hour incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) in the presence of 50 ug/ml Aronox, the level of TBARS was significantly decreased: P = 6.5 × 10−8, P = 7.0 × 10−6, and P = 3.0 × 10−5, respectively. Conclusion. Aronox causes a distinct reduction of lipid peroxidation induced by ziprasidone. PMID:25061527

  15. Increased non-protein bound iron in Down syndrome: contribution to lipid peroxidation and cognitive decline.

    PubMed

    Manna, Caterina; Officioso, Arbace; Trojsi, Francesca; Tedeschi, Gioacchino; Leoncini, Silvia; Signorini, Cinzia; Ciccoli, Lucia; De Felice, Claudio

    2016-12-01

    Down syndrome (DS, trisomy 21) is the leading cause of chromosomal-related intellectual disability. At an early age, adults with DS develop with the neuropathological hallmarks of Alzheimer's disease, associated with a chronic oxidative stress. To investigate if non-protein bound iron (NPBI) can contribute to building up a pro-oxidative microenvironment, we evaluated NPBI in both plasma and erythrocytes from DS and age-matched controls, together with in vivo markers of lipid peroxidation (F2-isoprostanes, F2-dihomo-isoprostanes, F4-neuroprostanes) and in vitro reactive oxygen species (ROS) formation in erythrocytes. The serum iron panel and uric acid were also measured. Second, we explored possible correlation between NPBI, lipid peroxidation and cognitive performance. Here, we report NPBI increase in DS, which correlates with increased serum ferritin and uric acid. High levels of lipid peroxidation markers and intraerythrocyte ROS formations were also reported. Furthermore, the scores of Raven's Colored Progressive Matrices (RCPM) test, performed as a measure of current cognitive function, are inversely related to NPBI, serum uric acid, and ferritin. Likewise, ROS production, F2-isoprostanes, and F4-neuroprostanes were also inversely related to cognitive performance, whereas serum transferrin positively correlated to RCPM scores. Our data reveal that increased availability of free redox-active iron, associated with enhanced lipid peroxidation, may be involved in neurodegeneration and cognitive decline in DS. In this respect, we propose chelation therapy as a potential preventive/therapeutic tool in DS.

  16. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles.

    PubMed

    Bowe, Whitney P; Logan, Alan C

    2010-12-09

    Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications.In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions.

  17. Sex-related differences in lipid peroxidation and photoprotection in Pistacia lentiscus.

    PubMed

    Juvany, Marta; Müller, Maren; Pintó-Marijuan, Marta; Munné-Bosch, Sergi

    2014-03-01

    Sex-related differences in the response of dioecious plants to abiotic stress have been poorly studied to date. This work explored to what extent sex may affect plant stress responses in Pistacia lentiscus L. (Anacardiaceae), a tree well adapted to Mediterranean climatic conditions. It was hypothesized that a greater reproductive effort in females may increase oxidative stress in leaves, particularly when plants are exposed to abiotic stress. Measurements of oxidative stress markers throughout the year revealed increased lipid peroxidation in females, but only during the winter. Enhanced lipid peroxidation in females was associated with reduced photoprotection, as indicated by reduced tocopherol levels and nonphotochemical quenching (NPQ) of chlorophyll fluorescence. Enhanced lipid peroxidation in females was also observed at predawn, which was associated with increased lipoxygenase activity and reduced cytokinin levels. An analysis of the differences between reproductive (R) and nonreproductive (NR) shoots showed an enhanced photoprotective capacity in R shoots compared to NR shoots in females. This capacity was characterized by an increased NPQ and a better antioxidant protection (increased carotenoid and tocopherol levels per unit of chlorophyll) in R compared to NR shoots. It is concluded that (i) females exhibit higher lipid peroxidation in leaves than males, but only during the winter (when sex-related differences in reproductive effort are the highest), (ii) this is associated with a lower photoprotective capacity at midday, as well as enhanced lipoxygenase activity and reduced cytokinin levels at predawn, and (iii) photoprotection capacity is higher in R relative to NR shoots in females.

  18. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles

    PubMed Central

    2010-01-01

    Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications. In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions. PMID:21143923

  19. N-3 Polyunsaturated Fatty Acids are Selective Targets of Ethanol Withdrawal-Induced Lipid Peroxidation

    USDA-ARS?s Scientific Manuscript database

    Ethanol withdrawal is a potentially life-threatening neurological syndrome owing to decreased GABA transmission and increased glutamatergic transmission resulting in a pro-excitotoxic state. Previous data indicate that ethanol withdrawal may increase CNS lipid peroxidation particularly to the n-3 fa...

  20. Sex-related differences in lipid peroxidation and photoprotection in Pistacia lentiscus

    PubMed Central

    Munné-Bosch, Sergi

    2014-01-01

    Sex-related differences in the response of dioecious plants to abiotic stress have been poorly studied to date. This work explored to what extent sex may affect plant stress responses in Pistacia lentiscus L. (Anacardiaceae), a tree well adapted to Mediterranean climatic conditions. It was hypothesized that a greater reproductive effort in females may increase oxidative stress in leaves, particularly when plants are exposed to abiotic stress. Measurements of oxidative stress markers throughout the year revealed increased lipid peroxidation in females, but only during the winter. Enhanced lipid peroxidation in females was associated with reduced photoprotection, as indicated by reduced tocopherol levels and nonphotochemical quenching (NPQ) of chlorophyll fluorescence. Enhanced lipid peroxidation in females was also observed at predawn, which was associated with increased lipoxygenase activity and reduced cytokinin levels. An analysis of the differences between reproductive (R) and nonreproductive (NR) shoots showed an enhanced photoprotective capacity in R shoots compared to NR shoots in females. This capacity was characterized by an increased NPQ and a better antioxidant protection (increased carotenoid and tocopherol levels per unit of chlorophyll) in R compared to NR shoots. It is concluded that (i) females exhibit higher lipid peroxidation in leaves than males, but only during the winter (when sex-related differences in reproductive effort are the highest), (ii) this is associated with a lower photoprotective capacity at midday, as well as enhanced lipoxygenase activity and reduced cytokinin levels at predawn, and (iii) photoprotection capacity is higher in R relative to NR shoots in females. PMID:24378602

  1. Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery

    PubMed Central

    Cristescu, Simona M.; Kiss, Rudolf; te Lintel Hekkert, Sacco; Dalby, Miles; Harren, Frans J. M.; Risby, Terence H.

    2014-01-01

    Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (>30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (>10-fold) and decreased over time. Reperfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene. PMID:25128523

  2. Almonds and Biomarkers of Lipid Peroxidation: A Randomized Controlled Cross-over Trial

    USDA-ARS?s Scientific Manuscript database

    Background: Nut consumption is associated with a reduced risk of coronary heart disease (CHD). Almonds, in addition to their cholesterol-lowering properties, have been shown to reduce oxidized LDL concentrations. However, their effect on other markers of lipid peroxidation is unknown. Methods: Twent...

  3. Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery.

    PubMed

    Cristescu, Simona M; Kiss, Rudolf; Hekkert, Sacco te Lintel; Dalby, Miles; Harren, Frans J M; Risby, Terence H; Marczin, Nandor

    2014-10-01

    Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (> 30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (> 10-fold) and decreased over time. Reperfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene.

  4. Lipid-induced peroxidation in the intestine is involved in glucose homeostasis imbalance in mice.

    PubMed

    Serino, Matteo; Waget, Aurélie; Marsollier, Nicolas; Masseboeuf, Myriam; Payros, Gaëlle; Kabani, Catherine; Denom, Jessica; Lacombe, Amélie; Thiers, Jean-Claude; Negre-Salvayre, Anne; Luquet, Serge; Burcelin, Rémy; Cruciani-Guglielmacci, Céline; Magnan, Christophe

    2011-01-01

    Daily variations in lipid concentrations in both gut lumen and blood are detected by specific sensors located in the gastrointestinal tract and in specialized central areas. Deregulation of the lipid sensors could be partly involved in the dysfunction of glucose homeostasis. The study aimed at comparing the effect of Medialipid (ML) overload on insulin secretion and sensitivity when administered either through the intestine or the carotid artery in mice. An indwelling intragastric or intracarotid catheter was installed in mice and ML or an isocaloric solution was infused over 24 hours. Glucose and insulin tolerance and vagus nerve activity were assessed. Some mice were treated daily for one week with the anti-lipid peroxidation agent aminoguanidine prior to the infusions and tests. The intestinal but not the intracarotid infusion of ML led to glucose and insulin intolerance when compared with controls. The intestinal ML overload induced lipid accumulation and increased lipid peroxidation as assessed by increased malondialdehyde production within both jejunum and duodenum. These effects were associated with the concomitant deregulation of vagus nerve. Administration of aminoguanidine protected against the effects of lipid overload and normalized glucose homeostasis and vagus nerve activity. Lipid overload within the intestine led to deregulation of gastrointestinal lipid sensing that in turn impaired glucose homeostasis through changes in autonomic nervous system activity.

  5. Substrate-selective Inhibition of Cyclooxygeanse-2 by Fenamic Acid Derivatives Is Dependent on Peroxide Tone.

    PubMed

    Orlando, Benjamin J; Malkowski, Michael G

    2016-07-15

    Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid (AA) and endocannabinoid substrates, placing the enzyme at a unique junction between the eicosanoid and endocannabinoid signaling pathways. COX-2 is a sequence homodimer, but the enzyme displays half-of-site reactivity, such that only one monomer of the dimer is active at a given time. Certain rapid reversible, competitive nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to inhibit COX-2 in a substrate-selective manner, with the binding of inhibitor to a single monomer sufficient to inhibit the oxygenation of endocannabinoids but not arachidonic acid. The underlying mechanism responsible for substrate-selective inhibition has remained elusive. We utilized structural and biophysical methods to evaluate flufenamic acid, meclofenamic acid, mefenamic acid, and tolfenamic acid for their ability to act as substrate-selective inhibitors. Crystal structures of each drug in complex with human COX-2 revealed that the inhibitor binds within the cyclooxygenase channel in an inverted orientation, with the carboxylate group interacting with Tyr-385 and Ser-530 at the top of the channel. Tryptophan fluorescence quenching, continuous-wave electron spin resonance, and UV-visible spectroscopy demonstrate that flufenamic acid, mefenamic acid, and tolfenamic acid are substrate-selective inhibitors that bind rapidly to COX-2, quench tyrosyl radicals, and reduce higher oxidation states of the heme moiety. Substrate-selective inhibition was attenuated by the addition of the lipid peroxide 15-hydroperoxyeicosatertaenoic acid. Collectively, these studies implicate peroxide tone as an important mechanistic component of substrate-selective inhibition by flufenamic acid, mefenamic acid, and tolfenamic acid.

  6. Liver Necrosis and Lipid Peroxidation in the Rat as the Result of Paraquat and Diquat Administration

    PubMed Central

    Burk, Raymond F.; Lawrence, Richard A.; Lane, James M.

    1980-01-01

    Paraquat and diquat facilitate formation of superoxide anion in biological systems, and lipid peroxidation has been postulated to be their mechanism of toxicity. Paraquat has been shown to be more toxic to selenium-deficient mice than to controls, presumably as the result of decreased activity of the selenoenzyme glutathione peroxidase. The present study was designed to measure lipid peroxidation and to assess toxicity in control and selenium-deficient rats given paraquat and diquat. Lipid peroxidation was measured by determining ethane production rates of intact animals; toxicity was assessed by survival and by histological and serum enzyme evidence of liver and kidney necrosis. Paraquat and diquat were both much more toxic to selenium-deficient rats than to control rats. Diquat (19.5 μmol/kg) caused rapid and massive liver and kidney necrosis and very high ethane production rates in selenium-deficient rats. The effect of paraquat (78 μmol/kg) was similar to that of diquat but was not as severe. Acutely lethal doses of paraquat (390 μmol/kg) and diquat (230 μmol/kg) in control rats caused very little ethane production and no evidence of liver necrosis. These findings suggest that paraquat and diquat exert their acute toxicity largely through lipid peroxidation in selenium-deficient rats. Selenium deficiency had no effect on superoxide dismutase activity in erythrocytes or in 105,000 g supernate of liver or kidney. Glutathione peroxidase, which represents the only well-characterized biochemical function of selenium in animals, was dissociated from the protective effect of selenium against diquat-induced lipid peroxidation and toxicity by a time-course study in which selenium-deficient rats were injected with 50 μg of selenium and later given diquat (19.5 μmol/kg). Within 10 h, the selenium injection provided significant protection against diquat-induced lipid peroxidation and mortality even though this treatment resulted in no rise in glutathione peroxidase

  7. Effects of inorganic iron and myoglobin on in vitro proximal tubular lipid peroxidation and cytotoxicity.

    PubMed

    Zager, R A; Foerder, C A

    1992-03-01

    Recent in vivo studies suggest that heme Fe causes proximal tubular lipid peroxidation and cytotoxicity, thereby contributing to the pathogenesis of myoglobinuric (Mgb) acute renal failure. Because hydroxyl radical (.OH) scavengers [dimethylthiourea (DMTU), benzoate, mannitol] can mitigate this injury, it is postulated that .OH is a mediator of Mgb-induced renal damage. The present study has tested these hypotheses using an isolated rat proximal tubular segment (PTS) system. An equal mixture of Fe2+/Fe3+ (4 mM total), when added to PTS, caused marked cytotoxicity [as defined by lactate dehydrogenase (LDH) release] and lipid peroxidation [assessed by malondialdehyde (MDA) increments]. Fe2+ or Fe3+ alone each induced massive MDA elevations, but only Fe2+ caused cytotoxicity. Although both DMTU and benzoate decreased LDH release during the Fe2+/Fe3+ challenge, mannitol and GSH did not, despite equivalent reductions in .OH (gauged by the salicylate trap method). GSH and catalase (but not DMTU, benzoate, or mannitol) decreased MDA concentrations, suggesting the Fe-driven lipid peroxidation was more H2O2 than .OH dependent. Deferoxamine totally blocked Fe-induced LDH release, even under conditions in which it caused an apparent increase in .OH generation. Mgb paradoxically protected against Fe-mediated PTS injury, an effect largely reproduced by albumin. In conclusion, these data suggest that: (a) Fe can cause PTS lipid peroxidation and cytotoxicity by a non-.OH-dependent mechanism; (b) Fe-mediated cytotoxicity and lipid peroxidation are not necessarily linked; and (c) Mgb paradoxically protects PTS against Fe-mediated injury, suggesting that: (i) Mgb Fe may require liberation from its porphyrin ring before exerting toxicity; and (ii) the protein residue may blunt the resulting injury.

  8. Involvement of lipid peroxidation-derived aldehyde-protein adducts in autoimmunity mediated by trichloroethene.

    PubMed

    Wang, Gangduo; Ansari, G A S; Khan, M Firoze

    2007-12-01

    Lipid peroxidation, a major contributor to cellular damage, is also implicated in the pathogenesis of autoimmune diseases (AD). The focus of this study was to elucidate the role of lipid peroxidation-derived aldehydes in autoimmunity induced and/or exacerbated by chemical exposure. Previous studies showed that trichloroethene (TCE) is capable of inducing/accelerating autoimmunity. To test whether TCE-induced lipid peroxidation might be involved in the induction/exacerbation of autoimmune responses, groups of autoimmune-prone female MRL +/+ mice were treated with TCE (10 mmol/kg, i.p., every 4th day) for 6 or 12 wk. Significant increases of the formation of malondialdehyde (MDA)- and 4-hydroxynonenal (HNE)-protein adducts were found in the livers of TCE-treated mice at both 6 and 12 wk, but the response was greater at 12 wk. Further characterization of these adducts in liver microsomes showed increased formation of MDA-protein adducts with molecular masses of 86, 65, 56, 44, and 32 kD, and of HNE-protein adducts with molecular masses of 87, 79, 46, and 17 kD in TCE-treated mice. In addition, significant induction of anti-MDA- and anti-HNE-protein adduct-specific antibodies was observed in the sera of TCE-treated mice, and showed a pattern similar to MDA- or HNE-protein adducts. The increases in anti-MDA- and anti-HNE-protein adduct antibodies were associated with significant elevation in serum anti-nuclear-, anti-ssDNA- and anti-dsDNA-antibodies at 6 wk and, to a greater extent, at 12 wk. These studies suggest that TCE-induced lipid peroxidation is associated with induction/exacerbation of autoimmune response in MRL+/+ mice, and thus may play an important role in disease pathogenesis. Further interventional studies are needed to establish a causal relationship between lipid peroxidation and TCE-induced autoimmune response.

  9. Effect of phytosterols on copper lipid peroxidation of human low-density lipoproteins.

    PubMed

    Ferretti, Gianna; Bacchetti, Tiziana; Masciangelo, Simona; Bicchiega, Virginia

    2010-03-01

    Phytosterols and stanols have received much attention in the past several years because of their cholesterol-lowering properties, and several studies have shown a protective effect against cardiovascular disease and colon and breast cancer development. A significant decrease of plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B has been demonstrated in subjects whose diet was supplemented with 2g/d of plant sterols. Changes in plasma lipoprotein levels were associated with a decrease of oxidized LDL, suggesting that plant sterols could exert an antioxidant effect. The aim of the present study was to further investigate the interaction between the major dietary phytosterols and plasma lipoproteins. Moreover, their antioxidant effect against in vitro-induced lipid peroxidation of human LDL was investigated. Susceptibility to copper-induced lipid peroxidation was investigated in LDLs isolated from plasma of normolipemic subjects. Concentrations of beta-sitosterol, campesterol, and stigmasterol ranging from 5 to 50 microM were studied. Analyses of the emission fluorescence spectra of tryptophan and of the probe 6-dodecanoyl-2-dimethyl-aminoaphthalene were used to investigate the effect of phytosterols on apoprotein structure and physicochemical properties of LDL. Our results demonstrated that phytosterols exert an inhibitory effect against copper-induced lipid peroxidation of LDLs, as shown by the lowered levels of conjugated dienes in oxidized lipoproteins incubated with different concentrations of plant sterols (5-50 microM). Moreover, analysis of fluorescence emission spectra of tryptophan and 6-dodecanoyl-2-dimethyl-aminoaphthalene demonstrated that phytosterols prevent the alterations of apoprotein structure and physicochemical properties associated with copper-triggered lipid peroxidation of lipoproteins. We suggest that the effect exerted by beta-sitosterol, stigmasterol, and campesterol against lipid peroxidation of LDL possibly related to

  10. Effects of lithium therapy on Na+-K+-ATPase activity and lipid peroxidation in bipolar disorder.

    PubMed

    Banerjee, Ushasi; Dasgupta, Anindya; Rout, Jayanta Kumar; Singh, Om Prakash

    2012-04-27

    Oxidative stress induced lipid peroxidation along with a reduced Na(+)-K(+)-ATPase activity has been implicated in the pathophysiology of bipolar disorders (BPD). Although, lithium therapy results in significant improvement in the symptoms of the disease, studies regarding its effect on the altered sodium pump activity and lipid peroxidation status have come out with conflicting results. The present study was undertaken to evaluate the status of lipid peroxidation and analyze the role of lithium and Na(+)-K(+)-ATPase activity in its regulation in BPD patients in our region. We measured RBC membrane Na(+)-K(+)-ATPase activity and serum thiobarbituric acid reacting substances (TBARS) level in 73 BPD patients and serum lithium, in addition, in 48 patients receiving lithium therapy among them. Na(+)-K(+)-ATPase activity and serum TBARS level were significantly decreased and increased respectively in all BPD patients compared to age and sex matched healthy controls. Same trend was observed in the BPD patients stabilized on lithium therapy compared to the lithium naive ones. Although, the enzyme activity showed a reciprocal relationship with TBARS in all patients of BPD, a significant positive correlation and dependence of the enzyme activity was evident with serum lithium level only in the lithium stabilized BPD group. BPD patients showed significantly compromised Na(+)-K(+)-ATPase activity and increased lipid peroxidation. Lithium induced improvement in the enzyme activity was associated with significant reduction in lipid peroxidation. Enhancement of the Na(+)-K(+)-ATPase activity by optimum dosage of lithium may be a potential contributing factor for reducing oxidative stress in BPD patients. Copyright © 2011 Elsevier Inc. All rights reserved.

  11. Effect of dietary melanoidins on lipid peroxidation during simulated gastric digestion: their possible role in the prevention of oxidative damage.

    PubMed

    Tagliazucchi, Davide; Verzelloni, Elena; Conte, Angela

    2010-02-24

    The ability of high molecular weight melanoidins extracted from coffee, barley coffee, and dark beer to inhibit lipid peroxidation during simulated gastric digestion of turkey meat has been investigated. Results showed that melanoidins decrease the synthesis of lipid hydroperoxides and secondary lipoxidation products. Coffee melanoidins at 3 mg/mL reversed the reaction and broke down hydroperoxides to concentrations lower than the initial value. Barley coffee and dark beer melanoidins were less effective, and even at 12 mg/mL did not reverse the reaction. The proposed mechanism of action involved Fe(2+) chelating capacity, heme-binding ability, and radical-scavenging activity. Melanoidins were characterized for their content in total proteins, carbohydrates, and phenolics, and the relationship between the chemical composition and the antioxidant activity of dietary melanoidins was investigated. Coffee melanoidins, which contain more phenolics and proteins with respect to the other melanoidins, showed greater antioxidant activity with respect to the other melanoidins tested.

  12. Reversal of noradrenergic depletion and lipid peroxidation in the pons after brain injury correlates with motor function recovery in rats.

    PubMed

    Bueno-Nava, Antonio; Montes, Sergio; DelaGarza-Montano, Paloma; Alfaro-Rodriguez, Alfonso; Ortiz, Ascencion; Gonzalez-Pina, Rigoberto

    2008-09-26

    Functional impairment after brain injury (BI) has been attributed to the inhibition of regions that are related to the injured site. Therefore, noradrenaline (NA) is thought to play a critical role in recovery from motor injury. However, the mechanism of this recovery process has not been completely elucidated. Moreover, the locus coeruleus (LC) projects from the pons through the rat sensorimotor cortex, and injury axotomizes LC fibers, depressing NA function. This was tested by measuring lipid peroxidation (LP) in the pons after sensorimotor cortex injury. Depression of function in the pons would be expected to alter areas receiving pontine efferents. Male Wistar rats were divided into three groups: control (n=16), injured (n=10) and recovering (n=16), and they were evaluated using a beam-walking assay between 2 and 20 days after cortical injury. We performed measures of NA and LP in both sides of the pons and cerebellum. We found a decrease of NA in the pons and the cerebellum, and a concomitant increase in the motor deficit and LP in the pons of injured animals. Recovering rats had NA and LP levels that were very similar to those observed in control rats. These observations suggest that the mechanism of remote inhibition after BI involves lipid peroxidation, and that the NA decrease found in the cerebellum of injured animals is mediated by a noradrenergic depression in the pons, or in areas receiving NA projections from the pons.

  13. An increase in lipoprotein oxidation and endogenous lipid peroxides in serum of obese women.

    PubMed

    Mutlu-Türkoğlu, U; Oztezcan, S; Telci, A; Orhan, Y; Aykaç-Toker, G; Sivas, A; Uysal, M

    2003-02-01

    Endogenous malondialdehyde and diene conjugate levels, the susceptibility of apolipoprotein B-containing lipoproteins to copper-induced lipid peroxidation, and antibody titer against oxidized low-density lipoproteins were increased, but serum antioxidant activity was unchanged in obese women. Serum cholesterol, low-density lipoproteincholesterol, and trigliceride levels were also elevated, but high-density lipoprotein-cholesterol levels remained unchanged in obese women. In vitro, oxidation of apolipoprotein B-containing lipoproteins and levels of antibody against oxidized low-density lipoprotein correlated with body mass index, serum total cholesterol, and low-density lipoproteincholesterol levels in obese women. These results indicate that obesity is associated with increases in endogenous lipid peroxides, oxidation of low-density lipoproteins, and lipids in serum.

  14. Simulation of lipid peroxidation in low-density lipoprotein by a basic "skeleton" of reactions.

    PubMed

    Abuja, P M; Esterbauer, H

    1995-01-01

    A minimal kinetic model describing lipid peroxidation in low-density lipoprotein (LDL) has been set up. Models have been calculated by numeric integration of the differential equations describing this system consisting of seven reactions and eleven reactants in a single compartment. The model describes the usually observed behavior of the reaction system, showing that the crucial intermediate is the lipid peroxyl radical (LOO.). During different stages of the reaction, depending on the presence of antioxidants (alpha-tocopherol), different pathways in the reaction scheme become active. Simulation also demonstrates that tocopherol-mediated propagation can occur under certain conditions, i.e., a low rate of initiation. This, however, does not mean that tocopherol enhances lipid peroxidation in LDL, as without tocopherol the process would be much faster. Further extension of the basic model by inclusion of a hypothetical antioxidant leads to a model which is capable of describing Cu(2+)-induced LPO over the whole lag phase up to full propagation.

  15. In Vitro effect of D-004, a lipid extract of the ground fruits of the Cuban royal palm (Roystonea regia), on rat microsomal lipid peroxidation.

    PubMed

    Menéndez, Roberto; Más, Rosa; Pérez, Yohani; González, R M

    2007-01-01

    D-004 is a lipid extract of the fruits of the Cuban royal palm (Roystonea regia) containing a mixture of saturated fatty acids. D-004 inhibits prostate hyperplasia (PH) induced with testosterone, in rodents. Since fatty acids inhibit lipid peroxidation (LP), this study investigated whether D-004 prevents in vitro LP. D-004 (0.9-1000 microg/mL) markedly and dose-dependently inhibited in vitro iron-induced LP in native brain and liver microsomes. D-004 showed hydroxyl radical scavenging activity, which could explain partially its antioxidant effect on microsomal iron-induced LP, but it was unable to scavenge superoxide and ABTS radicals, indicating a limited radical scavenging activity. Also, D-004 inhibited CCl4-mediated LP in active liver microsomes through a decreased generation of radical species rather than a radical trapping action on CCl(4)-derived radical species. D-004 also inhibited lipooxygenase (LOX) and cyclooxygenase (COX) activities, and the generation of protein-associated carbonyl groups after LP. Since increased oxidative stress has been linked to PH, the antioxidant effect of D-004 shown here could contribute to explaining its beneficial effects on T-induced PH in rodents. Nevertheless, this study shows only in vitro results. Further studies should investigate whether D-004 also exhibits antioxidant effects in vivo.

  16. Evidence for hydroxyl radical generation during lipid (linoleate) peroxidation.

    PubMed

    Frenette, Mathieu; Scaiano, Juan C

    2008-07-30

    The autoxidation of methyl linoleate in benzene at 37 degrees C by peroxyl radicals was found to generate hydroxyl radicals (.OH) from a secondary oxidation mechanism. The yield of hydroxyl radicals (approximately 2%) was determined by trapping these reactive radicals with benzene to give phenol. We propose that alphaC-H hydrogen abstraction from lipid hydroperoxides, the main autoxidation products, is the source of hydroxyl radicals.

  17. Myeloperoxidase-dependent Lipid Peroxidation Promotes the Oxidative Modification of Cytosolic Proteins in Phagocytic Neutrophils*

    PubMed Central

    Wilkie-Grantham, Rachel P.; Magon, Nicholas J.; Harwood, D. Tim; Kettle, Anthony J.; Vissers, Margreet C.; Winterbourn, Christine C.; Hampton, Mark B.

    2015-01-01

    Phagocytic neutrophils generate reactive oxygen species to kill microbes. Oxidant generation occurs within an intracellular phagosome, but diffusible species can react with the neutrophil and surrounding tissue. To investigate the extent of oxidative modification, we assessed the carbonylation of cytosolic proteins in phagocytic neutrophils. A 4-fold increase in protein carbonylation was measured within 15 min of initiating phagocytosis. Carbonylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhibited by butylated hydroxytoluene and Trolox, indicating a role for myeloperoxidase-dependent lipid peroxidation. Proteomic analysis of target proteins revealed significant carbonylation of the S100A9 subunit of calprotectin, a truncated form of Hsp70, actin, and hemoglobin from contaminating erythrocytes. The addition of the reactive aldehyde 4-hydroxynonenal (HNE) caused carbonylation, and HNE-glutathione adducts were detected in the cytosol of phagocytic neutrophils. The post-translational modification of neutrophil proteins will influence the functioning and fate of these immune cells in the period following phagocytic activation, and provides a marker of neutrophil activation during infection and inflammation. PMID:25697357

  18. The mechanism of cumene hydroperoxide-dependent lipid peroxidation: the significance of oxygen uptake.

    PubMed

    Weiss, R H; Estabrook, R W

    1986-11-15

    The addition of limiting amounts of cumene hydroperoxide to rat liver microsomes prepared from phenobarbital-treated rats resulted in the rapid uptake of molecular oxygen, the formation of thiobarbituric acid reactive products, and the loss of hydroperoxide over a similar time course. Maximal activity was observed at pH 7-8. The addition of cumene hydroperoxide to boiled microsomes did not initiate oxygen uptake or produce thiobarbituric acid reactive products. Oxygen uptake was required for the formation of thiobarbituric acid reactive products, but not for the loss of hydroperoxide. The extent of oxygen uptake and thiobarbituric acid reactive product formation was linearly dependent on the concentration of cumene hydroperoxide and independent of the amount of microsomes. For each nanomole of cumene hydroperoxide utilized, 1.5 nmol of oxygen was consumed and 0.11 nmol of thiobarbituric acid reactive products was formed. In addition, a saturable reaction having a high affinity for cumene hydroperoxide was observed that was associated with little or no oxygen uptake and thiobarbituric acid reactive product formation. Butylated hydroxytoluene at substoichiometric concentrations inhibited the extents and initial rates of oxygen uptake and thiobarbituric acid reactive product formation, indicating that cumene hydroperoxide-dependent lipid peroxidation may be an autocatalytic free radical process.

  19. Modification and inactivation of Cu,Zn-superoxide dismutase by the lipid peroxidation product, acrolein

    PubMed Central

    Kang, Jung Hoon

    2013-01-01

    Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments. [BMB Reports 2013; 46(11): 555-560] PMID:24152914

  20. Myeloperoxidase-dependent lipid peroxidation promotes the oxidative modification of cytosolic proteins in phagocytic neutrophils.

    PubMed

    Wilkie-Grantham, Rachel P; Magon, Nicholas J; Harwood, D Tim; Kettle, Anthony J; Vissers, Margreet C; Winterbourn, Christine C; Hampton, Mark B

    2015-04-10

    Phagocytic neutrophils generate reactive oxygen species to kill microbes. Oxidant generation occurs within an intracellular phagosome, but diffusible species can react with the neutrophil and surrounding tissue. To investigate the extent of oxidative modification, we assessed the carbonylation of cytosolic proteins in phagocytic neutrophils. A 4-fold increase in protein carbonylation was measured within 15 min of initiating phagocytosis. Carbonylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhibited by butylated hydroxytoluene and Trolox, indicating a role for myeloperoxidase-dependent lipid peroxidation. Proteomic analysis of target proteins revealed significant carbonylation of the S100A9 subunit of calprotectin, a truncated form of Hsp70, actin, and hemoglobin from contaminating erythrocytes. The addition of the reactive aldehyde 4-hydroxynonenal (HNE) caused carbonylation, and HNE-glutathione adducts were detected in the cytosol of phagocytic neutrophils. The post-translational modification of neutrophil proteins will influence the functioning and fate of these immune cells in the period following phagocytic activation, and provides a marker of neutrophil activation during infection and inflammation.

  1. Modification and inactivation of Cu,Zn-superoxide dismutase by the lipid peroxidation product, acrolein.

    PubMed

    Kang, Jung Hoon

    2013-11-01

    Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments.

  2. Regulation of NF-κB-Induced Inflammatory Signaling by Lipid Peroxidation-Derived Aldehydes

    PubMed Central

    Yadav, Umesh C. S.; Ramana, Kota V.

    2013-01-01

    Oxidative stress plays a critical role in the pathophysiology of a wide range of diseases including cancer. This view has broadened significantly with the recent discoveries that reactive oxygen species initiated lipid peroxidation leads to the formation of potentially toxic lipid aldehyde species such as 4-hydroxy-trans-2-nonenal (HNE), acrolein, and malondialdehyde which activate various signaling intermediates that regulate cellular activity and dysfunction via a process called redox signaling. The lipid aldehyde species formed during synchronized enzymatic pathways result in the posttranslational modification of proteins and DNA leading to cytotoxicity and genotoxicty. Among the lipid aldehyde species, HNE has been widely accepted as a most toxic and abundant lipid aldehyde generated during lipid peroxidation. HNE and its glutathione conjugates have been shown to regulate redox-sensitive transcription factors such as NF-κB and AP-1 via signaling through various protein kinase cascades. Activation of redox-sensitive transcription factors and their nuclear localization leads to transcriptional induction of several genes responsible for cell survival, differentiation, and death. In this review, we describe the mechanisms by which the lipid aldehydes transduce activation of NF-κB signaling pathways that may help to develop therapeutic strategies for the prevention of a number of inflammatory diseases. PMID:23710287

  3. Antioxidant depletion, lipid peroxidation, and impairment of calcium transport induced by air-blast overpressure in rat lungs.

    PubMed

    Elsayed, N M; Tyurina, Y Y; Tyurin, V A; Menshikova, E V; Kisin, E R; Kagan, V E

    1996-01-01

    Exposure to blast overpressure, or the sudden rise in atmospheric pressure after explosive detonation, results in damage mainly of the gas-filled organs. In addition to the physical damage, in the lung, injury may proceed via a hemorrhage-dependent mechanism initiating oxidative stress and accumulation of lipid peroxidation products. Massive rupture of capillaries and red blood cells, release of hemoglobin, its oxidation to met-hemoglobin and degradation sets the stage for heme-catalyzed oxidations. The authors hypothesized that lipid hydroperoxides interact with met-hemoglobin in the lungs of exposed animals to produce ferryl-hemoglobin, an extremely potent oxidant that induces oxidative damage by depleting antioxidants and initiating peroxidation reactions. Oxidation-induced disturbance of Ca2+ homeostasis facilitates further amplification of the damage. To test this hypothesis, groups of anesthetized rats (6 rats/group) were exposed to blast at 3 peak pressures: low (61.2 kPa), medium (95.2 kPa), high (136 kPa). One group served as an unexposed control. Immediately after exposure, the rats were euthanized and the lungs were analyzed for biochemical parameters. Blast overpressure caused: (1) depletion of total and water-soluble pulmonary antioxidant reserves and individual antioxidants (ascorbate, vitamin E, GSH), (2) accumulation of lipid peroxidation products (conjugated dienes, TBARS), and (3) inhibition of ATP-dependent Ca2+ transport. The magnitude of these changes in the lungs was proportional to the peak blast overpressure. Inhibition of Ca2+ transport strongly correlated with both depletion of antioxidants and enhancement of lipid peroxidation. In model experiments, met-hemoglobin/H2O2 produced damage to Ca2+ transport in the lungs from control animals similar to that observed in the lungs from blast overpressure-exposed animals. Ascorbate, which is known to reduce ferryl-hemoglobin, protected against met-hemoglobin/H2O2-induced damage of Ca2+ transport

  4. Modulation of keratinocyte expression of antioxidants by 4-hydroxynonenal, a lipid peroxidation end product

    SciTech Connect

    Zheng, Ruijin; Heck, Diane E.; Mishin, Vladimir; Black, Adrienne T.; Shakarjian, Michael P.; Kong, Ah-Ng Tony; Laskin, Debra L.; Laskin, Jeffrey D.

    2014-03-01

    4-Hydroxynonenal (4-HNE) is a lipid peroxidation end product generated in response to oxidative stress in the skin. Keratinocytes contain an array of antioxidant enzymes which protect against oxidative stress. In these studies, we characterized 4-HNE-induced changes in antioxidant expression in mouse keratinocytes. Treatment of primary mouse keratinocytes and PAM 212 keratinocytes with 4-HNE increased mRNA expression for heme oxygenase-1 (HO-1), catalase, NADPH:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) A1-2, GSTA3 and GSTA4. In both cell types, HO-1 was the most sensitive, increasing 86–98 fold within 6 h. Further characterization of the effects of 4-HNE on HO-1 demonstrated concentration- and time-dependent increases in mRNA and protein expression which were maximum after 6 h with 30 μM. 4-HNE stimulated keratinocyte Erk1/2, JNK and p38 MAP kinases, as well as PI3 kinase. Inhibition of these enzymes suppressed 4-HNE-induced HO-1 mRNA and protein expression. 4-HNE also activated Nrf2 by inducing its translocation to the nucleus. 4-HNE was markedly less effective in inducing HO-1 mRNA and protein in keratinocytes from Nrf2 −/− mice, when compared to wild type mice, indicating that Nrf2 also regulates 4-HNE-induced signaling. Western blot analysis of caveolar membrane fractions isolated by sucrose density centrifugation demonstrated that 4-HNE-induced HO-1 is localized in keratinocyte caveolae. Treatment of the cells with methyl-β-cyclodextrin, which disrupts caveolar structure, suppressed 4-HNE-induced HO-1. These findings indicate that 4-HNE modulates expression of antioxidant enzymes in keratinocytes, and that this can occur by different mechanisms. Changes in expression of keratinocyte antioxidants may be important in protecting the skin from oxidative stress. - Highlights: • Lipid peroxidation generates 4-hydroxynonenal, a reactive aldehyde. • 4-HNE induces antioxidant proteins in mouse keratinocytes. • Induction of

  5. Terazosin-induced alterations in catalase expression and lipid peroxidation in the rat seminal vesicles.

    PubMed

    Mitropoulos, D; Patris, E; Deliconstantinos, G; Kyroudi-Voulgari, A; Anastasiou, I; Perea, D

    2013-04-01

    Previous studies have shown that alpha1-adrenergic receptor antagonists may alter seminal vesicle contractility and impair fertility in male rats. This study was designed to investigate the effects of terazosin on the catalase expression in the seminal vesicles and the lipid peroxidation of the seminal fluid in normal adult rats. Wistar rats were treated with terazosin (1.2 mg kg(-1) body weight, given orally every second day) for 120 days. Catalase expression was assessed immunohistochemically in tissue sections of the seminal vesicles, and lipid peroxidation was estimated by measuring the malondialdehyde (MDA) levels in the seminal vesicles' fluid. The seminal vesicles in terazosin-treated rats were particularly distended in comparison with those of controls, and their secreting epithelium was suppressed. Cytoplasmic catalase expression in the secreting epithelial cells (% of cells) was increased in terazosin-treated specimens in comparison with controls (76.1 ± 17.1 versus 51.3 ± 25.1, P = 0.005). MDA levels (μm) were also higher in samples from treated subjects in comparison with controls (2.67 ± 1.19 versus 1.39 ± 0.19, P = 0.01). Although the direct effect of terazosin treatment on the seminal vesicles is that of impaired contractility, an indirect effect is that on fertility by increasing lipid peroxidation in the seminal fluid and/or through degrading of hydrogen peroxide that is essential for sperm capacitation.

  6. Effect of changes in plasma vitamin E level of vascular responses and lipid peroxidation in sickle cell anaemia subjects.

    PubMed

    Gbenebitse, S; Jaja, S I; Kehinde, M O

    2005-06-01

    The effect of vitamin E supplementation (300 mg/day for 6 weeks) on blood pressure, forearm blood flow, forearm vascular resistance, plasma vitamin E level and lipid peroxidation status was investigated in adult sickle cell anaemia subjects. Ten adults whose ages ranged from 19.0 to 25.0 years (mean 22.8+/-0.8 years) were studied. Vitamin E supplementation had little or no effect on arterial blood pressure but significantly increased forearm blood flow (p<0.001) and plasma vitamin E level (p<0.001). However it significantly decreased lipid peroxidation status (p<0.001) and forearm vascular resistance (p<0.001). The change in plasma vitamin E concentration correlated negatively with change in lipid peroxidation status (r=-0.8; p=0.003). However, change in plasma vitamin E concentration correlated positively with change in forearm blood flow (r=0.8; p=0.006). There was an inverse correlation between change in plasma lipid peroxidation and change in forearm blood flow (r=-0.7; p=0.03). The study therefore shows that in sickle cell anaemia subjects, vitamin E supplementation increases forearm blood flow and reduces forearm vascular resistance and lipid peroxidation. The increase in forearm blood flow correlates inversely with the reduction in lipid peroxidation. This suggests that in sickle cell anaemia subjects, vitamin E supplementation could cause an increase in forearm blood flow by decreasing plasma lipid peroxidation level.

  7. Astaxanthin Normalizes Epigenetic Modifications of Bovine Somatic Cell Cloned Embryos and Decreases the Generation of Lipid Peroxidation.

    PubMed

    Li, R; Wu, H; Zhuo, W W; Mao, Q F; Lan, H; Zhang, Y; Hua, S

    2015-10-01

    Astaxanthin is an extremely common antioxidant scavenging reactive oxygen species (ROS) and blocking lipid peroxidation. This study was conducted to investigate the effects of astaxanthin supplementation on oocyte maturation, and development of bovine somatic cell nuclear transfer (SCNT) embryos. Cumulus-oocyte complexes were cultured in maturation medium with astaxanthin (0, 0.5, 1.0, or 1.5 mg/l), respectively. We found that 0.5 mg/l astaxanthin supplementation significantly increased the proportion of oocyte maturation. Oocytes cultured in 0.5 mg/l astaxanthin supplementation were used to construct SCNT embryos and further cultured with 0, 0.5, 1.0 or 1.5 mg/l astaxanthin. The results showed that the supplementation of 0.5 mg/l astaxanthin significantly improved the proportions of cleavage and blastulation, as well as the total cell number in blastocysts compared with the control group, yet this influence was not concentration dependent. Chromosomal analyses revealed that more blastomeres showed a normal chromosomal complement in 0.5 mg/l astaxanthin treatment group, which was similar to that in IVF embryos. The methylation levels located on the exon 1 of the imprinted gene H19 and IGF2, pluripotent gene OCT4 were normalized, and global DNA methylation, H3K9 and H4K12 acetylation were also improved significantly, which was comparable to that in vitro fertilization (IVF) embryos. Moreover, we also found that astaxanthin supplementation significantly decreased the level of lipid peroxidation. Our findings showed that the supplementation of 0.5 mg/l astaxanthin to oocyte maturation medium and embryo culture medium improved oocyte maturation, SCNT embryo development, increased chromosomal stability and normalized the epigenetic modifications, as well as inhibited overproduction of lipid peroxidation. © 2015 Blackwell Verlag GmbH.

  8. Salidroside inhibits endogenous hydrogen peroxide induced cytotoxicity of endothelial cells.

    PubMed

    Zhao, Xingyu; Jin, Lianhai; Shen, Nan; Xu, Bin; Zhang, Wei; Zhu, Hongli; Luo, Zhengli

    2013-01-01

    Salidroside, a phenylpropanoid glycoside isolated from Rhodiola rosea L., shows potent antioxidant property. Herein, we investigated the protective effects of salidroside against hydrogen peroxide (H2O2)-induced oxidative damage in human endothelial cells (EVC-304). EVC-304 cells were incubated in the presence or absence of low steady states of H2O2 (3-4 µM) generated by glucose oxidase (GOX) with or without salidroside. 3(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) assays were performed, together with Hoechst 33258 staining and flow cytometric analysis using Annexin-V and propidium iodide (PI) label. The results indicated that salidroside pretreatment attenuated endogenous H2O2 induced apoptotic cell death in EVC-304 cells in a dose-dependent pattern. Furthermore, Western blot data revealed that salidroside inhibited activation of caspase-3, 9 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by endogenous H2O2. It also decreased the expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. All these results demonstrated that salidroside may present a potential therapy for oxidative stress in cardiovascular and cerebrovascular diseases.

  9. UVA photoirradiation of benzo[a]pyrene metabolites: induction of cytotoxicity, reactive oxygen species, and lipid peroxidation.

    PubMed

    Xia, Qingsu; Chiang, Hsiu-Mei; Yin, Jun-Jie; Chen, Shoujun; Cai, Lining; Yu, Hongtao; Fu, Peter P

    2015-10-01

    Benzo[a]pyrene (BaP) is a prototype for studying carcinogenesis of polycyclic aromatic hydrocarbons (PAHs). We have long been interested in studying the phototoxicity of PAHs. In this study, we determined that metabolism of BaP by human skin HaCaT keratinocytes resulted in six identified phase I metabolites, for example, BaP trans-7,8-dihydrodiol (BaP t-7,8-diol), BaP t-4,5-diol, BaP t-9,10-diol, 3-hydroxybenzo[a]pyrene (3-OH-BaP), BaP (7,10/8,9)tetrol, and BaP (7/8,9,10)tetrol. The photocytotoxicity of BaP, 3-OH-BaP, BaP t-7,8-diol, BaP trans-7,8-diol-anti-9,10-epoxide (BPDE), and BaP (7,10/8,9)tetrol in the HaCaT keratinocytes was examined. When irradiated with 1.0 J/cm(2) UVA light, these compounds when tested at doses of 0.1, 0.2, and 0.5 μM, all induced photocytotoxicity in a dose-dependent manner. When photoirradiation was conducted in the presence of a lipid (methyl linoleate), BaP metabolites, BPDE, and three related PAHs, pyrene, 7,8,9,10-tetrahydro-BaP trans-7,8-diol, and 7,8,9,10-tetrahydro-BaP trans-9,10-diol, all induced lipid peroxidation. The formation of lipid peroxides by BaP t-7,8-diol was inhibited by NaN3 and enhanced by deuterated methanol, which suggests that singlet oxygen may be involved in the generation of lipid peroxides. The formation of lipid hydroperoxides was partially inhibited by superoxide dismutase (SOD). Electron spin resonance spin trapping experiments indicated that both singlet oxygen and superoxide radical anion were generated from UVA photoirradiation of BPDE in a light dose responding manner.

  10. Identification of novel bioactive aldehyde-modified phosphatidylethanolamines formed by lipid peroxidation.

    PubMed

    Guo, Lilu; Chen, Zhongyi; Amarnath, Venkataraman; Davies, Sean S

    2012-09-15

    Lipid aldehydes generated by lipid peroxidation induce cell damage and inflammation. Recent evidence indicates that γ-ketoaldehydes (isolevuglandins, IsoLGs) form inflammatory mediators by modifying the ethanolamine headgroup of phosphatidylethanolamines (PEs). To determine if other species of aldehyde-modified PEs (al-PEs) with inflammatory bioactivity were generated by lipid peroxidation, we oxidized liposomes containing arachidonic acid and characterized the resulting products. We detected PE modified by IsoLGs, malondialdehyde (MDA), and 4-hydroxynonenal (HNE), as well as a novel series of N-acyl-PEs and N-carboxyacyl-PEs in these oxidized liposomes. These al-PEs were also detected in high-density lipoproteins exposed to myeloperoxidase. When we tested the ability of al-PEs to induce THP-1 monocyte adhesion to cultured endothelial cells, we found that PEs modified by MDA, HNE, and 4-oxononenal induced adhesion with potencies similar to those of PEs modified by IsoLGs (∼2μM). A commercially available medium-chain N-carboxyacyl-PE (C11:0CAPE) also stimulated adhesion, whereas C4:0CAPE and N-acyl-PEs did not. PEs modified by acrolein or by glucose were only partial agonists for adhesion. These studies indicate that lipid peroxidation generates a large family of al-PEs, many of which have the potential to drive inflammation. Copyright © 2012 Elsevier Inc. All rights reserved.

  11. Tocopherols Protect Synechocystis sp. Strain PCC 6803 from Lipid Peroxidation1

    PubMed Central

    Maeda, Hiroshi; Sakuragi, Yumiko; Bryant, Donald A.; DellaPenna, Dean

    2005-01-01

    Tocopherols (vitamin E) are lipid-soluble antioxidants synthesized only by photosynthetic eukaryotes and some cyanobacteria, and have been assumed to play important roles in protecting photosynthetic membranes from oxidative stress. To test this hypothesis, tocopherol-deficient mutants of Synechocystis sp. strain PCC 6803 (slr1736 and slr1737 mutants) were challenged with a series of reactive oxygen species-generating and lipid peroxidation-inducing chemicals in combination with high-light (HL) intensity stress. The tocopherol-deficient mutants and wild type were indistinguishable in their growth responses to HL in the presence and absence of superoxide and singlet oxygen-generating chemicals. However, the mutants showed enhanced sensitivity to linoleic or linolenic acid treatments in combination with HL, consistent with tocopherols playing a crucial role in protecting Synechocystis sp. strain PCC 6803 cells from lipid peroxidation. The tocopherol-deficient mutants were also more susceptible to HL treatment in the presence of sublethal levels of norflurazon, an inhibitor of carotenoid synthesis, suggesting carotenoids and tocopherols functionally interact or have complementary or overlapping roles in protecting Synechocystis sp. strain PCC 6803 from lipid peroxidation and HL stress. PMID:15965015

  12. 5-aminocoumarans: dual inhibitors of lipid peroxidation and dopamine release with protective effects against central nervous system trauma and ischemia.

    PubMed

    Ohkawa, S; Fukatsu, K; Miki, S; Hashimoto, T; Sakamoto, J; Doi, T; Nagai, Y; Aono, T

    1997-02-14

    A series of 2,3-dihydro-5-benzofuranamines (5-aminocoumarans) were developed for the treatment of traumatic and ischemic central nervous system (CNS) injury. Compounds within this class were extremely effective inhibitors of lipid peroxidation in vitro and antagonized excitatory behavior coupled with peroxidative injury induced by spinal intrathecal injection of FeCl2 (mouse-FeCl2-it assay) in vivo. Selected compounds were tested for antagonistic activity on methamphetamine (MAP)-induced hypermotility resulting from dopamine release in the mouse brain. Among the compounds synthesized, compound 26n (2,3-dihydro-2,4,6,7-tetramethyl-2-[(4-phenyl-1-piperidinyl) methyl]-5-benzofuranamine) exhibited potent effects in these assays (inhibition of lipid peroxidation, IC50 = 0.07 microM; mouse-FeCl2-it assay, ID50 = 10.4 mg/ kg, po; MAP-induced hypermotility, 98% inhibition, 10 mg/kg, ip). The S-(+)-form of compound 26n dihydrochloride (TAK-218), which has 30 times more potent antagonistic activity on MAP-induced hypermotility than the R-(-)-form, improved more significantly the survival rate in the cerebral ischemia model (rat, 1-3 mg/kg, ip) during the period of 1-14 days after ischemia and decreased functional disorders in the traumatic brain injury model (rat, 0.1-1 mg/kg, ip) 3-14 days after injury. These results imply a role for dopamine in deterioration of CNS function after ischemic and traumatic injury. TAK-218 is a promising compound for the treatment of stroke and CNS trauma and is now under clinical investigation.

  13. Studies on vitamin E and selenium deficiency in young pigs. II. The hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium status.

    PubMed Central

    Fontaine, M; Valli, V E

    1977-01-01

    The usefulness of the hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium deficiency in swine has been evaluated. Results indicated that although the hydrogen peroxide hemolysis test may be of some indication of the vitamin E status, it is not a reliable index of vitamin E deficiency in swine, at least on an individual basis. In contrast, the measure of red cell lipid peroxides can be considered a reliable test for vitamin E deficiency in swine. The hydrogen peroxide hemolysis test and the red cell lipid peroxides were not significantly affected by selenium deficiency. PMID:832189

  14. Effect of intracellular iron loading on lipid peroxidation of brain slices.

    PubMed

    Oubidar, M; Boquillon, M; Marie, C; Bouvier, C; Beley, A; Bralet, J

    1996-01-01

    The effect of artificially elevated cell iron content on oxygen-derived free radical production was assessed in brain slices by use of an iron ligand, 8-hydroxyquinoline (HQ). The iron complex Fe(3+)-HQ exhibited a high lipid solubility evidenced by n-octanol/water partition coefficient and was avidely taken up by brain slices. The catalytically active form of Fe3+ within the complex was evidenced by measuring the rate of ascorbate oxidation. Lipid peroxidation was assessed by measuring the thiobarbituric acid-reactive substances (TBARS) in brain homogenates or slices exposed to two doses of Fe(3+)-HQ (10 microM/20 microM, 100 microM/200 microM) or Fe(3+)-citrate (10 microM, 100 microM). Addition of the iron complexes to homogenates or slices resulted in a dose-dependent increase in lipid peroxidation. In homogenates, the effects were grossly similar with both complexes, whereas in slices the effects of Fe-HQ were significantly higher than those of Fe-citrate. Lipid peroxidation persisted in washed slices preexposed to Fe-HQ, but not in slices preexposed to the hydrophilic iron complex Fe-citrate. Fe-HQ-induced lipid peroxidation in slices was enhanced in the presence of H2O2, an effect that was not seen using Fe-citrate. Addition of Fe-HQ to brain homogenates in the presence of salicylic acid resulted in the production of 2,3-dihydroxybenzoic acid and the effect was potentiated in the presence of H2O2. This model of iron cell loading may be useful for evaluating the efficacy of antioxidant drugs.

  15. Tyrosine-lipid peroxide adducts from radical termination: para coupling and intramolecular Diels-Alder cyclization.

    PubMed

    Shchepin, Roman; Möller, Matias N; Kim, Hye-young H; Hatch, Duane M; Bartesaghi, Silvina; Kalyanaraman, Balaraman; Radi, Rafael; Porter, Ned A

    2010-12-15

    Free radical co-oxidation of polyunsaturated lipids with tyrosine or phenolic analogues of tyrosine gave rise to lipid peroxide-tyrosine (phenol) adducts in both aqueous micellar and organic solutions. The novel adducts were isolated and characterized by 1D and 2D NMR spectroscopy as well as by mass spectrometry (MS). The spectral data suggest that the polyunsaturated lipid peroxyl radicals give stable peroxide coupling products exclusively at the para position of the tyrosyl (phenoxy) radicals. These adducts have characteristic (13)C chemical shifts at 185 ppm due to the cross-conjugated carbonyl of the phenol-derived cyclohexadienone. The primary peroxide adducts subsequently undergo intramolecular Diels-Alder (IMDA) cyclization, affording a number of diastereomeric tricyclic adducts that have characteristic carbonyl (13)C chemical shifts at ~198 ppm. All of the NMR HMBC and HSQC correlations support the structure assignments of the primary and Diels-Alder adducts, as does MS collision-induced dissociation data. Kinetic rate constants and activation parameters for the IMDA reaction were determined, and the primary adducts were reduced with cuprous ion to give a phenol-derived 4-hydroxycyclohexa-2,5-dienone. No products from adduction of peroxyls at the phenolic ortho position were found in either the primary or cuprous reduction product mixtures. These studies provide a framework for understanding the nature of lipid-protein adducts formed by peroxyl-tyrosyl radical-radical termination processes. Coupling of lipid peroxyl radicals with tyrosyl radicals leads to cyclohexenone and cyclohexadienone adducts, which are of interest in and of themselves since, as electrophiles, they are likely targets for protein nucleophiles. One consequence of lipid peroxyl reactions with tyrosyls may therefore be protein-protein cross-links via interprotein Michael adducts.

  16. [Effect of phytic acid and its derivatives on blood lipid peroxidation state in vitro].

    PubMed

    Martusevich, A K; Sidorova, M V; Mel'nikova, N B; Solov'eva, A G; Peretiagin, S P

    2014-01-01

    We have studied specific features of lipid peroxidation in whole human blood under the action of aqueous solutions of xymedone (19.6 microM), phytic acid (117.9 microM) and its complex (237.6 microM) synthesized in distilled water and isotonic (0.9%) solution of sodium chloride. The estimated parameters included lipid peroxidation (LPO) rate, total antioxidant potential, superoxide dismutase (SOD) level, and malonic dialdehyde (MDA) level in blood plasma and erythrocytes. It was established that the effect of phytic acid on blood samples includes moderate stimulation of total antioxidant activity and SOD activity with predominant prooxidant effect. The phytic acid--xymedone complex synthesized in distilled water exhibits an antioxidant action, while its synthesis in saline solution yields a prooxidant.

  17. Breath pentane as a marker for lipid peroxidation and adverse outcome in preterm infants

    PubMed Central

    Nycyk, J; Drury, J; Cooke, R

    1998-01-01

    AIM—To test the hypothesis that complications of neonatal intensive care are related to increased oxygen derived free radical activity, using breath pentane as a marker of lipid peroxidation.
METHODS—Exhaled breath was collected daily from 57 ventilated preterm infants and pentane concentration measured by gas chromatography.
RESULTS—High peak pentane exhalation was significantly associated with low gestational age, mortality, intraventricular haemorrhage and retinopathy of prematurity. Peak pentane was not significantly associated with the development of chronic lung disease.
CONCLUSIONS—The demonstration that pentane exhalation is related to the course of neonatal disease and its outcome is consistent with the hypothesis that lipid peroxidation is associated with these illnesses, and may contribute to their severity. If this is a causal relation, antioxidant treatments could prove useful in reducing their severity. Measurement of breath pentane might assist in the assessment of antioxidant strategies prior to more extensive clinical trials.

 PMID:9797630

  18. Responses of a tropical tree species to ozone: visible leaf injury, growth, and lipid peroxidation.

    PubMed

    Cassimiro, Jéssica C; Moraes, Regina M

    2016-04-01

    The Brazilian native tree species Astronium graveolens was indicated as sensitive to ozone in a fumigation experiment. Thus, the objective of this study was to evaluate how sensitive A. graveolens is to ozone under realistic conditions in the field. Eighteen saplings were exposed to ozone in a contaminated area and in a greenhouse with filtered air during two exposure periods of approximately 63 days each (March-May 2012 and September-October 2012). Leaf injury was analyzed by means of its incidence and severity, the leaf injury index (LII) and the progression of leaf abscission. These variables were monitored weekly, whereas growth and lipid peroxidation were monitored monthly. Plants exposed to ozone showed significant growth decrease and visible leaf injury increase, but lipid peroxidation and leaf abscission remained unchanged. These results indicated that plants subjected to ozone possibly diverted energy from growth to the production of antioxidants necessary to cope with ozone-induced oxidative stress.

  19. Urea application promotes amino acid metabolism and membrane lipid peroxidation in Azolla.

    PubMed

    Chen, Jiana; Huang, Min; Cao, Fangbo; Pardha-Saradhi, P; Zou, Yingbin

    2017-01-01

    A pot experiment was conducted to evaluate the effect of urea on nitrogen metabolism and membrane lipid peroxidation in Azolla pinnata. Compared to controls, the application of urea to A. pinnata resulted in a 44% decrease in nitrogenase activity, no significant change in glutamine synthetase activity, 660% higher glutamic-pyruvic transaminase, 39% increase in free amino acid levels, 22% increase in malondialdehyde levels, 21% increase in Na+/K+- levels, 16% increase in Ca2+/Mg2+-ATPase levels, and 11% decrease in superoxide dismutase activity. In terms of H2O2 detoxifying enzymes, peroxidase activity did not change and catalase activity increased by 64% in urea-treated A. pinnata. These findings suggest that urea application promotes amino acid metabolism and membrane lipid peroxidation in A. pinnata.

  20. Vanadium-mediated lipid peroxidation in microsomes from human term placenta

    SciTech Connect

    Byczkowski, J.Z.; Wan, B.; Kulkarni, A.P.

    1988-11-01

    Vanadium is considered an essential element present in living organisms in trace amounts but it is toxic when introduced in excessive doses to animals and humans. Vanadium compounds are extensively used in modern industry and occupational exposure to high doses of vanadium is quite common. In pregnant mice, vanadium accumulates preferentially in the placenta and to lower extent in fetal skeleton and mammary gland during exposure to radioactive vanadium. Accumulation of vanadium in fetoplacental unit may present threat to the fetus by interacting with enzymes and ion-transporting systems in membranes. It is also possible that accumulation of vanadium with its concomitant reduction to vanadyl may lead to lipid peroxidation, followed by damage to biological membranes, lysosomal enzymes release and destruction of placental tissue. To explore some of these possibilities the authors decided to examine whether vanadate can undergo redox cycling in microsomes from human term placenta (HTP) that can lead to lipid peroxidation.

  1. [Opioid peptides effect on lipid peroxidation in long-term stress].

    PubMed

    Solin, A V; Liashev, Iu D

    2012-08-01

    It was shown in rats, that injection of opioid peptides (dynorphin A (1-13), DSLET and DAGO) decreased the stress-induced activation of lipid peroxidation in liver tissue and plasma. Dynorphin A (1-13) manifested the most expressed antioxidant effect in liver tissue. It not only decreased lipid peroxidation metabolites concentration, but also increased superoxiddismutase and catalase activity. Other peptides did not interfere enzyme activity. The use of DSLET or DAGO increased the superoxiddismutase plasma activity. Dynorphin A (1-13) injection increased catalase activity, but not superoxiddismutase. These effects could be explained by peculiarities of opioid receptors spread in liver tissue and stress-limiting action of peptides in entire organism.

  2. Functional disability of rat splenocytes provoked to lipid peroxidation by cumene hydroperoxide.

    PubMed

    Shimura, J; Shimura, F; Hosoya, N

    1985-04-22

    Rat splenocytes were provoked to lipid peroxidation in a dose-dependent manner by cumene hydroperoxide. After exposure to cumene hydroperoxide, formation of high molecular weight protein, presumably through cross-linking of lower molecular weight protein, was stimulated in splenocytes as well as in erythrocyte ghosts. The mitogenic response to concanavalin A of splenocytes was remarkably depressed by addition of cumene hydroperoxide to cultures. This depression was due rather to failures of splenocytes in responding to concanavalin A than deactivation of concanavalin A molecules. It is notworthy that the viability of splenocytes was unaffected by cumene hydroperoxide under the culture conditions where the mitogenic response was depressed. The addition of alpha-tocopherol or thiourea could block the depression of mitogenic response by cumene hydroperoxide, indicating that the depressed response to concanavalin A was related to radical formation. Overall evidence suggests that the function of immunocompetent cells can be depressed through lipid peroxidation-associated mechanisms without suffering from lethal damage.

  3. [Calcium transport in endoplasmic reticulum of the rat liver during lipid peroxidation].

    PubMed

    Gubskiĭ, Iu I; Kurskiĭ, M D; Zadorina, O V; Fedorov, A N; Briuzgina, T S; Iurzhenko, N N

    1990-01-01

    Some parameters of calcium transport in rat liver microsomes under conditions of lipoperoxidation activation modelled by antioxidant deficiency (AOD) were studied. This process was shown to be associated with a sharp stimulation of NADPH- and ascorbate-dependent lipid peroxidation in hepatocyte endoplasmic reticulum. The activation of lipid peroxidation was accompanied by disturbances in the kinetic properties of Ca2(+)-ATPase. This was paralleled with a considerable decrease of the ATP-dependent 45Ca-accumulation, increase in the passive permeability of microsomal vesicles for Ca2+ and Ca2+ elevation in the microsomal fraction. The AOD-induced diminution of the Ca2(+)-pump efficiency was slightly prevented by injections of rats with the antioxidants, alpha-tocopherol acetate and ionol which enable Ca2+ compartmentation correction in liver cytosol and membrane fractions.

  4. Seasonal variations in the antioxidant defence systems and lipid peroxidation of the digestive gland of mussels.

    PubMed

    Viarengo, A; Canesi, L; Pertica, M; Livingstone, D R

    1991-01-01

    1. The seasonal variations in the level of antioxidant compounds (glutathione (GSH), vitamin E, carotenoids) and in the activity of antioxidant enzymes, superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), GSH-peroxidase (EC 1.11.1.9) in the digestive gland of mussels (Mytilus sp.) were evaluated. The lipid peroxidation process was also measured by determining the tissue concentration of malondialdehyde (MDA). 2. The physiological fluctuations of the antioxidant defence systems were inversely related to the accumulation of lipid peroxidation products (MDA) in the tissue. The observed seasonal variations are presumably related to the changing metabolic status of the animals, itself dependent on such factors as gonad ripening and food availability. 3. In particular, the obtained data indicate that a reduction of the antioxidant defence systems, occurring during winter, could be directly responsible for an enhanced susceptibility of mussels tissues to oxidative stress, as indicated by the high MDA concentration observed in this period.

  5. β-Pinene inhibited germination and early growth involves membrane peroxidation.

    PubMed

    Chowhan, Nadia; Singh, Harminder Pal; Batish, Daizy R; Kaur, Shalinder; Ahuja, Nitina; Kohli, Ravinder K

    2013-06-01

    β-Pinene, an oxygenated monoterpene, is abundantly found in the environment and widely occurring in plants as a constituent of essential oils. We investigated the phytotoxicity of β-pinene against two grassy (Phalaris minor, Echinochloa crus-galli) and one broad-leaved (Cassia occidentalis) weeds in terms of germination and root and shoot growth. β-Pinene (0.02-0.80 mg/ml) inhibited the germination, root length, and shoot length of test weeds in a dose-response manner. The inhibitory effect of β-pinene was greater in grassy weeds and on root growth than on shoot growth. β-Pinene (0.04-0.80 mg/ml) reduced the root length in P. minor, E. crus-galli, and C. occidentalis over that in the control by 58-60, 44-92, and 26-85 %, respectively. In contrast, shoot length was reduced over the control by 45-97 % in P. minor, 48-78 % in E. crus-galli, and 11-75 % in C. occidentalis at similar concentrations. Further, we examined the impact of β-pinene on membrane integrity in P. minor as one of the possible mechanisms of action. Membrane integrity was evaluated in terms of lipid peroxidation, conjugated diene content, electrolyte leakage, and the activity of lipoxygenases (LOX). β-Pinene (≥0.04 mg/ml) enhanced electrolyte leakage by 23-80 %, malondialdehyde content by 15-67 %, hydrogen peroxide content by 9-39 %, and lipoxygenases activity by 38-383 % over that in the control. It indicated membrane peroxidation and loss of membrane integrity that could be the primary target of β-pinene. Even the enhanced (9-62 %) activity of protecting enzymes, peroxidases (POX), was not able to protect the membranes from β-pinene (0.04-0.20 mg/ml)-induced toxicity. In conclusion, our results show that β-pinene inhibits root growth of the tested weed species through disruption of membrane integrity as indicated by enhanced peroxidation, electrolyte leakage, and LOX activity despite the upregulation of POX activity.

  6. Protective effects of Emblica officinalis (Amla) on metal-induced lipid peroxidation in human erythrocytes.

    PubMed

    Krishnamoorthy, Vijay Kumar; Rather, Irfan Ahmad

    2016-05-01

    The protective potential of Emblica officinalis (amla) was investigated on metal-induced lipid per oxidation in human erythrocytes. Increases in the levels of MDA and catalase activity were assessed as lipid per oxidation. In addition, glutathione peroxidase (GPX), glutathione (GSH), and ascorbic acid levels were assessed as antioxidant indices. Preliminary investigation of the extract exhibited a significant reduction in lipid per oxidation and an increase in antioxidant abilities, such as a decrease in MDA, GPx and GSH (P<0.05). A significant reduction in erythrocyte hemolysis induced by hydrogen peroxide was observed using amla extract (P<0.05). These findings show that amla extract has significant protective potential against lipid per oxidation.

  7. Pyridine and pyrimidine analogs of acetaminophen as inhibitors of lipid peroxidation and cyclooxygenase and lipoxygenase catalysis†

    PubMed Central

    Nam, Tae-gyu; Nara, Susheel J.; Zagol-Ikapitte, Irène; Cooper, Thomas; Valgimigli, Luca; Oates, John A.; Porter, Ned A.; Boutaud, Olivier; Pratt, Derek A.

    2010-01-01

    Herein we report an investigation of the efficacy of pyridine and pyrimidine analogs of acetaminophen (ApAP) as peroxyl radical-trapping antioxidants and inhibitors of enzyme-catalyzed lipid peroxidation by cyclooxygenases (COX) and lipoxygenases (LOX). In inhibited autoxidations we find that ApAP, the common analgesic and antipyretic agent, is a very good antioxidant with a rate constant for reaction with peroxyl radicals (kinh = 5 × 105 M−1 s−1) that is higher than many widely-used phenolic antioxidants, such as the ubiquitous butylated hydroxytoluene (BHT). This reactivity is reduced substantially upon incorporation of nitrogen into the phenolic ring, owing to an increase in the O–H bond dissociation enthalpy of pyridinols and pyrimidinols with respect to phenols. Incorporation of nitrogen into the phenolic ring of ApAP was also found to decrease its efficacy as an inhibitor of prostaglandin biosynthesis by ovine COX-1 (oCOX-1). This is explained on the basis of an increase in its oxidation potential and its reduced reactivity as a reducing co-substrate of the peroxidase protoporphyrin. In contrast, the efficacy of ApAP as an inhibitor of lipid hydroperoxide biosynthesis by soybean LOX-1 (sLOX-1) increased upon incorporation of nitrogen into the ring, suggesting a different mechanism of inhibition dependent on the acidity of the phenolic O–H which may involve chelation of the catalytic non-heme iron atom. The greater stability of the 3-pyridinols and 5-pyrimidinols to air oxidation as compared to phenols allowed us to evaluate some electron-rich pyridinols and pyrimidinols as inhibitors of oCOX-1 and sLOX-1. While the pyridinols had the best combination of activities as antioxidants and inhibitors of oCOX-1 and sLOX-1, they were found to be more toxic than ApAP in preliminary assays in human hepatocellular carcinoma (HepG2) cell culture. The pyrimidinols, however, were up to 17-fold more reactive to peroxyl radicals and up to 25-fold better inhibitors

  8. Mechanism of chain termination in lipid peroxidation by carotenes: a theoretical study.

    PubMed

    Guo, Jian-Jhih; Hu, Ching-Han

    2010-12-23

    The reaction mechanism of carotenes (CARs) in chain termination against lipid peroxidation was studied using density functional theory. In the presence of peroxide (ROO(·)), the reaction barrier for its addition to CAR to form ROO-CAR(·) is smaller than those for its hydrogen abstractions from CAR and linoleic acid (LAH), respectively. In contrast, the reaction barriers for the O(2) additions of the carbon-centered radicals are ordered as ROO-CAR(·) > CAR(-H)(·) > LA(·). Thus, the chain-termination function of CAR is best demonstrated by trapping the addition radical and suppressing O(2) addition. For either the ROO-CAR(·) or CAR(-H)(·) radicals, β-carotene has noticeably higher O(2) addition barriers than those of their lycopene counterparts. The reaction barrier for the rearrangement of ROO-CAR(·) into RO(·) + epoxide is much smaller than that for the formation of cyclic ether and is comparable to that of O(2) addition. Since RO(·) has a stronger tendency toward hydrogen abstraction than ROO(·), the rearrangement of the addition adduct has to be recognized as an important factor while evaluating the chain-termination potency of a molecule. The overall reaction energy profile reveals that the protective function of CAR is mostly exhibited via formation of the addition adduct. Comparatively, β-carotene is a more potent antiradical agent than lycopene against peroxide-initiated lipid peroxidation.

  9. Exploration of scalp surface lipids reveals squalene peroxide as a potential actor in dandruff condition.

    PubMed

    Jourdain, Roland; Moga, Alain; Vingler, Philippe; El Rawadi, Charles; Pouradier, Florence; Souverain, Luc; Bastien, Philippe; Amalric, Nicolas; Breton, Lionel

    2016-04-01

    Dandruff is a common but complex disorder with three major contributing factors: (1) individual predisposition, (2) scalp sebum and (3) Malassezia yeast colonization. To obtain further insights into the role of sebum in dandruff biogenesis, we analyzed scalp lipid species in a cohort of ten dandruff-free (control) and ten dandruff-afflicted volunteers by gas chromatography coupled to mass spectrometry. Lipid peroxidation levels and biochemical markers of oxidative stress were also assessed. Squalene, a major sebum component, was significantly more peroxidized in dandruff-affected scalps, resulting in significantly higher ratios of squalene monohydroperoxide (SQOOH)/squalene. This was observed when comparing dandruff-affected zones of dandruff subjects to both their non-affected zones and control subjects. In addition, other biomarkers such as malondialdehyde indicated that oxidative stress levels were raised on dandruff scalps. Surprisingly, differences regarding either free or bound fatty acids were fairly rare and minor. Certain novel findings, especially squalene peroxidation levels, were then confirmed in a validation cohort of 24 dandruff-affected subjects, by comparing dandruff-affected and non-dandruff zones from the same individuals. As SQOOH can induce both keratinocyte inflammatory responses and hyperproliferation in vitro, we hypothesized that increased SQOOH could be considered as a new etiological dandruff factor via its ability to impair scalp barrier function. Our results also indicated that Malassezia could be a major source of squalene peroxidation on the scalp.

  10. Ethanol induces rapid lipid peroxidation and activation of nuclear factor-kappa B in cerebral vascular smooth muscle: relation to alcohol-induced brain injury in rats.

    PubMed

    Altura, Burton M; Gebrewold, Asefa; Zhang, Aimin; Altura, Bella T

    2002-06-07

    The present study was designed to test the hypothesis that acute administration of alcohol (ethanol) to primary cultured cerebral vascular smooth muscle cells will cause lipid peroxidation, inhibition of IkappaB phosphorylation, and inhibition of nuclear transcription factor-kappa B (NF-kappaB). Ethanol (10, 25, 100 mM) resulted in concentration-dependent rises in malondialdehyde in as little as 30-45 min after exposure to the alcohol, rising to levels 2.5-10x normal after 18-24 h. Using EMSA assays and specific antibodies, ethanol caused three DNA-binding proteins (p50, p65, c-Rel) to rise in nuclear extracts in a concentration-dependent manner. Using a rabbit antibody, IkappaB phosphorylation (and degradation) was stimulated by ethanol (in a concentration-dependent manner) and inhibited by a low concentration of the NF-kappaB inhibitor, pyrrolidine dithiocarbamate. These new biochemical and molecular data indicate that ethanol, even in physiologic concentrations, can elicit rapid lipid peroxidation and activation of NF-kappaB in cerebral vascular muscle cells. The present results when viewed in light of other recently published data suggest that ethanol-induced lipid peroxidation and activation of nuclear transcription factors probably play important roles in alcohol-induced brain-vascular damage, neurobehavioral actions and stroke.

  11. Biosynthesis of colloidal gold nanoparticles by Streptomyces sp. NK52 and its anti-lipid peroxidation activity.

    PubMed

    Prakash, Divya; Mahale, Vishal; Bankar, Ashok; Nawani, Neelu; Mahale, Vishal; Prakash, Divya

    2013-11-01

    Gold nanoparticles (Au-NPs) were synthesized from chloroauric acid using cell free supernatant of Streptomyces sp. NK52 grown in nutrient broth. These nanoparticles were synthesized by varying pH and temperature of the reaction mixture and chloroauric acid concentration. The nanoparticles were characterized by spectrometry, X-ray diffraction, Scanning electron microscopy and energy dispersive spectrometry. Au-NP ranged from 10-100 nm in size and exhibited a polydispersive nature with various shapes like rods, hexagons, triangles, spheres. The diffraction peaks at 2theta = 38.1 degrees and 44.5 degrees could be assigned to the (1 1 1) and (2 0 0) planes of a faced centre cubic (fcc) lattice of gold. Au-NP showed 47% inhibition of lipid peroxidation in vitro. To the best of our knowledge, this is the first report on the rapid biosynthesis of Au-NP using cell free supernatant of Streptomyces sp. and its evaluation for anti-lipid peroxidation.

  12. Lipid peroxidation is another potential mechanism besides pore-formation underlying hemolysis of tentacle extract from the jellyfish Cyanea capillata.

    PubMed

    Wang, Tao; Wen, Xiao-Juan; Mei, Xiao-Bin; Wang, Qian-Qian; He, Qian; Zheng, Jie-Min; Zhao, Jie; Xiao, Liang; Zhang, Li-Ming

    2013-01-09

    This study was performed to explore other potential mechanisms underlying hemolysis in addition to pore-formation of tentacle extract (TE) from the jellyfish Cyanea capillata. A dose-dependent increase of hemolysis was observed in rat erythrocyte suspensions and the hemolytic activity of TE was enhanced in the presence of Ca2+, which was attenuated by Ca2+ channel blockers (Diltiazem, Verapamil and Nifedipine). Direct intracellular Ca2+ increase was observed after TE treatment by confocal laser scanning microscopy, and the Ca2+ increase could be depressed by Diltiazem. The osmotic protectant polyethylenglycol (PEG) significantly blocked hemolysis with a molecular mass exceeding 4000 Da. These results support a pore-forming mechanism of TE in the erythrocyte membrane, which is consistent with previous studies by us and other groups. The concentration of malondialdehyde (MDA), an important marker of lipid peroxidation, increased dose-dependently in rat erythrocytes after TE treatment, while in vitro hemolysis of TE was inhibited by the antioxidants ascorbic acid-Vitamin C (Vc)-and reduced glutathione (GSH). Furthermore, in vivo hemolysis and electrolyte change after TE administration could be partly recovered by Vc. These results indicate that lipid peroxidation is another potential mechanism besides pore-formation underlying the hemolysis of TE, and both Ca2+ channel blockers and antioxidants could be useful candidates against the hemolytic activity of jellyfish venoms.

  13. Lipid Peroxidation Is another Potential Mechanism besides Pore-Formation Underlying Hemolysis of Tentacle Extract from the Jellyfish Cyanea capillata

    PubMed Central

    Wang, Tao; Wen, Xiao-Juan; Mei, Xiao-Bin; Wang, Qian-Qian; He, Qian; Zheng, Jie-Min; Zhao, Jie; Xiao, Liang; Zhang, Li-Ming

    2013-01-01

    This study was performed to explore other potential mechanisms underlying hemolysis in addition to pore-formation of tentacle extract (TE) from the jellyfish Cyanea capillata. A dose-dependent increase of hemolysis was observed in rat erythrocyte suspensions and the hemolytic activity of TE was enhanced in the presence of Ca2+, which was attenuated by Ca2+ channel blockers (Diltiazem, Verapamil and Nifedipine). Direct intracellular Ca2+ increase was observed after TE treatment by confocal laser scanning microscopy, and the Ca2+ increase could be depressed by Diltiazem. The osmotic protectant polyethylenglycol (PEG) significantly blocked hemolysis with a molecular mass exceeding 4000 Da. These results support a pore-forming mechanism of TE in the erythrocyte membrane, which is consistent with previous studies by us and other groups. The concentration of malondialdehyde (MDA), an important marker of lipid peroxidation, increased dose-dependently in rat erythrocytes after TE treatment, while in vitro hemolysis of TE was inhibited by the antioxidants ascorbic acid—Vitamin C (Vc)—and reduced glutathione (GSH). Furthermore, in vivo hemolysis and electrolyte change after TE administration could be partly recovered by Vc. These results indicate that lipid peroxidation is another potential mechanism besides pore-formation underlying the hemolysis of TE, and both Ca2+ channel blockers and antioxidants could be useful candidates against the hemolytic activity of jellyfish venoms. PMID:23303301

  14. Effects of isoquinoline alkaloid berberine on lipid peroxidation, antioxidant defense system, and liver damage induced by lead acetate in rats.

    PubMed

    Hasanein, Parisa; Ghafari-Vahed, Masumeh; Khodadadi, Iraj

    2017-01-01

    Liver is considered a target organ affected by lead toxicity. Oxidative stress is among the mechanisms involved in liver damage. Here we investigated the effects of the natural alkaloid berberine on oxidative stress and hepatotoxicity induced by lead in rats. Animals received an aqueous solution of lead acetate (500 mg Pb/l in the drinking water) and/or daily oral gavage of berberine (50 mg/kg) for 8 weeks. Rats were then weighed and used for the biochemical, molecular, and histological evaluations. Lead-induced oxidative stress, shown by increasing lipid peroxidation along with a concomitant decrease in hepatic levels of thiol groups, total antioxidant capacity, the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, and reduced versus oxidized glutathione ratio. Berberine corrected all the disturbances in oxidative stress markers induced by lead administration. Berberine also prevented the elevated levels of enzymes (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) and the decrease in body weight and albumin. The protective effects of berberine were comparable with silymarin. Furthermore, berberine attenuated liver damage, shown by decreased necrosis and inflammatory cell infiltration. Berberine represents a potential therapeutic option against lead-induced hepatotoxicity through inhibiting lipid peroxidation and enhancing antioxidant defenses. Berberine exerted protective effects on lead-induced oxidative stress and hepatotoxicity in rats.

  15. [Effects of exogenous spermidine on lipid peroxidation and membrane proton pump activity of cucumber seedling leaves under high temperature stress].

    PubMed

    Tian, Jing; Guo, Shi-Rong; Sun, Jin; Wang, Li-Ping; Yang, Yan-Juan; Li, Bin

    2011-12-01

    Taking a relatively heat-resistant cucumber (Cucumis sativus) cultivar 'Jinchun No. 4' as test material, a sand culture experiment was conducted in growth chamber to investigate the effects of foliar spraying spermidine (Spd) on the lipid peroxidation, membrane proton pump activity, and corresponding gene expression of cucumber seedling leaves under high temperature stress. Compared with the control, foliar spraying Spd increased the plant height, stem diameter, dry and fresh mass, and leaf area significantly, and inhibited the increase of leaf relative conductivity, malondialdehyde (MDA) content, and lipoxygenase (LOX) activity effectively. Foliar spraying Spd also helped to the increase of leaf plasma membrane- and tonoplast H(+)-ATPase activity, but no significant difference was observed in the gene expression levels. These results suggested that exogenous Spd could significantly decrease the leaf lipid peroxidation and increase the proton pump activity, and thus, stabilize the leaf membrane structure and function, alleviate the damage induced by high temperature stress, and enhance the heat tolerance of cucumber seedlings.

  16. Anti lipid peroxidation activity of Piper trioicum Roxb. and Physalis minima L. extracts.

    PubMed

    Dinakaran, Sathis Kumar; Saraswathi, Narasimha Raju; Nalini, Venkata Rama Rao; Srisudharson; Bodanapu, Venkat Ram Reddy; Avasarala, Harani; Banji, David

    2011-07-01

    Attempt has been made to evaluate free radical scavenging activity of ethanolic extract of Piper trioicum Roxb. and Physalis minima L. individually. In this study goat liver has been used as lipid source. This in vitro evaluation was done by measuring the malondialdehyde (MDA) of tissue homogenates. The results suggest that the ethanolic extract of the Piper trioicum Roxb. and Physalis minima L. has the ability to suppress the lipid peroxidation and it was also found that Piper trioicum Roxb. extract has more activity than Physalis minima L. extract.

  17. Effects of submicrometer particle compositions on cytokine production and lipid peroxidation of human bronchial epithelial cells.

    PubMed Central

    Huang, Song-Lih; Hsu, Miao-Kan; Chan, Chang-Chuan

    2003-01-01

    To identify the size and components related to toxicity of ambient particles, we used a trichotomous impactor to collect 17 sets of particles in three size ranges--submicrometer (diameters < 1 microm; PM1.0, fine (diameters between 1 and 2.5 microm; PM1.0-2.5, and coarse (diameters between 2.5 and 10 microm; PM2.5-10--at stations monitoring background, urban, traffic, and industrial air in Taiwan. Elemental contents, carbon contents, soluble ions, and endotoxin content of particles were determined by X-ray fluorescence spectrometry, thermal analysis, ion chromatography, and the Limulus amebocyte lysate assay, respectively. Human bronchial epithelial BEAS-2B cells were exposed to particle extracts at 100 micro g/mL for 8 hr, and interleukin-8 (IL-8) concentrations in the medium and lipid peroxidation products were measured. Particle-induced tumor necrosis factor-alpha (TNF-alpha) production by mouse macrophage RAW 264.7 cells was also measured. PM1.0 stimulation resulted in significantly higher IL-8 production and lipid peroxidation than PM2.5-10, whereas the responses elicited by PM1.0-2.5 were not significantly higher than blank filters. Untreated and polymyxin B-pretreated PM1.0 also stimulated more TNF-alpha production by RAW 264.7 cells than PM2.5-10 and PM1.0-2.5. Cytokine production was significantly associated with metal contents of PM1.0: IL-8 correlated with Cr and Mn, and TNF-alpha correlated with Fe and Cr. Lipid peroxidation in BEAS-2B cells correlated with elemental and organic carbon contents. Our study found that size and composition of ambient particles were both important factors in inducing cytokine production and lipid peroxidation. PMID:12676602

  18. Hydrogen sulfide decreases the plasma lipid peroxidation induced by homocysteine and its thiolactone.

    PubMed

    Olas, Beata; Kontek, Bogdan

    2015-06-01

    Hydrogen sulfide (H2S) has been investigated widely in recent years. H2S plays a variety of roles in different biological systems, including cardiovascular system. It is the final product of amino acids metabolism, which contains sulfur-cysteine and homocysteine (Hcy). In human plasma, there are several various forms of homocysteine: free Hcy, protein-bound Hcy (S-linked, and N-linked), and homocysteine thiolactone (HTL). Our previous works have shown that both Hcy in the reduced form and its thiolactone may modify fibrinolysis, coagulation process, and biological activity of blood platelets. Moreover, we have observed that HTL, like its precursor-Hcy stimulated the generation of superoxide anion radicals (O 2 (-•) ) in blood platelets. The aim of our study in vitro was to establish the influence of sodium hydrosulfide (NaHS, as a fast-releasing H2S donor; at tested concentrations: 10-1000 µM) on the plasma lipid peroxidation induced by the reduced Hcy (at final concentrations of 0.01-1 mM) and HTL (at final concentrations of 0.1-1 µM). Our results indicate that 10 and 100 µM NaHS decreased the lipid peroxidation in plasma treated with 1 mM Hcy or 1 µM HTL (when NaHS and Hcy/HTL were added to plasma together). The protective effect of 10 and 100 µM NaHS against the lipid peroxidation in plasma preincubated with 1 mM Hcy or 1 µM HTL was also observed. Considering the data presented in this study, we suggest that the lipid peroxidation (induced by different forms of homocysteine) may be reduced by hydrogen sulfide.

  19. Drought stress induced changes in lipid peroxidation and antioxidant system in genus Avena.

    PubMed

    Pandey, Harish C; Baig, M J; Chandra, A; Bhatt, R K

    2010-07-01

    Seven species of genus Avena viz., Avena sativa, Avena strigosa, Avena brevis, Avena vaviloviana, Avena abyssinica, Avena marocana and Avena sterilis were used to study the impact of drought stress on lipid peroxidation and other antioxidant enzymes. Maximum increase in the catalase activity was recorded in A. vaviloviana (129.97%) followed by A. sativa (122.82%) and A. brevis (83.38%) at vegetative stage; however at flowering stage the maximum increase was reported in A. sativa (25.62%) followed by A. sterilis (20.46%) and A. brevis (18.53%). At vegetative stage drought, maximum increase in peroxidase activity was recorded in A. sativa (122.82%) followed by A. brevis (83.38%) and A. sterilis (49.78%). Flowering stage drought, showed maximum increase in A. Sativa (27.09%) followed by A. marocana (23.50%) and A. sterilis (20.46%). A. sativa and A. sterilis showed stress tolerance at both the stages by accumulating higher percentage of peroxidase followed by A. brevis at vegetative and A. marocana at flowering stage. Level of lipid peroxidation in terms of Malondialdehyde (MDA) content was increased in the leaves when plants were subjected to moisture stress. The rate of increase in lipid peroxidation occurs irrespective of stage however; maximum increase was recorded in A. strigosa at both the stages. Avena species which showed high level of MDA content, indicates more lipid peroxidation and more membrane permeability and are comparatively more susceptible for water stress than those which produce less Malondialdehyde (MDA) content at higher magnitude of water stress such species have better capability for moisture stress tolerance.

  20. [Tissue specificity of antioxidant system functioning and lipid peroxidation in different age groups of Amur carp].

    PubMed

    Kras', S I; Tarasiuk, S I

    2011-01-01

    Key features of tissue enzymes functioning in antioxidant system (AOS) in sexually mature and immature individuals of Amur carp were studied. The activity of antioxidant enzymes was highest in the myocardium and subjected to age-related changes. It was concluded that changes in the functioning of AOS and intensity of lipid peroxidation processes are characterized by organ-tissue metabolic features and age peculiarities of metabolism that is most expressed in the myocardium.

  1. α-lipoic acid ameliorates n-3 highly-unsaturated fatty acids induced lipid peroxidation via regulating antioxidant defenses in grass carp (Ctenopharyngodon idellus).

    PubMed

    Shi, Xiao-Chen; Jin, Ai; Sun, Jian; Yang, Zhou; Tian, Jing-Jing; Ji, Hong; Yu, Hai-Bo; Li, Yang; Zhou, Ji-Shu; Du, Zhen-Yu; Chen, Li-Qiao

    2017-08-01

    This study evaluated the protective effect of α-lipoic acid (LA) on n-3 highly unsaturated fatty acids (HUFAs)-induced lipid peroxidation in grass carp. The result indicated that diets with n-3 HUFAs increased the production of malondialdehyde (MDA) (P < 0.05), thereby inducing lipid peroxidation in liver and muscle of grass carp. Meanwhile, compared with control group, the hepatosomatic index (HSI) and kidney index (KI) of grass carp were markedly increased in n-3 HUFAs-only group. However, diets with LA remarkably inhibited the n-3 HUFAs-induced increase of HSI, KI, and MDA level in serum, liver and muscle (P < 0.05). Interestingly, LA also significantly elevated the ratio of total n-3 HUFAs in fatty acid composition of muscle and liver (P < 0.05). Furthermore, LA significantly promoted the activity of antioxidant enzymes in serum, muscle and liver of grass carp (P < 0.05), including superoxide dismutase (SOD), catalase (CAT), and glutathione s-transferase (GST). The further results showed that LA significantly elevated mRNA expression of antioxidant enzymes with promoting the mRNA expression of NF-E2-related nuclear factor 2 (Nrf2) and decreasing Kelch-like-ECH-associated protein 1 (Keap1) mRNA level. From the above, these results suggested that LA could attenuate n-3 HUFAs-induced lipid peroxidation, remit the toxicity of the lipid peroxidant, and protect n-3 HUFAs against lipid peroxidation to promote its deposition in fish, likely strengthening the activity of antioxidant enzymes through regulating mRNA expressions of antioxidant enzyme genes via mediating Nrf2-Keap1 signaling pathways. Copyright © 2017 Elsevier Ltd. All rights reserved.

  2. Antioxidant properties of resveratrol and piceid on lipid peroxidation in micelles and monolamellar liposomes.

    PubMed

    Fabris, Sabrina; Momo, Federico; Ravagnan, Giampietro; Stevanato, Roberto

    2008-06-01

    The antioxidant activities of trans-resveratrol (trans-3,5,4'-trihydroxystilbene) and trans-piceid (trans-5,4'-dihydroxystilbene-3-O-beta-D-glucopyranoside), its more widespread glycosilate derivative, have been compared measuring their inhibitory action on peroxidation of linoleic acid (LA) and the radical scavenging ability towards different free radicals (such as DPPH) and radical initiators. It has been found that the two stilbenes have similar antioxidant capacity, while the comparison with BHT (2,6-di-tert-butyl-4-methylphenol) and alpha-tocopherol (vitamin E, vit. E), taken as reference, points out a slower but prolonged protective action against lipid peroxidation. Furthermore, piceid appears more efficacious than resveratrol as a consequence of the reaction of the latter with its radical form. The DSC profiles of phosphatidylcholine liposomes of various chain lengths, and EPR measurements of spin labelled liposomes demonstrated that the susceptible hydroxyl group of these compounds are located in the lipid region of the bilayer close to the double bonds of polyunsaturated fatty acids, making these stilbenes particularly suitable for the prevention and control of the lipid peroxidation of the membranes.

  3. Daily supplementation with iron increases lipid peroxidation in young women with low iron stores.

    PubMed

    King, Sarah M; Donangelo, Carmen M; Knutson, Mitchell D; Walter, Patrick B; Ames, Bruce N; Viteri, Fernando E; King, Janet C

    2008-06-01

    The aim of this study was to determine whether women with low iron stores (plasma ferritin lipid peroxidation as measured by ethane exhalation rates and plasma malondialdehyde. The women served as their own control as pre- and post-supplementation periods were compared. Twelve women participated in the study for a 70-day period and consumed daily iron supplements (98 mg of iron as ferrous sulfate) from day 14 to day 70. Baseline blood and expired air samples were obtained on days 1 and 14; measurements during supplementation were performed on days 56 and 70, that is at 6 and 8 weeks of supplementation. Iron status improved during the iron supplementation period; biochemical indicators of lipid peroxidation also increased. After 6 wks of iron supplementation, serum ferritin almost doubled and body iron more than doubled. Hemoglobin levels increased slightly and other indicators of iron status became normal. However, plasma malondialdehyde (MDA) and breath ethane exhalation rates (BEER) increased by more than 40% between baseline and 6 wks of supplementation; these increases correlated significantly with plasma iron and ferritin levels. MDA was positively correlated with BEER. BEER increased further after 8 wks of iron supplementation. The increased indicators of lipid peroxidation with duration of supplementation and as iron status improved suggest that providing daily nearly 100 mg iron may not be a totally innocuous regimen for correcting iron depletion in women.

  4. Liver and heart mitochondria obtained from Adelie penguin (Pygoscelis adeliae) offers high resistance to lipid peroxidation.

    PubMed

    Gavazza, Mariana; Marmunti, Mónica; Montalti, D; Gutiérrez, Ana María

    2008-06-01

    Lipid peroxidation is generally thought to be a major mechanism of cell injury in aerobic organisms subjected to oxidative stress. All cellular membranes are especially vulnerable to oxidation due to their high concentration of polyunsaturated fatty acids. However, birds have special adaptations for preventing membrane damage caused by reactive oxygen species. This study examines fatty acid profiles and susceptibility to lipid peroxidation in liver and heart mitochondria obtained from Adelie penguin (Pygoscelis adeliae). The saturated fatty acids in these organelles represent approximately 40-50% of total fatty acids whereas the polyunsaturated fatty acid composition was highly distinctive, characterized by almost equal amounts of 18:2 n-6; 20:4 n-6 and 22:6 n-3 in liver mitochondria, and a higher proportion of 18:2 n-6 compared to 20:4 n-6 and 22:6 n-3 in heart mitochondria. The concentration of total unsaturated fatty acids of liver and heart mitochondria was approximately 50% and 60%, respectively, with a prevalence of oleic acid C18:1 n9. The rate C20:4 n6/C18:2 n6 and the unsaturation index was similar in liver and heart mitochondria; 104.33 +/- 6.73 and 100.09 +/- 3.07, respectively. Light emission originating from these organelles showed no statistically significant differences and the polyunsaturated fatty acid profiles did not change during the lipid peroxidation process.

  5. IFN-γ ameliorates autoimmune encephalomyelitis by limiting myelin lipid peroxidation

    PubMed Central

    Sosa, Rebecca A.; Murphey, Cathi; Robinson, Rachel R.; Forsthuber, Thomas G.

    2015-01-01

    Evidence has suggested both a pathogenic and a protective role for the proinflammatory cytokine IFN-γ in experimental autoimmune encephalomyelitis (EAE). However, the mechanisms underlying the protective role of IFN-γ in EAE have not been fully resolved, particularly in the context of CNS antigen-presenting cells (APCs). In this study we examined the role of IFN-γ in myelin antigen uptake by CNS APCs during EAE. We found that myelin antigen colocalization with APCs was decreased substantially and that EAE was significantly more severe and showed a chronic-progressive course in IFN-γ knockout (IFN-γ−/−) or IFN-γ receptor knockout (IFN-γR−/−) mice as compared with WT animals. IFN-γ was a critical regulator of phagocytic/activating receptors on CNS APCs. Importantly, “free” myelin debris and lipid peroxidation activity at CNS lesions was increased in mice lacking IFN-γ signaling. Treatment with N-acetyl-l-cysteine, a potent antioxidant, abolished lipid peroxidation activity and ameliorated EAE in IFN-γ–signaling-deficient mice. Taken together the data suggest a protective role for IFN-γ in EAE by regulating the removal of myelin debris by CNS APCs and thereby limiting the substrate available for the generation of neurotoxic lipid peroxidation products. PMID:26305941

  6. Regulation of the hepatitis C virus RNA replicase by endogenous lipid peroxidation

    PubMed Central

    Yamane, Daisuke; McGivern, David R.; Wauthier, Eliane; Yi, MinKyung; Madden, Victoria J.; Welsch, Christoph; Antes, Iris; Wen, Yahong; Chugh, Pauline E.; McGee, Charles E.; Widman, Douglas G.; Misumi, Ichiro; Bandyopadhyay, Sibali; Kim, Seungtaek; Shimakami, Tetsuro; Oikawa, Tsunekazu; Whitmire, Jason K.; Heise, Mark T.; Dittmer, Dirk P.; Kao, C. Cheng; Pitson, Stuart M; Merrill, Alfred H.; Reid, Lola M.; Lemon, Stanley M.

    2014-01-01

    Although oxidative tissue injury often accompanies viral infection, there is little understanding of how it influences virus replication. We show that multiple hepatitis C virus (HCV) genotypes are exquisitely sensitive to oxidative membrane damage, a property distinguishing them from other pathogenic RNA viruses. Lipid peroxidation, regulated in part through sphingosine kinase 2, severely restricts HCV replication in Huh-7 cells and primary human hepatoblasts. Endogenous oxidative membrane damage lowers the 50% effective concentration of direct-acting antivirals, suggesting critical regulation of the conformation of the NS3/4A protease and NS5B polymerase, membrane-bound HCV replicase components. Resistance to lipid peroxidation maps genetically to trans-membrane and membrane-proximal residues within these proteins, and is essential for robust replication in cell culture, as exemplified by the atypical JFH1 strain. Thus, the typical, wild-type HCV replicase is uniquely regulated by lipid peroxidation, providing a novel mechanism for attenuating replication in stressed tissue and possibly facilitating long-term viral persistence. PMID:25064127

  7. Endogenous Intoxication and Saliva Lipid Peroxidation in Patients with Lung Cancer

    PubMed Central

    Bel’skaya, Lyudmila V.; Kosenok, Victor K.; Massard, Gilbert

    2016-01-01

    This research was aimed at a search for regularities in changes to parameters of endogenous intoxication and saliva lipid peroxidation in patients with lung cancer, non-malignant lung diseases, and apparently healthy people. All patients went through saliva sampling at an amount of 1 mL. A concentration of malondialdehyde (MDA) was measured according to a reaction with thiobarbituric acid, and a level of middle molecules (MM) was measured with UV spectroscopy at 254 and 280 nm, while the content of lipid peroxidation products was measured according to a degree of heptane extract light absorption at wavelengths of 220, 232, 278, and 400 nm. It has been revealed that in the context of lung cancer, the level of diene conjugates decreases, increasing the level of triene conjugates, Schiff’s bases, and MM. As a tumor grows, there is a decrease in the level of lipid peroxidation primary products and an increase in endotoxemia phenomena. The process is more apparent when going from local to locally advanced disease states. The nature of the MDA change is nonlinearly associated with tumor progression. The findings might be used to optimize traditional aids of diagnostics, in disease state forecasting, in treatment monitoring, etc. PMID:27854319

  8. [Relationship between lipid peroxidation in blood and neurobehavioral function changes in coke oven workers].

    PubMed

    Wang, Fang; Zhang, Hong-Mei; Nie, Ji-Sheng; Xue, Cui-E; Shi, Ying-Tao; Niu, Qiao

    2007-01-01

    To explore the coincidence of lipid peroxidation and neurobehavioral function changes in coke oven workers. One hundred and thirty-four coke oven workers were divided into three groups: 35 in the oven-bottom group, 49 in the oven-side group and 50 in oven-top group. WHO recommended NCTB was performed on coke oven workers and 36 controls from material conservation department; The contents of total superoxide dismutases (T-SOD), glutathione (GSH) and malondialdehyde (MDA) in blood were determined by test kits. Compared with the controls, the coke oven workers showed lower levels of T-SOD and GSH (P < 0.01), significantly higher MDA levels in blood (P < 0.01), higher score on negative mood state, lower scores on positive mood state, and poorer performance in NCTB test (P < 0.05). Further analysis revealed that there was a weak positive correlation between neurobehavioral function changes and the level of lipid peroxidation with a coefficient lower than 0.25. The level of lipid peroxidation in coke oven workers' blood increased and coincided with neurobehavioral function impairment.

  9. Metal-catalyzed oxidation of 2-alkenals generates genotoxic 4-oxo-2-alkenals during lipid peroxidation.

    PubMed

    Nuka, Erika; Tomono, Susumu; Ishisaka, Akari; Kato, Yoji; Miyoshi, Noriyuki; Kawai, Yoshichika

    2016-10-01

    Lipid peroxidation products react with cellular molecules, such as DNA bases, to form covalent adducts, which are associated with aging and disease processes. Since lipid peroxidation is a complex process and occurs in multiple stages, there might be yet unknown reaction pathways. Here, we analyzed comprehensively 2'-deoxyguanosine (dG) adducts with oxidized arachidonic acid using liquid chromatography-tandem mass spectrometry and found the formation of 7-(2-oxo-hexyl)-etheno-dG as one of the major unidentified adducts. The formation of this adduct was reproduced in the reaction of dG with 2-octenal and predominantly with 4-oxo-2-octenal (OOE). We also found that other 2-alkenals (with five or more carbons) generate corresponding 4-oxo-2-alkenal-type adducts. Importantly, it was found that transition metals enhanced the oxidation of C4-position of 2-octenal, leading to the formation of OOE-dG adduct. These findings demonstrated a new pathway for the formation of 4-oxo-2-alkenals during lipid peroxidation and might provide a mechanism for metal-catalyzed genotoxicity.

  10. Ranking antioxidants based on their effect on human serum lipids peroxidation.

    PubMed

    Pinchuk, Ilya; Shoval, Hila; Bor, Ariela; Schnitzer, Edit; Dotan, Yedidya; Lichtenberg, Dov

    2011-01-01

    Evaluation of the activity of antioxidants is commonly based on measurements of the effect of a specific antioxidant on redox reactions conducted in a solution. Given the difference between reactions that occur in homogeneous solutions and those that occur at lipid-water interfaces, as in biological membranes and lipoproteins, the relevance of the commonly-used assays (such as TEAC and ORAC) to the antioxidative activity in biological systems is questionable. The aim of the present investigation is to develop a more relevant assay. Based on our results, we propose an assay based on prolongation of the lag preceding fast peroxidation of serum lipids. The assay employs our previously developed procedure for determination of susceptibility of serum lipids to peroxidation. The effect of antioxidants is expressed in terms of the relative prolongation of the lag preceding peroxidation. It can be considered reliable because it is only marginally dependent on the specific sera used for the assay. The resultant ranking of antioxidants may be expressed either as the relative prolongation of the lag per 1μM of antioxidant or as the concentration of antioxidant required to double the lag. As expected, the observed ranking order is very different from that reported for TEAC or ORAC assays, undermining the relevance of these assays for oxidation that occurs at interfaces.

  11. Involvement of lipid peroxidation in the degradation of a non-phenolic lignin model compound by manganese peroxidase of the litter-decomposing fungus Stropharia coronilla.

    PubMed

    Kapich, Alexander N; Steffen, Kari T; Hofrichter, Martin; Hatakka, Annele

    2005-05-06

    Culture liquids of the litter-decomposing basidiomycete Stropharia coronilla showed pro-oxidant activity promoting the peroxidation of linoleic acid. This activity depended on the presence of manganese peroxidase (MnP) in the fungal culture. Pro-oxidant activity maxima coincided with maximum MnP activities during the separation of extracellular proteins by anion-exchange chromatography. Purified MnP1 showed substantial pro-oxidant activity in the presence of acetate and Mn2+ ions, even without the addition of hydrogen peroxide. A non-phenolic beta-O-4 lignin model compound [LMC; 1-(3,4-dimethoxyphenyl)-2-(2-methoxyphenoxy)-1,3-dihydroxypropane] was partially oxidized in an in vitro reaction system developing MnP-dependent lipid peroxidation. The chelating organic acids malonate and tartrate noticeably inhibited both the peroxidation of linoleic acid and the conversion of LMC in the system. The major product of the LMC oxidation was 1-(3,4-dimethoxyphenyl)-1-oxo-2-(2-methoxyphenoxy)-3-hydroxypropane; in addition, small amounts of 3,4-dimethoxybenzaldehyde (veratraldehyde) and 3,4-dimethoxybenzoic (veratric) acid were detected. Thus, MnP-initiated lipid peroxidation may be involved in the degradation of recalcitrant non-phenolic lignin substructures by litter-decomposing fungi similar to MnPs of wood-decaying fungi.

  12. Advanced oxidation protein products are more related to metabolic syndrome components than biomarkers of lipid peroxidation.

    PubMed

    Venturini, Danielle; Simão, Andréa Name Colado; Dichi, Isaias

    2015-09-01

    Although advanced oxidation protein products (AOPPs) have been reported as the most appropriate parameter for determination of oxidative stress in patients with metabolic syndrome (MetS), a direct comparison between protein and lipid peroxidation has not been performed yet. The aim of this study was to compare protein peroxidation with lipid peroxidation measured by 2 different methodologies (tert-butyl hydroperoxide-initiated chemiluminescence and ferrous oxidation-xylenol orange assay). The hypothesis of this study was that AOPPs would be more related to MetS than to oxidative markers of lipid peroxidation. This cross-sectional study evaluated 76 patients with MetS and 20 healthy subjects. Prooxidant-antioxidant index (PAI) assessed as AOPP/total radical-trapping antioxidant parameter ratio progressively increased (P < .05) according to the number of MetS components, whereas AOPPs and total radical-trapping antioxidant parameter increased (P < .05) when 5 components were compared with 3 components. Spearman test showed a positive correlation between AOPPs and waist circumference (r = 0.318, P < .01), fasting glucose (r = 0.250, P < .05), homeostasis model assessment insulin resistance (r = 0.043, P < .01), triacylglycerol (r = 0.713, P < .0001), highly sensitive C-reactive protein (r = 0.275, P < .05), and uric acid (r = 0.356, P < .01), whereas there was an inverse correlation with high-density lipoprotein cholesterol (r = -0.399, P < .001). Prooxidant-antioxidant index demonstrated a positive correlation with waist circumference (r = 0.386, P < .01), fasting glucose (r = 0.388, P < .01), fasting insulin (r = 0.344, P < .05), homeostasis model assessment insulin resistance (r = 0.519, P < .001), triacylglycerol (r = 0.687, P < .0001), highly sensitive C-reactive protein (r = 0.278, P < .05), and uric acid (r = 0.557, P < .0001), whereas there was an inverse correlation with high-density lipoprotein cholesterol (r = -0.480, P < .0001). In conclusion, protein

  13. Shengmai San reduces hepatic lipids and lipid peroxidation in rats fed on a high-cholesterol diet.

    PubMed

    Yao, Hsien-Tsung; Chang, Yi-Wei; Chen, Chiung-Tong; Chiang, Meng-Tsan; Chang, Ling; Yeh, Teng-Kuang

    2008-02-28

    Shengmai San (SMS), which is comprised of the medicinal herbs of Panax ginseng C.A. Meyer, Schisandra chinensis Baill., and Ophiopogon japonicus Ker-Gawl (2:1:2)., is a traditional Chinese medicine being used for treating coronary heart disease. The aim of this study was to investigate the effects of SMS on the plasma and liver lipids, lipid peroxidation and antioxidant systems in liver and heart of cholesterol-fed rats. Rats were fed on a high-cholesterol (0.5%) diet (control group), high-cholesterol diet containing 2% SMS (2% SMS group) and 4% SMS (4% SMS group) for four weeks. The oxidative stress marker (thiobarbituric acid reactive substances, TBARS) and antioxidant defense systems including glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in rat liver and heart were evaluated. Results showed that rats fed with SMS-containing diet had reduced the H(2)O(2)-induced erythrocytes susceptibility to hemolysis, and 4% SMS feeding rats had higher plasma GSH concentration compared to the animals fed with the control diet. However, SMS had no effect on plasma lipids (total cholesterol, triglyceride and high-density lipoprotein cholesterol) and TBARS concentration. On the other hand, rats fed with the 4% SMS diet reduced the hepatic cholesterol and triglyceride contents. Fecal bile acid excretion was significantly increased in rats fed with the SMS-containing diet. Higher hepatic GSH and lower TBARS concentrations were observed in rats fed with the 4% SMS diet compared with the rats fed with the control diet. No significant difference in activities of GSH-Px, GST and SOD was found in liver and heart after the SMS treatment. Results from this study indicate that the SMS may reduce hepatic lipids and lipid peroxidation in rats.

  14. Effects of D-003, a mixture of very long chain saturated fatty acids, and policosanol on in vivo lipid peroxidation in rats.

    PubMed

    Pérez, Yohani; Más, Rosa; González, Rosa María; Jiménez, Sonia; Molina, Vivian

    2008-01-01

    D-003 and policosanol (CAS 557-61-9), specific and distinct mixtures of high molecular weight primary aliphatic acids and alcohols, respectively, have shown to inhibit lipid peroxidation in vivo, but comparative studies between their effects on lipid peroxidation processes had not been conducted before. To compare the effects of D-003 and policosanol on markers of lipid peroxidation in vivo in rats. Male Wistar rats were distributed into 9 groups: a control group treated with acacia gum/water vehicle, 4 with policosanol and 4 with D-003, both treatments at 5, 25, 100 and 250 mg/kg. Treatments were administered during 4 weeks. Both treatments significantly and dose-dependently reduced plasma malondyaldehide (MDA) and total peroxides. Nevertheless, while D-003 was effective from 5 mg/kg, the lowest effective dose of policosanol was 25 mg/kg. The maximal effects of both treatments were obtained with 100 mg/kg, but greater in D-003 than in policosanol group, and the same occurred across all doses tested. MDA concentrations generated with the enzymatic system in liver homogenates were also significantly and dose-dependently inhibited with both treatments. The lowest effective doses of D-003 and policosanol were 5 and 100 mg/kg, respectively, and the highest inhibitions of about 80% (D-003) and 11% (policosanol). D-003 was more effective than policosanol in all comparisons. D-003 was also more effective than policosanol for lowering MDA concentrations generated with the no enzymatic system, but in these conditions policosanol was effective from 25 mg/kg and produced an inhibition somewhat greater (about 29%) than on MDA-generated by the enzymatic system. Both policosanol and D-003 did not modify the activity of endogenous antioxidant enzymes compared with the controls. D-003 (5-250 mg/kg) orally administered for 4 weeks was more effective than policosanol for lowering all the lipid peroxidation markers assessed, like plasma MDA and total peroxides, and MDA concentrations

  15. Production of lipid peroxidation products in osteoarthritic tissues: new evidence linking 4-hydroxynonenal to cartilage degradation.

    PubMed

    Morquette, Barbara; Shi, Qin; Lavigne, Patrick; Ranger, Pierre; Fernandes, Julio C; Benderdour, Mohamed

    2006-01-01

    The lipid peroxidation product 4-hydroxynonenal (HNE) is prominently produced in osteoarthritic (OA) synovial cells, but its specific contribution to cartilage destruction is not understood. This study was designed to test whether HNE signaling and binding are involved in OA cartilage degradation through type II collagen (CII) and matrix metalloproteinase 13 (MMP-13) modulation. HNE levels in synovial fluid and in isolated OA chondrocytes treated with free radical donors were determined by enzyme-linked immunosorbent assay. The formation of the HNE/CII adducts was measured in cartilage explants by immunoprecipitation. Levels of CII and MMP-13 messenger RNA and protein were determined by reverse transcription-polymerase chain reaction, Western blotting, and by the use of commercial kits. Levels of HNE/protein adducts were higher in OA synovial fluid compared with normal synovial fluid and were higher in OA chondrocytes treated with free radical donors compared with untreated cells. In cartilage explants, HNE induced CII cleavage, as established by the generation of neoepitopes. The level of HNE/CII adducts was increased in OA cartilage explants incubated with free radical donors. Modification of CII by HNE accelerated its degradation by active MMP-13. In isolated OA chondrocytes, HNE inhibited the expression of CII and tissue inhibitor of metalloproteinases 1 and induced MMP-13 mainly through activation of p38 MAPK. In vitro, HNE binding to MMP-13 activated this enzyme at a molar ratio of 1:100 (MMP-13 to HNE). The increased level of HNE in OA cartilage and the ability of HNE to induce transcriptional and posttranslational modifications of CII and MMP-13 suggest that this aldehyde could play a role in OA.

  16. Silymarin alleviates bleomycin-induced pulmonary toxicity and lipid peroxidation in mice.

    PubMed

    Razavi-Azarkhiavi, Kamal; Ali-Omrani, Mehdi; Solgi, Reza; Bagheri, Pezhman; Haji-Noormohammadi, Mehdi; Amani, Nahid; Sepand, Mohammad-Reza

    2014-10-01

    The application of bleomycin is limited due to its side effects including lung toxicity. Silymarin is a flavonoid complex isolated from milk thistle [Silybum marianum L. (Asteraceae)] which has been identified as an antioxidant and anti-inflammatory compound. This study evaluates the effect of silymarin on oxidative and inflammatory parameters in the lungs of mice exposed to bleomycin. BALB/c mice were divided into four groups of control, bleomycin (1.5 U/kg), bleomycin plus silymarin (50 and 100 mg/kg). After bleomycin administration, mice received 10 d intraperitoneal silymarin treatment. On 10th day, blood and lung samples were collected for measurement of oxidative and inflammatory factors. Silymarin led to a decrease in lung lipid peroxidation (0.19 and 0.17 nmol/mg protein) in bleomycin-injected animals. Glutathione-S-transferase (GST) which was inhibited by bleomycin (32.4 nmol/min/mg protein) induced by higher dose of silymarin (41 nmol/min/mg protein). Silymarin caused an elevation in glutathione (GSH): 2.6 and 3.1 µmol/g lung compare with bleomycin-injected animals 1.8 µmol/g lung. Catalase (CAT) was increased due to high dose of silymarin (65.7 µmol/min/ml protein) compare with bleomycin treated-mice. Myeloperoxidase (MPO) which was induced due to bleomycin (p < 0.05) reduced again by high dose of silymarin (0.51 U/min/mg protein). Bleomycin led to an increase in TNF-α and interleukin-6 (IL-6) (7.9 and 11.8 pg/ml). These parameters were reduced by silymarin (p < 0.05). Silymarin attenuated bleomycin induced-pulmonary toxicity. This protective effect may be due to the ability of silymarin in keeping oxidant-antioxidant balance and regulating of inflammatory mediator release.

  17. Modulation of keratinocyte expression of antioxidants by 4-hydroxynonenal, a lipid peroxidation end product.

    PubMed

    Zheng, Ruijin; Heck, Diane E; Mishin, Vladimir; Black, Adrienne T; Shakarjian, Michael P; Kong, Ah-Ng Tony; Laskin, Debra L; Laskin, Jeffrey D

    2014-03-01

    4-Hydroxynonenal (4-HNE) is a lipid peroxidation end product generated in response to oxidative stress in the skin. Keratinocytes contain an array of antioxidant enzymes which protect against oxidative stress. In these studies, we characterized 4-HNE-induced changes in antioxidant expression in mouse keratinocytes. Treatment of primary mouse keratinocytes and PAM 212 keratinocytes with 4-HNE increased mRNA expression for heme oxygenase-1 (HO-1), catalase, NADPH:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) A1-2, GSTA3 and GSTA4. In both cell types, HO-1 was the most sensitive, increasing 86-98 fold within 6h. Further characterization of the effects of 4-HNE on HO-1 demonstrated concentration- and time-dependent increases in mRNA and protein expression which were maximum after 6h with 30 μM. 4-HNE stimulated keratinocyte Erk1/2, JNK and p38 MAP kinases, as well as PI3 kinase. Inhibition of these enzymes suppressed 4-HNE-induced HO-1 mRNA and protein expression. 4-HNE also activated Nrf2 by inducing its translocation to the nucleus. 4-HNE was markedly less effective in inducing HO-1 mRNA and protein in keratinocytes from Nrf2-/- mice, when compared to wild type mice, indicating that Nrf2 also regulates 4-HNE-induced signaling. Western blot analysis of caveolar membrane fractions isolated by sucrose density centrifugation demonstrated that 4-HNE-induced HO-1 is localized in keratinocyte caveolae. Treatment of the cells with methyl-β-cyclodextrin, which disrupts caveolar structure, suppressed 4-HNE-induced HO-1. These findings indicate that 4-HNE modulates expression of antioxidant enzymes in keratinocytes, and that this can occur by different mechanisms. Changes in expression of keratinocyte antioxidants may be important in protecting the skin from oxidative stress. Copyright © 2014 Elsevier Inc. All rights reserved.

  18. [Effect of cordyceps polysaccharide on lipid peroxidation of rats with dimethylnitrosamine-induced liver fibrosis].

    PubMed

    Peng, Jing-Hua; Li, Xue-Mei; Hu, Yi-Yang; Feng, Qin

    2013-02-01

    polysaccharide can significantly inhibit DMN-induced liver fibrosis and lipid peroxidation in rats.

  19. Alterations of metabolic activity in human osteoarthritic osteoblasts by lipid peroxidation end product 4-hydroxynonenal

    PubMed Central

    Shi, Qin; Vaillancourt, France; Côté, Véronique; Fahmi, Hassan; Lavigne, Patrick; Afif, Hassan; Di Battista, John A; Fernandes, Julio C; Benderdour, Mohamed

    2006-01-01

    4-Hydroxynonenal (HNE), a lipid peroxidation end product, is produced abundantly in osteoarthritic (OA) articular tissues, but its role in bone metabolism is ill-defined. In this study, we tested the hypothesis that alterations in OA osteoblast metabolism are attributed, in part, to increased levels of HNE. Our data showed that HNE/protein adduct levels were higher in OA osteoblasts compared to normal and when OA osteoblasts were treated with H2O2. Investigating osteoblast markers, we found that HNE increased osteocalcin and type I collagen synthesis but inhibited alkaline phosphatase activity. We next examined the effects of HNE on the signaling pathways controlling cyclooxygenase-2 (COX-2) and interleukin-6 (IL-6) expression in view of their putative role in OA pathophysiology. HNE dose-dependently decreased basal and tumour necrosis factor-α (TNF-α)-induced IL-6 expression while inducing COX-2 expression and prostaglandin E2 (PGE2) release. In a similar pattern, HNE induces changes in osteoblast markers as well as PGE2 and IL-6 release in normal osteoblasts. Upon examination of signaling pathways involved in PGE2 and IL-6 production, we found that HNE-induced PGE2 release was abrogated by SB202190, a p38 mitogen-activated protein kinase (MAPK) inhibitor. Overexpression of p38 MAPK enhanced HNE-induced PGE2 release. In this connection, HNE markedly increased the phosphorylation of p38 MAPK, JNK2, and transcription factors (CREB-1, ATF-2) with a concomitant increase in the DNA-binding activity of CRE/ATF. Transfection experiments with a human COX-2 promoter construct revealed that the CRE element (-58/-53 bp) was essential for HNE-induced COX-2 promoter activity. However, HNE inhibited the phosphorylation of IκBα and subsequently the DNA-binding activity of nuclear factor-κB. Overexpression of IKKα increased TNF-α-induced IL-6 production. This induction was inhibited when TNF-α was combined with HNE. These findings suggest that HNE may exert multiple

  20. UVA Photoirradiation of Nitro-Polycyclic Aromatic Hydrocarbons—Induction of Reactive Oxygen Species and Formation of Lipid Peroxides

    PubMed Central

    Xia, Qingsu; Yin, Jun J.; Zhao, Yuewei; Wu, Yuh-Sen; Wang, Yu-Qui; Ma, Liang; Chen, Shoujun; Sun, Xin; Fu, Peter P.; Yu, Hongtao

    2013-01-01

    Nitro-polycyclic aromatic hydrocarbons (nitro-PAHs) are a class of genotoxic environmental contaminants. We have long been interested in determining the mechanisms by which nitro-PAHs induce genotoxicity. Although the metabolic activation of nitro-PAHs leading to toxicological activities has been well studied, the photo-induced activation of nitro-PAHs has seldom been reported. In this paper, we report photo-induced lipid peroxidation by 19 nitro-PAHs. The results indicated that all but two of the nitro-PAHs can induce lipid peroxidation. Mechanistic studies suggest that lipid peroxidation by nitro-PAHs is mediated by free radicals generated in the reaction. There was no structural correlation between the nitro-PAHs and their ability to induce lipid peroxidation upon UVA irradiation, or between the HOMO-LUMO gap and the ability to cause lipid peroxidation. Most of the nitro-PAHs are less potent in terms of causing lipid peroxidation than their parent PAHs. The lack of correlation is attributed to the complex photophysics and photochemistry of the nitro-PAHs and the yield of reactive oxygen species (ROS) and other factors. PMID:23493032

  1. Lipid peroxidation and antioxidative protection mechanism in rat lungs upon acute and chronic exposure to nitrogen dioxide.

    PubMed Central

    Sagai, M; Ichinose, T

    1987-01-01

    This work was done to clarify the relation between the changes of lipid peroxidation and the activities of antioxidative protective enzymes in lungs of rats exposed acutely, subacutely, and chronically to nitrogen dioxide. It was confirmed that the activities of the antioxidative enzymes to protect cells from oxidative stress increased in an early phase, and then the activities decreased gradually. Lipid peroxides increased once in an early phase and then returned to the control level; thereafter, lipid peroxides increased gradually again. Lipid peroxidation as measured by ethane exhalation increased significantly with 0.04, 0.4, and 4 ppm nitrogen dioxide exposure for 9, 18, and 27 months, and a dose-response relationship was clearly observed. The temporal changes of lipid peroxidation varied inversely with that of the activities of antioxidative protective enzymes. From these results, it was suggested that the increments of antioxidative protective enzyme activities in an early phase were complementary effects to protect cells from damage by lipid peroxides which were increased by nitrogen dioxide exposure, and that the complementary effects are lost in later phases of life-span exposure. Finally, loss of such protective complementary effects might relate to some chronic diseases in lungs. Therefore, the temporal changes described above are important characteristics in chronic exposure of air pollutants. PMID:3665862

  2. UVA photoirradiation of nitro-polycyclic aromatic hydrocarbons-induction of reactive oxygen species and formation of lipid peroxides.

    PubMed

    Xia, Qingsu; Yin, Jun-Jie; Zhao, Yuewei; Wu, Yuh-Sen; Wang, Yu-Qui; Ma, Liang; Chen, Shoujun; Sun, Xin; Fu, Peter P; Yu, Hongtao

    2013-03-14

    Nitro-polycyclic aromatic hydrocarbons (nitro-PAHs) are a class of genotoxic environmental contaminants. We have long been interested in determining the mechanisms by which nitro-PAHs induce genotoxicity. Although the metabolic activation of nitro-PAHs leading to toxicological activities has been well studied, the photo-induced activation of nitro-PAHs has seldom been reported. In this paper, we report photo-induced lipid peroxidation by 19 nitro-PAHs. The results indicated that all but two of the nitro-PAHs can induce lipid peroxidation. Mechanistic studies suggest that lipid peroxidation by nitro-PAHs is mediated by free radicals generated in the reaction. There was no structural correlation between the nitro-PAHs and their ability to induce lipid peroxidation upon UVA irradiation, or between the HOMO-LUMO gap and the ability to cause lipid peroxidation. Most of the nitro-PAHs are less potent in terms of causing lipid peroxidation than their parent PAHs. The lack of correlation is attributed to the complex photophysics and photochemistry of the nitro-PAHs and the yield of reactive oxygen species (ROS) and other factors.

  3. Application of FTIR-ATR Spectroscopy to Determine the Extent of Lipid Peroxidation in Plasma during Haemodialysis

    PubMed Central

    Oleszko, Adam; Olsztyńska-Janus, Sylwia; Grzeszczuk-Kuć, Karolina; Bujok, Jolanta; Gałecka, Katarzyna; Czerski, Albert; Witkiewicz, Wojciech; Komorowska, Małgorzata

    2015-01-01

    During a haemodialysis (HD), because of the contact of blood with the surface of the dialyser, the immune system becomes activated and reactive oxygen species (ROS) are released into plasma. Particularly exposed to the ROS are lipids and proteins contained in plasma, which undergo peroxidation. The main breakdown product of oxidized lipids is the malondialdehyde (MDA). A common method for measuring the concentration of MDA is a thiobarbituric acid reactive substances (TBARS) method. Despite the formation of MDA in plasma during HD, its concentration decreases because it is removed from the blood in the dialyser. Therefore, this research proposes the Fourier Transform Infrared Attenuated Total Reflectance (FTIR-ATR) spectroscopy, which enables determination of primary peroxidation products. We examined the influence of the amount of hydrogen peroxide added to lipid suspension that was earlier extracted from plasma specimen on lipid peroxidation with use of TBARS and FTIR-ATR methods. Linear correlation between these methods was shown. The proposed method was effective during the evaluation of changes in the extent of lipid peroxidation in plasma during a haemodialysis in sheep. A measurement using the FTIR-ATR showed an increase in plasma lipid peroxidation after 15 and 240 minutes of treatment, while the TBARS concentration was respectively lower. PMID:25961007

  4. Effect of dietary docosahexaenoic acid connecting phospholipids on the lipid peroxidation of the brain in mice.

    PubMed

    Hiratsuka, Seiichi; Ishihara, Kenji; Kitagawa, Tomoko; Wada, Shun; Yokogoshi, Hidehiko

    2008-12-01

    The effect of dietary docosahexaenoic acid (DHA, C22:6n-3) with two lipid types on lipid peroxidation of the brain was investigated in streptozotocin (STZ)-induced diabetic mice. Each group of female Balb/c mice was fed a diet containing DHA-connecting phospholipids (DHA-PL) or DHA-connecting triacylglycerols (DHA-TG) for 5 wk. Safflower oil was fed as the control. The lipid peroxide level of the brain was significantly lower in the mice fed the DHA-PL diet when compared to those fed the DHA-TG and safflower oil diets, while the alpha-tocopherol level was significantly higher in the mice fed the DHA-PL diet than in those fed the DHA-TG and safflower oil diets. The DHA level of phosphatidylethanolamine in the brain was significantly higher in the mice fed the DHA-PL diet than in those fed the safflower oil diet. The dimethylacetal levels were significantly higher in the mice fed the DHA-PL diet than in those fed the safflower oil and DHA-TG diets. These results suggest that the dietary DHA-connecting phospholipids have an antioxidant activity on the brain lipids in mice, and the effect may be related to the brain plasmalogen.

  5. 6-mo aerobic exercise intervention enhances the lipid peroxide transport function of HDL.

    PubMed

    Tiainen, Sanna; Luoto, Riitta; Ahotupa, Markku; Raitanen, Jani; Vasankari, Tommi

    2016-01-01

    During acute exercise, the concentration of oxidized high-density lipoprotein (HDL) lipids (ox-HDL) is reported to increase suggesting that HDL may function in decreasing the concentration of oxidized low-density lipoprotein (LDL) lipids. However, the effect of exercise intervention on the lipid peroxide transport function of HDL is unknown. A randomized controlled trial with sedentary women (N = 161), aged 43-63, with no current use of hormone therapy, were randomized into a 6-month (mo) exercise group and a control group. During the 6-mo intervention, the concentration of ox-HDL increased in the exercise group by 5% and decreased in the control group by 2% (p = .003). Also, the ratio of ox-HDL to HDL-cholesterol increased by 5% in the exercise group and decreased by 1.5% in the control group (p = .036). The concentrations of cholesteryl ester transfer protein (CETP) and adiponectin did not change during the intervention. The concentration of serum triglycerides trended to decrease by 6% in the intervention group (p = .051). We found that the concentration of ox-HDL increased during the 6-mo aerobic exercise intervention, but the increase was not related to changes in the levels of CETP or adiponectin. These results, together with earlier studies, suggest that HDL has an active role in the reverse transport of lipid peroxides.

  6. [Intensity of lipid peroxidation and protein oxidative modification of goat and cow milk].

    PubMed

    Vysokogorskiĭ, V E; Gavrilova, N B; Arkhipenko, Iu A

    2014-01-01

    Indices of free-radical peroxidation have been estimated: intensity of lipid per- oxidation and protein oxidative modification of goat and cow milk of specific breeds of forest-steppe zone of Omsk region. The obtained results indicate that processes of lipid peroxidation and protein oxidative destruction in goat and cow milk of different breeds occur with different gradation. The content of carbonile derivatives in goat milk of Saan breed 1.4 (0.95; 1.5) u/ml was lower than in cow's milk of black-and-white breed 4.6 (1.1; 6.0) u/ml (p = 0.005) what could be caused by large content of protein thiol groups of this kind of milk and lower quantity of amino acid residues that are available for carbonylation. This kind of milk is characterized by higher SH-group content than cow milk for 31% and Switzerland goat milk for 20% (p = 0.005). The content of cetodiens and attached triens in isopropanol phase of the lipid extract of goat milk of Swiss breed is lower by 30% than in cow milk. In isopropanol phase of the milk lipid extracts contain- ing phospholipids the level of Schiff grounding did not differ. The results obtained prove that goat milk contain less protein subjected to oxidative modification.

  7. [Effect of phensuccinal on lipid metabolism, lipid peroxidation, and antioxidant system activity in rabbits with dithiazone-induced diabetes].

    PubMed

    Gorbenko, N I; Poltorak, V V; Gladkikh, A I; Ivanova, O V

    2003-01-01

    A three-month administration of phensuccinal improved glucose homeostasis, decreased the levels of total cholesterol, triglycerides, fatty acids, and low-density lipoproteins in the blood serum, and reduced the lipid peroxidation rate as compared to the untreated diabetic control. In addition, phensuccinal increased the content of the antiatherogenic high-density lipoprotein fraction and the related paraoxonase enzyme activity. The preventive effect of phensuccinal with respect to diabetic dyslipidemia development, together with the antioxidant action, show this compound to be a promising therapeutic means of preventing and/or reducing macrovascular complications in diabetic patients.

  8. Effects of idebenone (CV-2619) and its metabolites on respiratory activity and lipid peroxidation in brain mitochondria from rats and dogs.

    PubMed

    Sugiyama, Y; Fujita, T; Matsumoto, M; Okamoto, K; Imada, I

    1985-12-01

    The effects of idebenone (CV-2619) and its metabolites on respiratory activity and lipid peroxidation in isolated brain mitochondria from rats and dogs were studied. CV-2619 was easily reduced by canine brain mitochondria in the presence of respiratory substrates. Reduced CV-2619 (2H-CV-2619) was rapidly oxidized through the cytochrome b chain, indicating that the compound functioned simply as an electron carrier of mitochondrial respiratory system. Both nicotinamide adenine dinucleotide (NADH)- and nicotinamide adenine dinucleotide phosphate (NADPH)-dependent lipid peroxidations were examined in canine brain mitochondria in the presence of adenosine diphosphate (ADP) and Fe3+. NADH-cytochrome c reductase activity was sensitive to NADPH-dependent lipid peroxidation. CV-2619 (10(-5)M) strongly inhibited both types of the lipid peroxidation reactions and protected the resultant inactivation of the NADH-cytochrome c reductase activity. Activities of succinate oxidase in rat and canine brain mitochondria were virtually unaffected by CV-2619 and its metabolites (10(-5)-10(-6) M). On the other hand, CV-2619 markedly suppressed the state 3 respiration in glutamate oxidation in a dose dependent manner without any effect on the state 4 respiration and the ADP/O ratio in intact rat brain mitochondria. The inhibitory effect of CV-2619 was also observed in NADH-cytochrome c reductase, but not in NADH-2,6-dichlorophenolindophenol (DCIP) and NADH-ubiquinone reductases in canine brain mitochondria. These facts and results of inhibitor analysis suggest that the action site of CV-2619 is NADH-linked complex I in the mitochondrial respiratory chain and is different from that of inhibitors of oxidative phosphorylation such as rotenone, oligomycin and 2,4-dinitrophenol. Finally, the above findings suggest that CV-2619 acts as an electron carrier in respiratory chains and functions as an antioxidant against membrane damage caused by lipid peroxidation in brain mitochondria. It appears

  9. Electron paramagnetic resonance study of lipid and protein membrane components of erythrocytes oxidized with hydrogen peroxide

    PubMed Central

    Mendanha, S.A.; Anjos, J.L.V.; Silva, A.H.M.; Alonso, A.

    2012-01-01

    Electron paramagnetic resonance (EPR) spectroscopy of spin labels was used to monitor membrane dynamic changes in erythrocytes subjected to oxidative stress with hydrogen peroxide (H2O2). The lipid spin label, 5-doxyl stearic acid, responded to dramatic reductions in membrane fluidity, which was correlated with increases in the protein content of the membrane. Membrane rigidity, associated with the binding of hemoglobin (Hb) to the erythrocyte membrane, was also indicated by a spin-labeled maleimide, 5-MSL, covalently bound to the sulfhydryl groups of membrane proteins. At 2% hematocrit, these alterations in membrane occurred at very low concentrations of H2O2 (50 µM) after only 5 min of incubation at 37°C in azide phosphate buffer, pH 7.4. Lipid peroxidation, suggested by oxidative hemolysis and malondialdehyde formation, started at 300 µM H2O2 (for incubation of 3 h), which is a concentration about six times higher than those detected with the probes. Ascorbic acid and α-tocopherol protected the membrane against lipoperoxidation, but did not prevent the binding of proteins to the erythrocyte membrane. Moreover, the antioxidant (+)-catechin, which also failed to prevent the cross-linking of cytoskeletal proteins with Hb, was very effective in protecting erythrocyte ghosts from lipid peroxidation induced by the Fenton reaction. This study also showed that EPR spectroscopy can be useful to assess the molecular dynamics of red blood cell membranes in both the lipid and protein domains and examine oxidation processes in a system that is so vulnerable to oxidation. PMID:22473321

  10. Nitroxide free radicals protect macular carotenoids against chemical destruction (bleaching) during lipid peroxidation.

    PubMed

    Zareba, M; Widomska, J; Burke, J M; Subczynski, W K

    2016-12-01

    Macular xanthophylls (MXs) lutein and zeaxanthin are dietary carotenoids that are selectively concentrated in the human eye retina, where they are thought to protect against age-related macular degeneration (AMD) by multiple mechanisms, including filtration of phototoxic blue light and quenching of singlet oxygen and triplet states of photosensitizers. These physical protective mechanisms require that MXs be in their intact structure. Here, we investigated the protection of the intact structure of zeaxanthin incorporated into model membranes subjected to oxidative modification by water- and/or membrane-soluble small nitroxide free radicals. Model membranes were formed from saturated, monounsaturated, and polyunsaturated phosphatidylcholines (PCs). Oxidative modification involved autoxidation, iron-mediated, and singlet oxygen-mediated lipid peroxidation. The extent of chemical destruction (bleaching) of zeaxanthin was evaluated from its absorption spectra and compared with the extent of lipid peroxidation evaluated using the thiobarbituric acid assay. Nitroxide free radicals with different polarity (membrane/water partition coefficients) were used. The extent of zeaxanthin bleaching increased with membrane unsaturation and correlated with the rate of PC oxidation. Protection of the intact structure of zeaxanthin by membrane-soluble nitroxides was much stronger than that by water-soluble nitroxides. The combination of zeaxanthin and lipid-soluble nitroxides exerted strong synergistic protection against singlet oxygen-induced lipid peroxidation. The synergistic effect may be explained in terms of protection of the intact zeaxanthin structure by effective scavenging of free radicals by nitroxides, therefore allowing zeaxanthin to quench the primary oxidant, singlet oxygen, effectively by the physical protective mechanism. The redox state of nitroxides was monitored using electron paramagnetic resonance spectroscopy. Both nitroxide free radicals and their reduced form

  11. Aerobic training suppresses exercise-induced lipid peroxidation and inflammation in overweight/obese adolescent girls.

    PubMed

    Youssef, Hala; Groussard, Carole; Lemoine-Morel, Sophie; Pincemail, Joel; Jacob, Christophe; Moussa, Elie; Fazah, Abdallah; Cillard, Josiane; Pineau, Jean-Claude; Delamarche, Arlette

    2015-02-01

    This study aimed to determine whether aerobic training could reduce lipid peroxidation and inflammation at rest and after maximal exhaustive exercise in overweight/obese adolescent girls. Thirty-nine adolescent girls (14-19 years old) were classified as nonobese or overweight/obese and then randomly assigned to either the nontrained or trained group (12-week multivariate aerobic training program). Measurements at the beginning of the experiment and at 3 months consisted of body composition, aerobic fitness (VO2peak) and the following blood assays: pre- and postexercise lipid peroxidation (15F2a-isoprostanes [F2-Isop], lipid hydroperoxide [ROOH], oxidized LDL [ox-LDL]) and inflammation (myeloperoxidase [MPO]) markers. In the overweight/ obese group, the training program significantly increased their fat-free mass (FFM) and decreased their percentage of fat mass (%FM) and hip circumference but did not modify their VO2peak. Conversely, in the nontrained overweight/obese group, weight and %FM increased, and VO2peak decreased, during the same period. Training also prevented exercise-induced lipid peroxidation and/or inflammation in overweight/obese girls (F2-Isop, ROOH, ox-LDL, MPO). In addition, in the trained overweight/obese group, exercise-induced changes in ROOH, ox-LDL and F2-Isop were correlated with improvements in anthropometric parameters (waist-to-hip ratio, %FM and FFM). In conclusion aerobic training increased tolerance to exercise-induced oxidative stress in overweight/obese adolescent girls partly as a result of improved body composition.

  12. Early involvement of lysosome dysfunction in the degeneration of cerebral cortical neurons caused by the lipid peroxidation product 4-hydroxynonenal.

    PubMed

    Zhang, Shi; Eitan, Erez; Mattson, Mark P

    2017-03-01

    Free radical-mediated oxidative damage to proteins, lipids, and DNA occurs in neurons during acute brain injuries and in neurodegenerative disorders. Membrane lipid peroxidation contributes to neuronal dysfunction and death, in part by disrupting neuronal ion homeostasis and cellular bioenergetics. Emerging findings suggest that 4-hydroxynonenal (HNE), an aldehyde produced during lipid peroxidation, impairs the function of various proteins involved in neuronal homeostasis. Here we tested the hypothesis that HNE impairs the cellular system that removes damaged proteins and organelles, the autophagy-lysosome pathway in rat primary cortical neurons. We found that HNE, at a concentration that causes apoptosis over a 48-72 h period, increases protein levels of LC3 II and p62 and within 1 and 4 h of exposure, respectively; LC3 II and p62 immunoreactive puncta were observed in the cytoplasm of HNE-treated neurons at 6 h. The extent of up-regulation of p62 and LC3 II in response to HNE was not affected by co-treatment with the lysosome inhibitor bafilomycin A1, suggesting that the effects of HNE on autophagy were secondary to lysosome inhibition. Indeed, we found that neurons exposed to HNE exhibit elevated pH levels, and decreased protein substrate hydrolysis and cathepsin B activity. Neurons exposed to HNE also exhibited the accumulation of K63-linked polyubiquitinated proteins, which are substrates targeted for lysosomal degradation. Moreover, we found that the levels of LAMP2a and constitutively active heat-shock protein 70, and numbers of LAMP2a-positive lysosomes, are decreased in neurons exposed to HNE. Our findings demonstrate that the lipid peroxidation product HNE causes early impairment of lysosomes which may contribute to the accumulation of damaged and dysfunctional proteins and organelles and consequent neuronal death. Because impaired lysosome function is increasingly recognized as an early event in the neuronal death that occurs in neurodegenerative

  13. Alteration of lipid status and lipid metabolism, induction of oxidative stress and lipid peroxidation by 2,4-dichlorophenoxyacetic herbicide in rat liver.

    PubMed

    Tayeb, Wafa; Nakbi, Amel; Cheraief, Imed; Miled, Abdelhedi; Hammami, Mohamed

    2013-07-01

    This study aims to investigate the effects of the 2,4-dichlorophenoxyacetic herbicide (2,4-D) on plasma lipids, lipoproteins concentrations, hepatic lipid peroxidation, fatty acid composition and antioxidant enzyme activities in rats. Animals were randomly divided into four groups of 10 each: control group and three 2,4-D-treated groups G1, G2 and G3 were administered 15, 75 and 150 mg/kg/BW/d 2,4-D by gavage for 28 d, respectively. Results showed that 2,4-D caused significant negative changes in the biochemical parameters investigated. The malondialdehyde level was significantly increased in 2,4-D-treated groups. Fatty acid composition of the liver was also significantly changed with 2,4-D exposure. Furthermore, the hepatic antioxidant enzyme activities were significantly affected. Finally, 2,4-D at the studied doses modifies lipidic status, disrupt lipid metabolism and induce hepatic oxidative stress. In conclusion, at higher doses, 2,4-D may play an important role in the development of vascular disease via metabolic disorder of lipoproteins, lipid peroxidation and oxidative stress.

  14. Follicular fluid lipid peroxidation levels in women with endometriosis during controlled ovarian hyperstimulation.

    PubMed

    de Lima, Camila Bruna; Cordeiro, Fernanda Bertuccez; Camargo, Mariana; Zylbersztejn, Daniel Suslik; Cedenho, Agnaldo Pereira; Bertolla, Ricardo Pimenta; Lo Turco, Edson Guimarães

    2017-04-01

    This observational study aimed to establishing a relationship between lipid peroxidation and endometriosis in women undergoing controlled ovarian hyperstimulation. A total of 79 women were divided into two groups: (i) controls (tubal or male factor); and (ii) endometriosis (stages III/IV). The endometriosis diagnosis was confirmed by videolaparoscopy and the controlled ovarian stimulation protocol was similar to all patients. Follicular fluid (FF) lipid peroxidation levels were determined through the quantification of malondialdehyde. Statistical analysis was performed using parametric and non-parametric tests, logistic regression was performed to estimate the chance of achieving a pregnancy in each group and a moving average was calculated for the endometriosis group. Peroxidation levels in the endometriosis group were significantly higher when compared to controls. The moving average showed a decrease of MDA levels in the endometriosis group with increasing female age. Moreover, women with endometriosis who were under 33 years of age were 4.3 times more likely to achieve a pregnancy than women above that age. In conclusion, endometriosis is associated with increased FF oxidative stress (OS) in patients undergoing in vitro fertilization (IVF). Also, increasing age is associated with a decrease in severity of the oxidative status, but a decreased chance of pregnancy.

  15. Plasma lipid peroxidation in sporadic Parkinson's disease. Role of the L-dopa.

    PubMed

    Agil, Ahmad; Durán, Raquel; Barrero, Francisco; Morales, Blas; Araúzo, Mariano; Alba, Francisco; Miranda, Ma Teresa; Prieto, Isabel; Ramírez, Manuel; Vives, Francisco

    2006-01-15

    Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease (PD). There are several methods to measure oxidative stress, being lipid peroxidation (LPO) one of the most frequently used. Endogenous plasma LPO was determined by a spectrofluorimetric method in fifty two patients with sporadic PD and in forty controls. To know the maximum capacity of lipids to peroxidate, LPO was also measured after co-incubation with Fe2+/H2O2 (exogenous LPO). All PD patients were taken L-dopa and the effect of this treatment on LPO levels was additionally studied. Urine catecholamines and their main metabolites were also analyzed, and their possible correlation to LPO statistically studied. Endogenous plasma LPO levels were 33% higher in PD group than in control group (P<0.001). Exogenous plasma or oxidizability was also higher in PD patients compared to controls (20%, P<0.05). The intake of L-dopa was negatively dose-related to endogenous and exogenous plasma LPO. In conclusion, plasma of PD patients has elevated levels of LPO and also is more prone to peroxidation than that in the control group. The results also suggest an antioxidant effect of L-dopa.

  16. Fluorescent products in high-density lipoproteins (HDL) and their association with other lipid peroxide products (LPPs)

    NASA Astrophysics Data System (ADS)

    Plavinski, Swiatoslav L.; Kuznetsov, Alexandr S.; Kopilevich, Yurij I.; Svetlykh, Alexander A.; Melnikov, Nikita O.

    1998-01-01

    The lipid peroxidation products of the lipofuscin type can be measured in plasma with the help of fluorimeters. Such products are increasing during whole plasm oxidation in parallel with other indices of lipid peroxidation damage. Preformed fluorescent products are located in all lipoprotein classes. The study of lipofuscin-type pigments fluorescence in HDL showed, that they contain substantial amounts of fluorescent compounds and that it rises in parallel with concentration of other lipid peroxidation products, especially thiobarbituric acid-reacting substances. Neither total plasma cholesterol, nor triglycerides influenced content of fluorescent products in HDL. The HDL subfractions contained different types of the fluorescent products but the bulk of these lipoproteins were almost free of them. The obtained data show that measurement of lipofuscin-type fluorescence in HDL gives a good and sensitive index of these lipoproteins damage by peroxidation.

  17. Lipid Peroxidation by the Manganese Peroxidase of Phanerochaete chrysosporium Is the Basis for Phenanthrene Oxidation by the Intact Fungus

    PubMed Central

    Moen, Mark A.; Hammel, Kenneth E.

    1994-01-01

    The manganese peroxidase (MnP) of Phanerochaete chrysosporium supported Mn(II)-dependent, H2O2-independent lipid peroxidation, as shown by two findings: linolenic acid was peroxidized to give products that reacted with thiobarbituric acid, and linoleic acid was peroxidized to give hexanal. MnP also supported the slow oxidation of phenanthrene to 2,2′-diphenic acid in a reaction that required Mn(II), oxygen, and unsaturated lipids. Phenanthrene oxidation to diphenic acid by intact cultures of P. chrysosporium occurred to the same extent that oxidation in vitro did and was stimulated by Mn. These results support a role for MnP-mediated lipid peroxidation in phenanthrene oxidation by P. chrysosporium. PMID:16349285

  18. [The intensity of lipid peroxidation and enzymatic antioxidative activity in potato leaves under action of drought and polystimulin K].

    PubMed

    Nyzhnyk, T P; Hryhoriuk, I P; Mykhal's'ka, L M

    2004-01-01

    The influence long-term soil drought and potato plants treatment by synthetic analog of cytokinin--polystimulin K on intensity of lipid peroxidation processes and enzymatic antioxidative activity have been investigated. It has been found, that the drought induced the shift of prooxidative-antioxidative balance in respect of lipid peroxidation activation in the potato leaves. It was accompanied by the increase of the ethylene output, membrane permeability, as well as decrease of the lipids content and increase in the enzymatic antioxidative activity (catalase and peroxidase). It is shown, that the intensity of peroxidation processes was higher in budding phases, while enzymatic antioxidative activity was higher in flowering phases in potato plants. Plant exogenous treatment by polystimulin K induced both the decrease in peroxidate oxidation processes, stabilization of catalase and peroxidase activity, as well as the increase in potato resistance to drought.

  19. Sn-protoporphyrin plus photoirradiation induces lipid peroxidation in vivo and in vitro in nonjaundiced Gunn rats.

    PubMed

    Mimura, S; Nagae, H; Keino, H; Watanabe, K; Kashiwamata, S

    1991-01-01

    Lipid peroxidation induced by Sn-protoporphyrin (SnPP) plus photoirradiation was investigated in vivo and in vitro using nonjaundiced Gunn rats. Membrane lipids from young adult rat brain were peroxidized by SnPP plus photoirradiation depending on the SnPP concentration and photoirradiance. Similarly, coadministration of SnPP and photoirradiation to suckling rats increased lipid peroxides in the whole blood and was found lethal. The influence of the wavelength distribution of light sources was also examined by using blue-white and green fluorescent lights. The photodynamic effect by green light irradiation whose energy distribution had no overlap with the Soret band of SnPP was about half of that produced by blue-white light with regard to the membrane peroxidation and the lethal effect on neonatal rats. We therefore conclude that the combination of SnPP and photoirradiation is a potentially hazardous treatment of neonatal jaundice.

  20. Polyhexanide and hydrogen peroxide inhibit proteoglycan synthesis of human chondrocytes.

    PubMed

    Röhner, Eric; Hoff, Paula; Winkler, Tobias; von Roth, Philipp; Seeger, Jörn Bengt; Perka, Carsten; Matziolis, Georg

    2011-03-01

    The use of local antiseptics is a common method in septic joint surgery. We tested polyhexanide and hydrogen peroxide, two of the most frequently used antiseptics with high efficacy and low toxicity. The purpose of this study was to evaluate the effects of both antiseptics on the extracellular cartilaginous matrix synthesis of human chondrocytes. Chondrocytes were isolated from donated human knee joints, embedded in alginate beads, and incubated for 10 and 30 minutes with polyhexanide (0.04%), hydrogen peroxide (3%), or phosphate-buffered saline (PBS) for control. Cartilaginous matrix production was quantified through light microscopic analysis of Alcian blue staining. Cell number and morphology were detected by histological analysis. Chondrocytes showed a decreased intensity of blue colouring after antiseptic treatment versus PBS. In contrast to that, neither the cell number per view field nor the cell morphology differed between the groups. Polyhexanide has more toxic potential than hydrogen peroxide. Based on the fact that the cell number and morphology was not altered by the substances at the examined concentrations, the lower intensity of Alcian blue staining of treated chondrocytes indicates a decreased cartilage-specific matrix synthesis by polyhexanide more than by hydrogen peroxide and control.

  1. Antioxidant enzyme expression, lipid peroxidation, and protein oxidation in human myometrium with parturition.

    PubMed

    Khan, Raheela N; Matharoo-Ball, B; Shaw, R W

    2010-01-01

    Oxygen levels fluctuate considerably during human labor leading to hypoxia and reoxygenation of the uteroplacental unit and in some cases may compromise the progression of labor. Our aim was to assess the possible contribution of oxidative stress to the onset of labor. Thiobarbituric acid was used as a marker of lipid peroxidation along with Western blotting using anti-dinitrophenylhydrazine (DNPH) to assess protein carbonylation in myometrial samples obtained before and after the onset of term and preterm labor. Levels of key antioxidative enzymes were also compared. Higher levels of lipid peroxidation were observed in myometrial samples obtained during term or preterm labor. Reduced levels of glutathione peroxidase (GSHPx) were also encountered in these 2 groups. Conversely, protein carbonyl content was higher in laboring term and preterm myometrial samples. Levels of catalase (CAT) and superoxide dismutase (SOD) were unaltered across all 4 groups. Lipids in the laboring myometrium are susceptible to oxidative injury possibly due to diminished protection as a result of lower GSHPx activity. The reason for enhanced protein carbonylation suggests differential mechanisms governing protein turnover in the pregnant compared with the parturient uterus. Localized, oxidant damage of human myometrium may be a causal factor in difficult deliveries.

  2. The mechanism of cumene hydroperoxide-dependent lipid peroxidation: the function of cytochrome P-450.

    PubMed

    Weiss, R H; Estabrook, R W

    1986-11-15

    The addition of limiting amounts of cumene hydroperoxide to rat liver microsomes resulted in the rapid uptake of molecular oxygen, the formation of thiobarbituric acid reactive products, and the loss of hydroperoxide. The stoichiometry of lipid peroxidation and the yields of 2-phenyl-2-propanol (a major product of the reaction) and acetophenone (a minor product) observed with liver microsomes prepared from untreated rats is greater than that seen with liver microsomes from ciprofibrate-treated rats which, in turn, is greater than that observed with liver microsomes from phenobarbital-treated rats. The Km's and Vmax's of oxygen uptake varied with the type of rat liver microsomes used. Cytochrome P-450 substrates and inhibitors decreased the extents and initial rates of oxygen uptake and thiobarbituric acid reactive product formation. A mechanism is proposed involving the cytochrome P-450-catalyzed homolytic cleavage of the cumene hydroperoxide O-O bond to give the cumyloxyl radical. It is proposed that this oxygen-centered radical abstracts a hydrogen atom from an unsaturated fatty acid associated with a lipid (initiating lipid peroxidation) to give 2-phenyl-2-propanol or that the radical undergoes beta-scission to produce acetophenone and a methyl radical.

  3. Phototoxicity of kava - formation of reactive oxygen species leading to lipid peroxidation and DNA damage.

    PubMed

    Xia, Qingsu; Chiang, Hsiu-Mei; Zhou, Yu-Ting; Yin, Jun-Jie; Liu, Fang; Wang, Cheng; Guo, Lei; Fu, Peter P

    2012-01-01

    Kava is one of the most widely sold herbal dietary supplements in the United States. It has been reported that, besides exhibiting hepatotoxicity, kava also possesses photosensitivity and induces dermopathy in humans. In this study, we determined that UVA irradiation of kava in the presence of a lipid, methyl linoleate, generated lipid peroxidation which was mediated by singlet oxygen generated during photoirradiation. The six major kavalactones(yangonin, 7,8-dihydrokawa in, kawain, 7,8-dihydromethysticin, methysticin, and 5,6-dehydrokawain) were also studied in parallel; only 5,6-dehydrokawain and yangonin-induced a low level of lipid peroxidation. UVA irradiation of kava in human HaCaT skin keratinocytes induced cytotoxicity which was mediated by oxidative stress, led to DNA strand cleavage, and produced 8-hydroxy-2'-deoxyguanosine (8-OHdG) adduct. Study by the electron spin resonance (ESR) method revealed that UVA irradiation of kava produced singlet oxygen and carbon-centered radicals. The overall results suggest that kava is photocytotoxic and photogenotoxic, both mediated by free radicals generated during photoirradiation.

  4. Lipofuscins prepared by modification of photoreceptor cells via glycation or lipid peroxidation show the similar phototoxicity

    PubMed Central

    Dontsov, Alexander; Koromyslova, Anna; Ostrovsky, Mikhail; Sakina, Natalia

    2016-01-01

    AIM To investigate the effect of two ways of lipofuscin production (lipid peroxidation and glycation) on lipofuscin fluorescence characteristics and phototoxicity and to compare them with the properties of natural lipofuscin. METHODS Model lipofuscins were prepared on the basis of bovine photoreceptor outer segments (POS) with bisretinoid A2E addition. One set of samples was prepared from POS modified by lipid peroxidation, while another set from POS modified by glycation with fructose. Fluorescent properties and kinetics of photoinduced superoxide generation of model lipofuscins and human retinal pigment epithelium (RPE) lipofuscin were compared. The fluorescence spectra of samples were measured at 365 nm excitation wavelength and 380-650 emission wavelength. RESULTS The fluorescence spectra of model lipofuscins are almost the same as the spectrum of natural lipofuscin. Visible light irradiation of both model lipofuscins and natural lipofuscin isolated from RPE cells leads to decrease of a fluorescence maximum at 550 nm and to appearance of a distinct, new maximum at 445-460 nm. The rate of photogeneration of reactive oxygen forms by both model lipofuscins was almost the same and approximately two times less than that of RPE lipofuscin granules. CONCLUSION These data suggest that fluorescent characteristics and phototoxicity of lipofuscin granules depend only to an insignificant degree on the oxidative modification of POS proteins and lipids, and generally are defined by the bisretinoid fluorophores contained in them. PMID:27909686

  5. Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.

    PubMed

    Sultana, Rukhsana; Perluigi, Marzia; Allan Butterfield, D

    2013-09-01

    Lipid peroxidation involves a cascade of reactions in which production of free radicals occurs selectively in the lipid components of cellular membranes. Polyunsaturated fatty acids easily undergo lipid peroxidation chain reactions, which, in turn, lead to the formation of highly reactive electrophilic aldehydes. Among these, the most abundant aldehydes are 4-hydroxy-2-nonenal (HNE) and malondialdehyde, while acrolein is the most reactive. Proteins are susceptible to posttranslational modifications caused by aldehydes binding covalently to specific amino acid residues, in a process called Michael adduction, and these types of protein adducts, if not efficiently removed, may be, and generally are, dangerous for cellular homeostasis. In the present review, we focused the discussion on the selective proteins that are identified, by redox proteomics, as selective targets of HNE modification during the progression and pathogenesis of Alzheimer disease (AD). By comparing results obtained at different stages of the AD, it may be possible to identify key biochemical pathways involved and ideally identify therapeutic targets to prevent, delay, or treat AD.

  6. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death.

    PubMed

    Zilka, Omkar; Shah, Ron; Li, Bo; Friedmann Angeli, José Pedro; Griesser, Markus; Conrad, Marcus; Pratt, Derek A

    2017-03-22

    Ferroptosis is a form of regulated necrosis associated with the iron-dependent accumulation of lipid hydroperoxides that may play a key role in the pathogenesis of degenerative diseases in which lipid peroxidation has been implicated. High-throughput screening efforts have identified ferrostatin-1 (Fer-1) and liproxstatin-1 (Lip-1) as potent inhibitors of ferroptosis - an activity that has been ascribed to their ability to slow the accumulation of lipid hydroperoxides. Herein we demonstrate that this activity likely derives from their reactivity as radical-trapping antioxidants (RTAs) rather than their potency as inhibitors of lipoxygenases. Although inhibited autoxidations of styrene revealed that Fer-1 and Lip-1 react roughly 10-fold more slowly with peroxyl radicals than reactions of α-tocopherol (α-TOH), they were significantly more reactive than α-TOH in phosphatidylcholine lipid bilayers - consistent with the greater potency of Fer-1 and Lip-1 relative to α-TOH as inhibitors of ferroptosis. None of Fer-1, Lip-1, and α-TOH inhibited human 15-lipoxygenase-1 (15-LOX-1) overexpressed in HEK-293 cells when assayed at concentrations where they inhibited ferroptosis. These results stand in stark contrast to those obtained with a known 15-LOX-1 inhibitor (PD146176), which was able to inhibit the enzyme at concentrations where it was effective in inhibiting ferroptosis. Given the likelihood that Fer-1 and Lip-1 subvert ferroptosis by inhibiting lipid peroxidation as RTAs, we evaluated the antiferroptotic potential of 1,8-tetrahydronaphthyridinols (hereafter THNs): rationally designed radical-trapping antioxidants of unparalleled reactivity. We show for the first time that the inherent reactivity of the THNs translates to cell culture, where lipophilic THNs were similarly effective to Fer-1 and Lip-1 at subverting ferroptosis induced by either pharmacological or genetic inhibition of the hydroperoxide-detoxifying enzyme Gpx4 in mouse fibroblasts, and glutamate

  7. On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death

    PubMed Central

    2017-01-01

    Ferroptosis is a form of regulated necrosis associated with the iron-dependent accumulation of lipid hydroperoxides that may play a key role in the pathogenesis of degenerative diseases in which lipid peroxidation has been implicated. High-throughput screening efforts have identified ferrostatin-1 (Fer-1) and liproxstatin-1 (Lip-1) as potent inhibitors of ferroptosis − an activity that has been ascribed to their ability to slow the accumulation of lipid hydroperoxides. Herein we demonstrate that this activity likely derives from their reactivity as radical-trapping antioxidants (RTAs) rather than their potency as inhibitors of lipoxygenases. Although inhibited autoxidations of styrene revealed that Fer-1 and Lip-1 react roughly 10-fold more slowly with peroxyl radicals than reactions of α-tocopherol (α-TOH), they were significantly more reactive than α-TOH in phosphatidylcholine lipid bilayers − consistent with the greater potency of Fer-1 and Lip-1 relative to α-TOH as inhibitors of ferroptosis. None of Fer-1, Lip-1, and α-TOH inhibited human 15-lipoxygenase-1 (15-LOX-1) overexpressed in HEK-293 cells when assayed at concentrations where they inhibited ferroptosis. These results stand in stark contrast to those obtained with a known 15-LOX-1 inhibitor (PD146176), which was able to inhibit the enzyme at concentrations where it was effective in inhibiting ferroptosis. Given the likelihood that Fer-1 and Lip-1 subvert ferroptosis by inhibiting lipid peroxidation as RTAs, we evaluated the antiferroptotic potential of 1,8-tetrahydronaphthyridinols (hereafter THNs): rationally designed radical-trapping antioxidants of unparalleled reactivity. We show for the first time that the inherent reactivity of the THNs translates to cell culture, where lipophilic THNs were similarly effective to Fer-1 and Lip-1 at subverting ferroptosis induced by either pharmacological or genetic inhibition of the hydroperoxide-detoxifying enzyme Gpx4 in mouse fibroblasts, and glutamate

  8. Interactions of amiodarone with model membranes and amiodarone-photoinduced peroxidation of lipids.

    PubMed

    Sautereau, A M; Tournaire, C; Suares, M; Tocanne, J F; Paillous, N

    1992-06-23

    The potent antiarrhythmic drug, amiodarone (AMIO) exhibits phototoxicity, which is thought to be related to its interaction with biological membranes. We report here a spectroscopic study of the interactions of this drug with phosphatidylglycerol (PG) and phosphatidylcholine (PC) liposomes used as membrane model systems. A linear increase in absorbance at 300 nm was observed with increasing addition of AMIO to dimyristoyl-DL-PC (DMPC) liposomes over all the drugs-lipid molar ratio (Ri)s tested. In contrast, in the dimyristoyl-DL-PG (DMPG) liposomes, there was a dramatic increase in absorbance at values of Ri above unity. Light scattering by DMPG liposomes at 350 nm increased with increasing AMIO concentration up to a Ri = 1, and then decreased with increasing drug concentration. Such changes were not observed with the DMPC liposomes. Moreover, addition of AMIO changed the fluorescence polarization rate of 1,6-diphenyl 1,3,5-hexatriene embedded in these liposomes. It reduced the rate below the phase transition temperature (Tt) of the lipid, but increased it above this temperature. These effects on the lipidic phases observed at low Ri were more pronounced on the DMPG than on the DMPC liposomes. The strong interactions of AMIO with phospholipids, especially the acidic ones, were confirmed by liposome size determinations. All these data strongly suggest that the drug was incorporated in the core of the lipid bilayers. Such a penetration would favor a drug-photoinduced peroxidation of lipids. Indeed, UV irradiation of AMIO-DOPG mixtures led to the disappearance of the unsaturated fatty acids of phospholipids, checked by gas chromatography measurements, which was correlated with the amount of oxygen consumed. This showed that AMIO did photosensitize phospholipid peroxidation.

  9. Diazepam blocks striatal lipid peroxidation and improves stereotyped activity in a rat model of acute stress.

    PubMed

    Méndez-Cuesta, Luis A; Márquez-Valadez, Berenice; Pérez-De La Cruz, Verónica; Escobar-Briones, Carolina; Galván-Arzate, Sonia; Alvarez-Ruiz, Yarummy; Maldonado, Perla D; Santana, Ricardo A; Santamaría, Abel; Carrillo-Mora, Paul

    2011-11-01

    In this work, the effect of a single dose of diazepam was tested on different markers of oxidative damage in the striatum of rats in an acute model of immobilization (restraint) stress. In addition, the locomotor activity was measured at the end of the restraint period. Immobilization was induced to animals for 24 hr, and then, lipid peroxidation, superoxide dismutase activity and content, and mitochondrial function were all estimated in striatal tissue samples. Corticosterone levels were measured in serum. Diazepam was given to rats as a pre-treatment (1 mg/kg, i.p.) 20 min. before the initiation of stress. Our results indicate that acute stress produced enhanced striatal levels of lipid peroxidation (73% above the control), decreased superoxide dismutase activity (54% below the control), reduced levels of mitochondrial function (35% below the control) and increased corticosterone serum levels (86% above the control). Pre-treatment of stressed rats with diazepam decreased the striatal lipid peroxidation levels (68% below the stress group) and improved mitochondrial function (18% above the stress group), but only mild preservation of superoxide dismutase activity was detected (17% above the stress group). In regard to the motor assessment, only the stereotyped activity was increased in the stress group with respect to control (46% above the control), and this effect was prevented by diazepam administration (30% below the stress group). The preventive actions of diazepam in this acute model of stress suggest that drugs exhibiting anxiolytic and antioxidant properties might be useful for the design of therapies against early acute phases of physic stress.

  10. Perinatal complications, lipid peroxidation, and mental health problems in a large community pediatric sample.

    PubMed

    Mansur, Rodrigo B; Cunha, Graccielle R; Asevedo, Elson; Zugman, André; Rios, Adiel C; Salum, Giovanni A; Pan, Pedro M; Gadelha, Ary; Levandowski, Mateus L; Belangero, Síntia I; Manfro, Gisele G; Stertz, Laura; Kauer-Sant'anna, Márcia; Miguel, Eurípedes C; Bressan, Rodrigo A; Mari, Jair J; Grassi-Oliveira, Rodrigo; Brietzke, Elisa

    2016-10-26

    Replicated evidence indicates that perinatal complications are associated with increased markers of oxidative stress and with mental health problems in children. However, there are fewer reports on the impact of perinatal complications in later phases of development. We aimed to investigate the estimated effects of perinatal complications on levels of lipid peroxidation and on psychopathology in children and adolescents. The study is part of the High Risk Cohort Study for Psychiatric Disorders; the population was composed by 554 students, 6-14 years of age. Serum levels of malondialdehyde, a product of lipid peroxidation, were measured by the TBARS method. A household interview with parents and caregivers was conducted and included inquiries about perinatal history, the Child Behavior Checklist (CBCL), and parent's evaluation, using the Mini International Psychiatric Interview (MINI). We created a cumulative risk index, conceptualized as each individual's cumulative exposure to perinatal complications. Results indicate that perinatal complications were associated with higher levels of TBARS. After adjusting for age, gender, socio-economic status, CBCL total problems score, parental psychopathology, and childhood maltreatment, children exposed to 3 or more perinatal complications had an 26.9% (95% CI 9.9%, 46.6%) increase in TBARS levels, relative to the unexposed group. Exploratory mediation analysis indicated that TBARS levels partially mediated the association between perinatal complications and externalizing problems. In conclusion, an adverse intrauterine and/or early life environment, as proxied by the cumulative exposure to perinatal complications, was independently associated with higher levels of lipid peroxidation in children and adolescents.

  11. Effect of Launaea procumbens on thyroid glands lipid peroxidation and hormonal dysfunction: a randomized control trial.

    PubMed

    Khan, Rahmat Ali

    2017-09-11

    Launaea procumbens (Roxb.) Amin is traditionally used in Pakistan for the treatment of hormonal disorders and oxidative stress. The present study was aimed to evaluate the efficacy of Launaea procumbens methanol extract (LPME) against KBrO3-induced oxidative stress and hormonal dysfunction in thyroid. To examine the effects of LPME against the oxidative stress of KBrO3 in thyroid tissue, 36 male albino rats were used. Protective effects of LPME were observed on thyroid hormonal levels, activities of antioxidant enzymes, lipid peroxidation (TBARS) and DNA damage. Treatment with KBrO3 significantly (P < 0.01) reduced the levels of T3 (55.13 ± 1.93) and T4 (14.7 ± 1.78) and increased TSH (55.13 ± 1.93) levels. KBrO3 exposure in rats reduced the activities of antioxidant enzymes viz.; CAT (1.16 ± 0.08); SOD (12.0 ± 0.08), GST (17.7 ± 1.1) and GSR (54.3 ± 2.1) but increased lipid peroxidation (20.3 ± 0.71) and DNA (30.4 ± 2.0) damage. Co-administration of LPME significantly (P < 0.01) improved these alterations with respect to hormonal levels, activities of antioxidant enzymes and lipid peroxidation close to those seen in control rats. These results suggest that LPME can protect thyroid tissue against oxidative damage, possibly through the antioxidant effects of its bioactive compounds.

  12. Antioxidant systems and lipid peroxidation in Bathymodiolus azoricus from Mid-Atlantic Ridge hydrothermal vent fields.

    PubMed

    Bebianno, M J; Company, R; Serafim, A; Camus, L; Cosson, R P; Fiala-Médoni, A

    2005-11-30

    Enzymatic defenses involved in protection from oxygen radical damage were determined in gills and mantle of Bathymodiolus azoricus collected from three contrasting Mid-Atlantic Ridge (MAR) hydrothermal vent fields (Menez-Gwen, Lucky Strike and Rainbow). The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx) (total and Se-dependent), and levels of total oxyradical scavenging capacity (TOSC), metallothioneins (MT) and lipid peroxidation (LPO) were determined in B. azoricus tissues and the impact of metal concentrations on these antioxidant systems and lipid peroxidation assessed. SOD, CAT, TOSC, MTs and LPO levels were higher in B. azoricus gills while glutathione peroxidases (total and Se-dependent) were higher in the mantle, and with the exception of CAT, were of the same order of magnitude as in other molluscs. TOSC levels from Menez-Gwen indicate that the vent environment at this site is less stressful and the formation of ROS in mussels is effectively counteracted by the antioxidant defense system. TOSC depletion indicates an elevated ROS production in molluscs at the other two vent sites. Cytosolic SOD, GPx and LPO were more relevant at Lucky Strike (Bairro Alto) where levels of essential (Cu and Zn) and toxic metals (Cd and Ag) were highest in the organisms. CAT activity and LPO were predominant at the Rainbow vent site, where an excess of Fe in mussel tissues and in vent fluids (the highest of all three vent sites) may have contributed to increased LPO. Therefore, three distinct pathways for antioxidant enzyme systems and LPO based on environmental metal speciation of MAR vent fields are proposed for Bathymodiolus gills. At Menez-Gwen, TOSC towards peroxyl and hydroxyl radicals and peroxynitrite are predominant, while at Lucky Strike cytosolic SOD activity and GPx are the main antioxidant mechanisms. Finally at Rainbow, catalase and lipid peroxidation are dominant, suggesting that resistance of mussels to metal toxicity at

  13. Zinc supplementation ameliorates electromagnetic field-induced lipid peroxidation in the rat brain.

    PubMed

    Bediz, Cem Seref; Baltaci, Abdulkerim Kasim; Mogulkoc, Rasim; Oztekin, Esma

    2006-02-01

    Extremely low-frequency (0-300 Hz) electromagnetic fields (EMFs) generated by power lines, wiring and home appliances are ubiquitous in our environment. All populations are now exposed to EMF, and exposure to EMF may pose health risks. Some of the adverse health effects of EMF exposure are lipid peroxidation and cell damage in various tissues. This study has investigated the effects of EMF exposure and zinc administration on lipid peroxidation in the rat brain. Twenty-four male Sprague-Dawley rats were randomly allocated to three groups; they were maintained untreated for 6 months (control, n = 8), exposed to low-frequency (50 Hz) EMF for 5 minutes every other day for 6 months (n = 8), or exposed to EMF and received zinc sulfate daily (3 mg/kg/day) intraperitoneally (n = 8). We measured plasma levels of zinc and thiobarbituric acid reactive substances (TBARS), and levels of reduced glutathione (GSH) in erythrocytes. TBARS and GSH levels were also determined in the brain tissues. TBARS levels in the plasma and brain tissues were higher in EMF-exposed rats with or without zinc supplementation, than those in controls (p < 0.001). In addition, TBARS levels were significantly lower in the zinc-supplemented rats than those in the EMF-exposed rats (p < 0.001). GSH levels were significantly decreased in the brain and erythrocytes of the EMF-exposed rats (p < 0.01), and were highest in the zinc-supplemented rats (p < 0.001). Plasma zinc was significantly lower in the EMF-exposed rats than those in controls (p < 0.001), while it was highest in the zinc-supplemented rats (p < 0.001). The present study suggests that long-term exposure to low-frequency EMF increases lipid peroxidation in the brain, which may be ameliorated by zinc supplementation.

  14. Differential effects of antipsychotics on expression of antioxidant enzymes and membrane lipid peroxidation in rat brain.

    PubMed

    Parikh, Vinay; Khan, Mohammad M; Mahadik, Sahebarao P

    2003-01-01

    Typical and atypical antipsychotics significantly differ in their neurotransmitter receptor affinity profiles, and their efficacy and side effects in schizophrenic patients. Typical antipsychotics have been found to increase the oxidative (i.e. free radical-mediated) cellular injury in rats. Since schizophrenia also involves oxidative injury, the understanding of differential effects of these antipsychotics on expression of antioxidant enzymes and oxidative injury may be very critical. The effect of chronic exposure of haloperidol (HAL), a typical antipsychotic, was compared to effects of risperidone (RIS) or clozapine (CLZ) or olanzapine (OLZ), atypical antipsychotics on antioxidant defense enzymes and lipid peroxidation in the rat brain. The levels of antioxidant enzymes and hydroxyalkenals (HAEs) were measured in rat brain cytosol and fatty acids were measured in brain cell membranes. Chronic HAL treatment for both 45 and 90 days significantly decreased manganese-superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD) and catalase (CAT) activity with parallel marked increase in (HAEs), a marker of lipid peroxidation in rat brain. The levels of enzymatic activity very well correlated with the levels of enzyme proteins indicating that the changes were probably in the expression of net protein. However, RIS, CLZ and OLZ treatments did not produce any alterations in the levels of antioxidant enzymes and HAEs, both after 45 and 90 days. There were no alterations in the levels of saturated as well as polyunsaturated fatty acids in brain membranes. These findings indicate that chronic administration of HAL, but none of the studied atypicals induce oxidative stress by persistent changes in the levels of antioxidant enzymes and cause membrane lipid peroxidation.

  15. N,N-diethyldithiocarbamate produces copper accumulation, lipid peroxidation, and myelin injury in rat peripheral nerve.

    PubMed

    Tonkin, Elizabeth G; Valentine, Holly L; Milatovic, Dejan M; Valentine, William M

    2004-09-01

    Previous studies have demonstrated the ability of the dithiocarbamate, disulfiram, to produce a peripheral neuropathy in humans and experimental animals and have also provided evidence that N,N-diethyldithiocarbamate (DEDC) is a proximate toxic species of disulfiram. The ability of DEDC to elevate copper levels in the brain suggests that it may also elevate levels of copper in peripheral nerve, possibly leading to oxidative stress and lipid peroxidation from redox cycling of copper. The study presented here investigates the potential of DEDC to promote copper accumulation and lipid peroxidation in peripheral nerve. Rats were administered either DEDC or deionized water by ip osmotic pumps and fed a normal diet or diet containing elevated copper, and the levels of metals, isoprostanes, and the severity of lesions in peripheral nerve and brain were assessed by ICP-AES/AAS, GC/MS, and light microscopy, respectively. Copper was the only metal that demonstrated any significant compound-related elevations relative to controls, and total copper was increased in both brain and peripheral nerve in animals administered DEDC on both diets. In contrast, lesions and elevated F2-isoprostanes were significantly increased only in peripheral nerve for the rats administered DEDC on both diets. Autometallography staining of peripheral nerve was consistent with increased metal content along the myelin sheath, but in brain, focal densities were observed, and a periportal distribution occurred in liver. These data are consistent with the peripheral nervous system being more sensitive to DEDC-mediated demyelination and demonstrate the ability of DEDC to elevate copper levels in peripheral nerve. Additionally lipid peroxidation appears to either be a contributing event in the development of demyelination, possibly through an increase of redox active copper, or a consequence of the myelin injury.

  16. [Study of the processes of lipid peroxidation in patients with endogenous psychoses using gas chromatography].

    PubMed

    Kovaleva, E S; Orlov, O N; Bogdanova, E D; Beliaev, B S; Tsutsul'kovskaia, M Ia

    1989-01-01

    The processes of lipid peroxidation were studied in healthy subjects and patients with manic-depressive psychosis and schizophrenia using a non-invasive method based on chromatographic determination of endogenic pentane in the expired air. In patients with circular psychosis pentane concentration in the expired air did not differ from the norm, yet with advancing age it decreased (in contrast to an elevation in normal subjects). In schizophrenic patients pentane levels were significantly higher than in age-matched normal subjects. The level of the studied parameter was not correlated with the duration of the disease but showed a definite correlation with the severity of adverse disturbances in schizophrenia.

  17. The potent antioxidant activity of the vitamin K cycle in microsomal lipid peroxidation.

    PubMed

    Vervoort, L M; Ronden, J E; Thijssen, H H

    1997-10-15

    In the vitamin K cycle, vitamin K-hydroquinone, the active cofactor for gamma-glutamylcarboxylase, is continuously regenerated. The successive pathways contain oxidation of the hydroquinone to the epoxide, followed by reduction to the quinone and reduction to the hydroquinone. Vitamin K-hydroquinone is a potent radical scavenging species (Mukai et al., J Biol Chem 267: 22277-22281, 1992). We tested the potential antioxidant activity of the vitamin K cycle in lipid peroxidation reactions (thiobarbituric acid reactive substances, TBARS) in rat liver microsomes. As prooxidant we used Fe2+/ascorbate, NADPH-Fe3+/ATP, and NADPH/CCl4. Vitamin K (< or = 50 microM) on its own did not influence the formation of TBARS. In combination with 1 mM dithiothreitol (DTT), the reductive cofactor for the microsomal enzyme vitamin K epoxide reductase, vitamin K suppressed lipid peroxidation with a concentration that blocked the maximal response by 50% (IC50) of ca. 0.2 microM. Vitamin K1 (phylloquinone) and vitamin K2 (menaquinone-4) were equally active. Warfarin (5 microM) and chloro-vitamin K (50 microM), inhibitors of vitamin K epoxide reductase and gamma-glutamylcarboxylase, respectively, were able to completely abolish the antioxidant effect. Lipid peroxidation was inversely related to the amount of vitamin K hydroquinone in the reaction. Vitamin K epoxide reductase seemed sensitive to lipid peroxidation, with half of the activity being lost within 10 min during oxidation with NADPH/CCl4. The inactivation could be attenuated by antioxidants such as vitamin E, reduced glutathione, and menadione and also by a K vitamin in combination with DTT, but not by superoxide dismutase and catalase. The results show that the vitamin K cycle could act as a potent antioxidant, that the active species in all probability is vitamin K-hydroquinone, and that the primary reaction product is the semiquinone. The results also show that the reaction product is processed in the vitamin K cycle to

  18. Redox-derived damage-associated molecular patterns: Ligand function of lipid peroxidation adducts.

    PubMed

    Uchida, Koji

    2013-02-12

    Endogenous electrophiles, such as α,β-unsaturated aldehydes and ketones generated during lipid peroxidation, exhibit a facile reactivity with proteins, generating a variety of intra and intermolecular covalent adducts. It has been postulated that these host-derived, modified proteins with electrophiles, which constitute the products of diverse classes of oxidative reactions, represent damage-associated molecular patterns (DAMPs). The DAMPs, that occur in vivo, can be a ligand of multiple proteins, which in turn, may lead to the profound innate and adaptive immune responses and mediate homeostatic functions consequent to inflammation and cell death.

  19. Serum copper, zinc and lipid peroxidation in pregnant women with preeclampsia in gorgan.

    PubMed

    Rafeeinia, Arash; Tabandeh, Afsaneh; Khajeniazi, Safoura; Marjani, Abdol J

    2014-01-01

    The aim of study was to assay serum copper, zinc and lipid peroxidation levels in pregnant women with and without preeclampsia. There were significant differences between systolic, diastolic blood pressures and copper, Cu/Zn ratio and malondialdehyde among two groups. There were significant differences in weight, pre-pregnancy body mass index, systolic, diastolic blood pressures and copper, Cu/Zn ratio and malondialdehyde levels when compared to healthy pregnant women with mild and severe preeclampsia patients. A positive correlation was observed between systolic and diastolic blood pressure and copper, malondialdehyde and Cu/Zn ratio. Copper and malondialdehyde may play a role in the pathophysiology of preeclampsia.

  20. Mechanisms involved in the modulation of astroglial resistance to oxidative stress induced by activated microglia: antioxidative systems, peroxide elimination, radical generation, lipid peroxidation.

    PubMed

    Röhl, Claudia; Armbrust, Elisabeth; Herbst, Eva; Jess, Anne; Gülden, Michael; Maser, Edmund; Rimbach, Gerald; Bösch-Saadatmandi, Christine

    2010-05-01

    Microglia and astrocytes are the cellular key players in many neurological disorders associated with oxidative stress and neuroinflammation. Previously, we have shown that microglia activated by lipopolysaccharides (LPS) induce the expression of antioxidative enzymes in astrocytes and render them more resistant to hydrogen peroxide (H2O2). In this study, we examined the mechanisms involved with respect to the cellular action of different peroxides, the ability to detoxify peroxides, and the status of further antioxidative systems. Astrocytes were treated for 3 days with medium conditioned by purified quiescent (microglia-conditioned medium, MCM[-]) or LPS-activated (MCM[+]) microglia. MCM[+] reduced the cytotoxicity of the organic cumene hydroperoxide in addition to that of H2O2. Increased peroxide resistance was not accompanied by an improved ability of astrocytes to remove H2O2 or an increased expression/activity of peroxide eliminating antioxidative enzymes. Neither peroxide-induced radical generation nor lipid peroxidation were selectively affected in MCM[+] treated astrocytes. The glutathione content of peroxide resistant astrocytes, however, was increased and superoxide dismutase and heme oxygenase were found to be upregulated. These changes are likely to contribute to the higher peroxide resistance of MCM[+] treated astrocytes by improving their ability to detoxify reactive oxygen radicals and oxidation products. For C6 astroglioma cells a protective effect of microglia-derived factors could not be observed, underlining the difference of primary cells and cell lines concerning their mechanisms of oxidative stress resistance. Our results indicate the importance of microglial-astroglial cell interactions during neuroinflammatory processes.

  1. Effect of Repeatedly Heated Palm Olein on Blood Pressure—Regulating Enzymes Activity and Lipid Peroxidation in Rats

    PubMed Central

    Xin-Fang, Leong; Jumat, Salimon; Mohd Rais, Mustafa; Kamsiah, Jaarin

    2012-01-01

    Background: Oxidative stress is associated with the pathogenesis of cardiovascular diseases. The process of deep-fat frying in dietary cooking oil plays a role in the generation of free radicals. In this study, palm olein heated to 180 °C was tested for its effect on the activity of blood pressure–regulating enzymes and lipid peroxidation. Methods: Forty-two adult male Sprague-Dawley rats were equally assigned into 6 groups.The first group was fed with normal rat chow as the control group, and the subsequent groups were fed with rat chow fortified with 15% weight/weight of the following: fresh palm olein, palm olein heated once, palm olein heated twice, palm olein heated 5 times, or palm olein heated 10 times. The duration of feeding was 6 months. Fatty acid analyses of oil were performed using gas chromatography. Peroxide values were determined using standard titration. Plasma was collected for biochemical analyses. Results: Repeatedly heated palm olein increased the levels of peroxide, angiotensin-converting enzyme, and lipid peroxidation as well as reduced the level of heme oxygenase. Fresh palm olein and palm olein heated once had lesser effects on lipid peroxidation and a better effect on the activity of blood pressure–regulating enzymes than repeatedly heated palm olein. Conclusion: Repeatedly heated palm olein may negatively affect the activity of blood pressure–regulating enzymes and increase lipid peroxidation. PMID:22977371

  2. Radiosensitization by fullerene-C60 dissolved in squalene on human malignant melanoma through lipid peroxidation and enhanced mitochondrial membrane potential

    NASA Astrophysics Data System (ADS)

    Kato, Shinya; Kimura, Masatsugu; Miwa, Nobuhiko

    2014-04-01

    We examined fullerene-C60 dissolved in squalene (C60/Sqe) for the ability to potentiate the radiosensitization under X-ray irradiation on human malignant melanoma HMV-II cells, which were treated with C60/Sqe and thereafter irradiated with X-ray. The cell proliferation for C60/Sqe was inhibited more markedly than for Sqe alone. Meanwhile, cell proliferation was almost unaltered for C60/squalane (Sqa) or Sqa, a hydrogenated form of Sqe, as compared to no-additive control. Thus radiosensitization of C60/Sqe is attributed to peroxidation of unsaturated bonds of squalene by X-ray-excited C60 in contrast to squalane. The fluorescence images of HMV-II cells stained with Rhodamine123, an indicator for mitochondrial membrane potential, were monitored for 6 h after X-ray irradiation. C60/Sqe obviously exhibited more augmented fluorescence intensity on perinuclear region of HMV-II cells than Sqe alone. TBARS assay showed that the lipid peroxidation level as malondialdehyde-equivalent increased by combination of C60/Sqe and X-ray dose-dependently on X-ray doses. C60/Sqe exhibited lipid peroxidation more markedly by 1.2-fold than Sqe alone. Thus the level of lipid peroxidation of squalene was sufficiently higher in C60/Sqe than in Sqe in the absence of C60 under X-ray irradiation, suggesting the combination of C60/Sqe and X-ray irradiation induced radiosensitization on HMV-II cells by peroxidation of absorbed Sqe in mitochondrial membrane via oxidative stress mediated by fullerene-C60.

  3. The important role of lipid peroxidation processes in aging and age dependent diseases.

    PubMed

    Spiteller, Gerhard

    2007-09-01

    Any change in the cell membrane structure activates lipoxygenases (LOX). LOX transform polyunsaturated fatty acids (PUFAs) to lipidhydroperoxide molecules (LOOHs). When cells are severely wounded, this physiological process switches to a non-enzymatic lipid peroxidation (LPO) process producing LOO* radicals. These oxidize nearly all-biological molecules such as lipids, sugars, and proteins. The LOO* induced degradations proceed by transfer of the radicals from cell to cell like an infection. The chemical reactions induced by LO* and LOO* radicals seem to be responsible for aging and induction of age dependent diseases.Alternatively, LO* and LOO* radicals are generated by frying of fats and involve cholesterol-PUFA esters and thus induce atherogenesis. Plants and algae are exposed to LOO* radicals generating radiation. In order to remove LOO* radicals, plants and algae transform PUFAs to furan fatty acids, which are incorporated after consumption of vegetables into mammalian tissues where they act as excellent scavengers of LOO* and LO* radicals.

  4. Potato peel extract-a natural antioxidant for retarding lipid peroxidation in radiation processed lamb meat.

    PubMed

    Kanatt, Sweetie R; Chander, Ramesh; Radhakrishna, P; Sharma, Arun

    2005-03-09

    The effective utilization of potato peel, a waste generated in large quantities by the food industry, as an antioxidant was investigated. Potato peel extract (PPE) exhibited high phenolic content (70.82 mg of catechin equivalent/100 g), chlorogenic acid (27.56 mg/100 g of sample) being the major component. The yield of total phenolics and chlorogenic acid increased by 26 and 60%, respectively, when the extract was prepared from gamma irradiated (150 Gy) potatoes. PPE showed excellent antioxidant activity as determined by beta-carotene bleaching and radical scavenging activity of 1,1-diphenyl-2-picrylhydrazyl (DPPH). The suitability of PPE for controlling lipid oxidation of radiation processed lamb meat was also investigated. PPE (0.04%) when added to meat before radiation processing was found to retard lipid peroxidation of irradiated meat as measured by TBA number and carbonyl content. The antioxidant activity of PPE was found to be comparable to butylated hydroxytoluene (BHT).

  5. Rapid determination of lipid peroxidation using a novel pyridoxamine-participating ferrous oxidation-sulfosalicylic acid spectrophotometric method.

    PubMed

    Chen, Jingnan; Cai, Danqian; Zhang, Yu

    2016-11-15

    A novel method is developed to rapidly analyze lipid peroxidation in edible oils and fatty foods at room temperature, which is called the pyridoxamine-participating ferrous oxidation-sulfosalicylic acid (PFOS) method. The PFOS method evaluates the lipid peroxide value colorimetrically via detecting the pyridoxamine-mediated pigment produced by 5-sulfosalicylic acid and Fe(3+) at 500nm, while the latter is converted from Fe(2+) in the presence of lipid peroxides. The optimized formulation was ethanol (70%, v/v), Fe(2+) (4mmol/L), 5-sulfosalicylic acid (40mmol/L) and pyridoxamine (18mmol/L). The limit of quantitation is 0.087mmol Fe(3+)/L with acceptable reproducibility. In addition, current method has a significant linear correlation with both conventional thiobarbituric acid (R(2)=0.9999) and ferric thiocyanate assays (R(2)=0.9675). This method offers a rapid technique for evaluating lipid peroxidation without heating and sophisticated instrumental procedures. Besides, current method provides a new option to evaluate the lipid peroxidation state and improve the reproducibility of ferrous-oxidation. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. Artepillin C isoprenomics: design and synthesis of artepillin C isoprene analogues as lipid peroxidation inhibitor having low mitochondrial toxicity.

    PubMed

    Uto, Yoshihiro; Ae, Shutaro; Koyama, Daisuke; Sakakibara, Mitsutoshi; Otomo, Naoki; Otsuki, Mamoru; Nagasawa, Hideko; Kirk, Kenneth L; Hori, Hitoshi

    2006-08-15

    We designed and synthesized isoprene analogues of artepillin C, a major component of Brazilian propolis, and investigated the inhibitory activity on lipid peroxidation of rat liver mitochondria (RLM) and RLM toxicity based on isoprenomics. We succeeded in the synthesis of artepillin C isoprene analogues using regioselective prenylation within the range from 22% to 53% total yield. Reactivity of artepillin C and its isoprene analogues with ABTS (2,2'-Azinobis(3-ethylbenzothiazoline-6-sulfonate)) radical cations showed only a slight difference among the molecules. The isoprene side-chain elongation analogues of artepillin C showed almost the same inhibitory activity against RLM lipid peroxidation as artepillin C. Artepillin C and its isoprene analogues had very weak RLM uncoupling activity. Moreover, artepillin C and its isoprene analogues exhibited a lower inhibitory activity against adenosine 5'-triphosphate (ATP) synthesis by about two orders of magnitude than the effective inhibitory activity against RLM lipid peroxidation. From these results we conclude that artepillin C isoprene analogues could be potent lipid peroxidation inhibitors having low mitochondrial toxicity. We also conclude that elongation of the isoprene side chain of artepillin C to increase lipophilicity had little influence on the inhibitory activity toward RLM lipid peroxidation.

  7. Effects of lycopene on in vitro quality and lipid peroxidation in refrigerated and cryopreserved turkey spermatozoa.

    PubMed

    Rosato, M P; Centoducati, G; Santacroce, M P; Iaffaldano, N

    2012-01-01

    1. The effects of lycopene-enriched extenders on the in vitro quality of turkey semen including lipid peroxidation were examined after chilled and frozen storage. 2. Five pools of semen diluted in extenders containing 0, 0·05 or 0·1 mg/ml of lycopene were stored at 5°C for 48 h or cryopreserved as pellets and the following variables determined in fresh samples and samples stored chilled or frozen: sperm motility, viability, osmotic resistance, DNA integrity and lipid peroxidation (as malonaldehyde production). 3. Semen quality was generally compromised after storage, especially post-freezing. However, in the presence of the highest dose of lycopene, both the viability and osmotic-resistance of chilled spermatozoa and the DNA integrity of frozen spermatozoa were similar to those of fresh spermatozoa. 4. Greater lipid peroxidation was detected in refrigerated compared to fresh or cryopreserved spermatozoa. However, spermatozoa chilled in lycopene-enriched extenders showed significantly lower malonaldehyde levels than those chilled without lycopene, while the addition of lycopene to the freezing medium served to maintain the lipid peroxidation levels observed in fresh semen. 5. In conclusion, the presence of lycopene in the extender improved the survival of turkey spermatozoa after liquid-storage and protected DNA integrity against cryodamage. The beneficial effects of lycopene observed could be related to its capacity to diminish sperm lipid peroxidation during refrigeration or cryopreservation.

  8. Effect of Danofloxacin on Reactive Oxygen Species Production, Lipid Peroxidation and Antioxidant Enzyme Activities in Kidney Tubular Epithelial Cell Line, LLC-PK1.

    PubMed

    Yu, Chun-Hong; Liu, Zhao-Ying; Sun, Lei-Sheng; Li, Yu-Juan; Zhang, Da-Sheng; Pan, Ren-Tao; Sun, Zhi-Liang

    2013-12-01

    The purpose of this study was to investigate the possibility that oxidative stress was involved in danofloxacin-induced toxicity in renal tubular cells epithelial cell line (LLC-PK1). Confluent LLC-PK1 cells were incubated with various concentrations of danofloxacin. The extent of oxidative damage was assessed by measuring the reactive oxygen species (ROS) level, lipid peroxidation, cell apoptosis and antioxidative enzyme activities. Danofloxacin induced a concentration-dependent increase in the ROS production, not even cytotoxic conditions. Similarly, danofloxacin caused an about 4 times increase in the level of thiobarbituric acid reactive substances at the concentration of 400 μM for 24 hr, but it did not induce cytotoxicity and apoptosis. Antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), were increased after treatment with 100, 200 and 400 μM of danofloxacin for 24 hr. The activity of glutathione peroxidase (GPX) was significantly decreased in a concentration-dependent manner. In addition, ROS production, lipid peroxidation and GPX decline were inhibited by additional glutathione and N-acetyl cysteine. These data suggested that danofloxacin could not induce oxidative stress in LLC-PK1 cells at the concentration (≤400 μM) for 24 hr. The increase levels of ROS and lipid peroxidation could be partly abated by the increase activities of SOD and CAT. © 2013 Nordic Pharmacological Society. Published by John Wiley & Sons Ltd.

  9. Evaluation of liver function impairment and lipid peroxidation induced by lantana camara leaf powder administration in adult rat serum and liver.

    PubMed

    Saini, N; Singh, J; Sehgal, R; Ojha, S

    2007-05-30

    Lantana camara is a common weed and certain medicinal properties have been attributed to this plant, but most varieties of this plant are reported to be highly toxic to animals. The plant is a native of America but a few varieties are indigenous to tropical Asia and Africa. The present investigation was done to study the hepatotoxic and lipid peroxidative effects of this noxious weed on female Wistar rats. Eighty four percent (84%) increase was observed in the activity of AST in group B and 120% increase was noted in group C in serum. In, liver tissue this increase was 66% and 258%. In the case of ALT, 165% increase was observed in group B and 219% increase was observed in group C in serum. In, liver there was 46% increase in group B and 216% increase in group C in the ALT activity. Similarly, 30% and 50% increase in group B and 120% and 300% increase in group C in the activity of ALP was observed with respect to control group. The overall protein concentration was increased in serum and decreased in liver tissue. Lipid peroxidation in liver tissue was inhibited by 22% in group B and 55% in group C. Thus Lantana camara is a toxic plant which produces severe hepatotoxicity in rats, but it also prevented lipid peroxidation that may suggest that Lantana camara may be acting as antioxidant but, exactly which of its component is responsible for this activity is not known and needs future investigations.

  10. Effect of barbiturates on hydroxyl radicals, lipid peroxidation, and hypoxic cell death in human NT2-N neurons.

    PubMed

    Almaas, R; Saugstad, O D; Pleasure, D; Rootwelt, T

    2000-03-01

    Barbiturates have been shown to be neuroprotective in several animal models, but the underlying mechanisms are unknown. In this study, the authors investigated the effect of barbiturates on free radical scavenging and attempted to correlate this with their neuroprotective effects in a model of hypoxic cell death in human NT2-N neurons. Hydroxyl radicals were generated by ascorbic acid and iron and were measured by conversion of salicylate to 2,3-dihydroxybenzoic acid. The effect of barbiturates on lipid peroxidation measured as malondialdehyde and 4-hydroxynon-2-enal was also investigated. Hypoxia studies were then performed on human NT2-N neurons. The cells were exposed to 10 h of hypoxia or combined oxygen and glucose deprivation for 3 or 5 h in the presence of thiopental (50-600 microM), methohexital (50-400 microM), phenobarbital (10-400 microM), or pentobarbital (10-400 microM), and cell death was evaluated after 24 h by lactate dehydrogenase release. Pentobarbital, phenobarbital, methohexital, and thiopental dose-dependently inhibited formation of 2,3-dihydroxybenzoic acid and iron-stimulated lipid peroxidation. There were significant but moderate differences in antioxidant action between the barbiturates. While phenobarbital (10-400 microM) and pentobarbital (10-50 microM) increased lactate dehydrogenase release after combined oxygen and glucose deprivation, thiopental and methohexital protected the neurons at all tested concentrations. At a higher concentration (400 microM), pentobarbital also significantly protected the neurons. At both 50 and 400 microM, thiopental and methohexital protected the NT2-N neurons significantly better than phenobarbital and pentobarbital. Barbiturates differ markedly in their neuroprotective effects against combined oxygen and glucose deprivation in human NT2-N neurons. The variation in neuroprotective effects could only partly be explained by differences in antioxidant action.

  11. Antioxidant and lipid peroxidation responses in Mytilus galloprovincialis exposed to mixtures of benzo(a)pyrene and copper.

    PubMed

    Maria, V L; Bebianno, M J

    2011-06-01

    This study aimed to assess the antioxidant system potential and lipid peroxidative effects, in the gill and digestive gland of Mytilus galloprovincialis exposed to individual and binary mixtures of benzo(a)pyrene (BaP) and Cu for 7 days. Data demonstrated that in mussels exposed to BaP antioxidant enzymes (catalase--CAT, total glutathione peroxidase--tGPx, glutathione S-transferase--GST and glutathione reductase--GR) and lipid peroxidation (LPO) increased in the gill. On the contrary, in the digestive gland inhibitory antioxidant effects (superoxide dismutase-SOD, GR, metallothioneins-MT) and no changes in LPO levels were detected. Cu was also a potent oxidant agent since MT and LPO levels increased in mussel gill, despite no LPO effect in the digestive gland. For both single contaminants the organ specificity and distinct physiologic/metabolism roles were evident in terms of antioxidant capacity. Gill SOD inhibition, MT and GST unchanged was a result of "simple independent action" of exposure to BaP and Cu. "Interactions" in the binary mixtures, led to absence of changes in LPO effects. In the digestive gland, BaP and Cu interactions were also responsible for the GST and LPO enhancement (antagonistic effects). The current findings demonstrate the differences in antioxidant responses where the organ dependency highlights each contaminant particular mode of action. Generally, in the gill "non-interactive" effects occurred with the lowest Cu concentration while "interactions" exist for the mixture with the highest Cu concentrations. In the digestive gland, "interactions" and "no interaction" effects occurred in all the binary mixtures. Complex contaminant mixtures interact differently based on target tissue which may lead to an imbalance in the mussels health status.

  12. [Status of the lipid peroxidation system in the tissues of rats following a 7-day flight on the Kosmos-1667 biosatellite].

    PubMed

    Delenian, N V; Markin, A A

    1989-01-01

    Rats flown for 7 days on Cosmos-1667 were for the first time used to measure antioxidative enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase), lipid peroxidation products (diene conjugates, malonic dialdehyde, Schiff bases) and tocopherol. Enhanced lipid peroxidation in the heart was completely compensated by activation of antioxidative enzymes. The content of all lipid peroxidation products measured in the liver increased; this was accompanied by a decrease of glutathione peroxidase and an increase of superoxide dismutase activities. It is suggested that lipid peroxidation was activated in response to altered gravity.

  13. [The effect of middle molecules isolated from the serum of burn patients on the state of lipid peroxidation in animal tissues].

    PubMed

    Tupikova, Z A; Osipovich, V K

    1990-01-01

    Intensity of ascorbate-, NADPH-dependent and spontaneous lipid peroxidation were studied in mice brain and liver tissues after intravenous administration of middle molecular mass peptides, isolated from blood serum of animals with thermic burns. Positive effect of these peptides on lipid peroxidation was detected in tissues of animals with altered rate of lipid peroxidation (strong burns of 10-12% of body surface served as a biological model). The data obtained suggest that individual components of blood serum middle molecular fraction appear to exhibit the regulating effects on lipid peroxidation in animal tissues.

  14. Effect of mild iron overload on liver and kidney lipid peroxidation.

    PubMed

    Galleano, M; Puntarulo, S

    1994-10-01

    1. Hepatotoxicity is the most common finding in patients with iron overload since the liver is the major recipient of iron excess, even though the kidney could be a target of iron toxicity. The effect of iron overload was studied in the early stages after iron-dextran injection in rats, as a model for secondary hemocromatosis. 2. Total hepatic and kidney iron content was markedly elevated over control values 20 h after the iron administration. Plasma GOT, GPT and LDH activities were not affected, suggesting that liver cell permeability was not affected by necrosis. 3. Spontaneous liver chemiluminescence was measured as an indicator of oxidative stress and lipid peroxidation. Light emission was increased four-fold 6 h after iron supplementation. 4. Increases in the generation of thiobarbituric acid reactive substances (TBARS in liver and kidney homogenates were detected after iron administration. 5. The activities of catalase, SOD and glutathione peroxidase were determined. Enzymatic activities declined in liver homogenates by 25, 36 and 32%, respectively, 20 h after iron injection. These activities were not affected in kidney as compared to control values, except for SOD activity that was decreased by 26%. 6. The content of alpha-tocopherol was decreased by 31% in whole kidney homogenates and by 40% in plasma. 7. Our data indicate that lipid peroxidation occurs after mild iron overload both in liver and kidney. Enzymatic antioxidants are consumed significantly in liver and alpha-tocopherol content decreases in kidney, suggesting an organ-specific antioxidant effect.

  15. Lipid peroxidation markers in adult attention deficit hyperactivity disorder: new findings for oxidative stress.

    PubMed

    Bulut, Mahmut; Selek, Salih; Bez, Yasin; Cemal Kaya, Mehmet; Gunes, Mehmet; Karababa, Fatih; Celik, Hakim; Savas, Haluk Asuman

    2013-10-30

    Malondialdehyde (MDA) is a reliable marker of lipid peroxidation where paraoxonase and arylesterase are two enzymes against it. Although increased MDA has been previously shown in adults with attention deficit/hyperactivity disorder (A-ADHD), levels of paraoxonase and arylesterase enzymes have not been studied yet. We aimed to determine the status of both MDA level and paraoxonase and arylesterase enzyme activities in A-ADHD patients. A total of 35 adults with ADHD diagnosis according to Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV) criteria and 29 healthy volunteers were included in the study. Serum MDA, paraoxonase and arylesterase levels of the participants were measured. The disease severity of the patients was determined by using Turgay's Adult Attention Deficit Disorder/Attention Deficit Hyperactivity Disorder (ADD/ADHD) DSM IV Based Diagnostic Screening and Rating Scale. The serum MDA level of patients was significantly higher than that of healthy control subjects, whereas their paraoxonase and arylesterase levels were significantly lower. There was no correlation between the levels of biochemical parameters (MDA, paraoxonase and arylesterase) and the disease severity. Sub-types of A-ADHD were similar in terms of these biochemical parameters. Increased lipid peroxidation, a part of oxidative stress, in adults with ADHD appears to be unbuffered by antioxidant enzymes, namely paraoxonase and arylesterase.

  16. WO3/Pt nanoparticles promote light-induced lipid peroxidation and lysosomal instability within tumor cells

    NASA Astrophysics Data System (ADS)

    Clark, Andrea J.; Petty, Howard R.

    2016-02-01

    Although metal-metal oxide nanoparticles have attracted considerable interest as catalysts, they have attracted little interest in nanomedicine. This is likely due to the fact that metal oxide semiconductors generally require biologically harmful ultraviolet excitation. In contrast, this study focuses upon WO3/Pt nanoparticles, which can be excited by visible light. To optimize the nanoparticles’ catalytic performance, platinization was performed at alkaline pH. These nanoparticles destroyed organic dyes, consumed dissolved oxygen and produced hydroxyl radicals. 4T1 breast cancer cells internalized WO3/Pt nanoparticles within the membrane-bound endo-lysosomal compartment as shown by electron and fluorescence microscopy. During visible light exposure, but not in darkness, WO3/Pt nanoparticles manufacture reactive oxygen species, promote lipid peroxidation, and trigger lysosomal membrane disruption. As cells of the immune system degrade organic molecules, produce reactive oxygen species, and activate the lipid peroxidation pathway within target cells, these nanoparticles mimic the chemical attributes of immune effector cells. These biomimetic nanoparticles should become useful in managing certain cancers, especially ocular cancer.

  17. Lipid Peroxidation, Nitric Oxide Metabolites, and Their Ratio in a Group of Subjects with Metabolic Syndrome

    PubMed Central

    Caimi, Gregorio; Lo Presti, Rosalia; Montana, Maria; Canino, Baldassare; Averna, Maurizio R.

    2014-01-01

    Our aim was to evaluate lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), nitric oxide metabolites (nitrite + nitrate) expressed as NOx, and TBARS/NOx ratio in a group of subjects with metabolic syndrome (MS). In this regard we enrolled 106 subjects with MS defined according to the IDF criteria, subsequently subdivided into diabetic (DMS) and nondiabetic (NDMS) and also into subjects with a low triglycerides/HDL-cholesterol (TG/HDL-C) index or with a high TG/HDL-C index. In the entire group and in the four subgroups of MS subjects we found an increase in TBARS and NOx levels and a decrease in TBARS/NOx ratio in comparison with normal controls. Regarding all these parameters no statistical difference between DMS and NDMS was evident, but a significant increase in NOx was present in subjects with a high TG/HDL-C index in comparison with those with a low index. In MS subjects we also found a negative correlation between TBARS/NOx ratio and TG/HDL-C index. Considering the hyperactivity of the inducible NO synthase in MS, these data confirm the altered redox and inflammatory status that characterizes the MS and suggest a link between lipid peroxidation, inflammation, and insulin resistance, evaluated as TG/HDL-C index. PMID:24987495

  18. In vitro lipid peroxidation of intestinal bile salt-based nanoemulsions: potential role of antioxidants.

    PubMed

    Courraud, J; Charnay, C; Cristol, J P; Berger, J; Avallone, S

    2013-12-01

    Over the last decades, oxidative stress has been described as a deleterious phenomenon contributing to numerous noncommunicable diseases such as cardiovascular disease, diabetes, and cancers. As many authors ascribed the healthy effect of fruit and vegetable consumption mainly to their antioxidant contents, it has been hypothesized that their protection could occur from the gut. Therefore, the aim of this study was to develop an original and physiological model of nanoemulsions to study lipid peroxidation within the intestine and to assess the properties of potential antioxidants in this setting. Several nanoemulsions were compared in terms of physical characteristics and reactivity to 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced oxidation. Formulations included different types of lipids, a detergent (a conjugated bile salt or sodium dodecyl sulfate) and, finally, lipophilic antioxidants. Hemin and myoglobin were also tested as relevant potential oxidants. Fatty acid (FA) peroxidation was monitored by gas chromatography while malondialdehyde and antioxidant contents were measured by HPLC. Investigated nanoemulsions were composed of spherical or cylindrical mixed micelles, the latter being the least resistant to oxidation. In the experimental conditions, AAPH was the only efficient oxidant. Alpha-tocopherol and lutein significantly slowed FA degradation from 4 to 1 μM, respectively. On the contrary, beta-carotene did not show any protective capacity at 4 μM. In conclusion, the tested nanoemulsions were appropriate to assess antioxidant capacity during the intestinal phase of digestion.

  19. Effects of Resveratrol Supplementation on Oxidative Damage and Lipid Peroxidation Induced by Strenuous Exercise in Rats.

    PubMed

    Xiao, Ning-Ning

    2015-07-01

    The purpose of the present study was to investigate the effects of resveratrol supplementation on oxidative damage and lipid peroxidation induced by strenuous exercise in rats. The rats were randomly divided into five groups: a sedentary control group, an exercise control group, and three treatment exercise groups administered increasing doses of resveratrol (25, 50, and 100 mg/kg body weight). Resveratrol was administered by oral gavage once daily for four weeks. At the end of the four-week period, the rats performed a strenuous exercise on the treadmill, and the levels of lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured. The results showed that resveratrol supplementation had protective effects against strenuous exercise-induced oxidative damage and lipid peroxidation by lowering the levels of LDH, CK, MDA, 4-HNE, and 8-OHdG in the serum or muscle of rats. These beneficial effects are probably owing to the inherent antioxidant activities of resveratrol.

  20. Morin, a flavonoid, on lipid peroxidation and antioxidant status in experimental myocardial ischemic rats.

    PubMed

    Al-Numair, Khalid S; Chandramohan, Govindasamy; Alsaif, Mohammed A; Veeramani, Chinnadurai; El Newehy, Ahmed S

    2014-01-01

    Myocardial infarction affects a large population in the world. Lipid peroxide metabolism plays an important role in the pathology of myocardial infarction. The present study was designed to investigate the antioxidant potential of morin, a flavonoid in isoproterenol (ISO)-induced myocardial infarction (MI), in rats. Male albino Wistar rats were pre-treated with morin (40 mg/kg), daily for a period of 30 days. After the treatment period, ISO (85 mg/kg), was subcutaneously injected in rats at an interval of 24 h for 2 days. ISO-administered rats showed elevated levels of thiobarbituric acid reactive substances (TBARS), and lipid hydro-peroxide (LOOH), in plasma and heart. Pretreatment with morin, the above changes were significantly reduced to near normal level. ISO-administered rats showed decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) in heart. In addition, decrease the levels non enzymatic antioxidants such as reduced glutathione (GSH), vitamin C and vitamin E in plasma and heart while ceruloplasmin in plasma. Pretreatment with morin, reversed these above biochemical changes towards normalcy. These findings revealed that, the morin possess antioxidant activity in experimentally induced cardiac toxicity.

  1. Effect of Soybean Hypocotyl Extract on Lipid Peroxidation in GK Rats

    PubMed Central

    Quan, Jishu; Yin, Xuezhe; Kanazawa, Takemichi

    2009-01-01

    Vascular complications, as a consequence of atherosclerosis, are main causes of morbidity and mortality in patients with diabetes mellitus. There is increasing evidence that lipid peroxidation and oxidative modification of low density lipoprotein (LDL) is important in atherogenesis. In this study we investigated the effect of soybean hypocotyl extract (SHE), rich in isoflavones and saponins, on lipid peroxide (LPO) levels in liver, plasma and lipoproteins in GK diabetic rats, and its efficacy on the reduction of susceptibility of LDL and high density lipoprotein (HDL) to oxidation. The oxidative modification of LDL and HDL was determined with the lag time of copper ion-induced oxidation curve identified by the conjugated dienes. In SHE group which were fed diet containing 40 g/kg of SHE for 16 weeks, LPO levels in liver, plasma and HDL fraction were significantly decreased compared with the control group. The lag phage of LDL oxidation curve was prolonged noticeably by a mean of 27 min in SHE group as compared to the control group, indicating a reduced susceptibility to oxidation. The results suggest that intake of soybean hypocotyl extract might be useful for the prevention and treatment of diabetes mellitus and diabetes-associated diseases. PMID:19430608

  2. Effect of occupation on lipid peroxidation and antioxidant status in coal-fired thermal plant workers