Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.5.1.18 (glutathione S-transferase)
22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythrocytes are a convenient model to understand the membrane oxidative damage induced by various xenobiotic-prooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LC), a type II pyrethroid, to induce oxidative stress response in rabbit erythrocytes in vitro and its effect on selected antioxidant enzymes and (2) the role of vitamin C (VC; 20mM) and vitamin E (VE; 2mM) in alleviating the cytotoxic effects of LC. Erythrocytes were divided into three groups. The first group, previously prepared erythrocytes was incubated for 4h at 37 degrees C with different concentrations (0, 0.1, 0.5, 1, 2.5, 5mM) of LC. The second and third groups were preincubated with VC or VE, respectively for 20 min and followed by LC incubation for 4h. Following in vitro exposure, LC caused a significant induction of oxidative damage in erythrocytes at different concentrations as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels. However, a significant decrease in the content of sulfhydryl groups (SH-groups), and the activities of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) were observed. The response was concentration dependent. VC or VE pretreated erythrocytes showed a significant protection against the cytotoxic effects induced by LC on the studied parameters. In conclusion, antioxidant vitamins especially VE could be able to ameliorate LC-induced oxidative stress by decreasing lipid peroxidation and altering antioxidant defense system in erythrocytes.
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PMID:Lambda-cyhalothrin-induced changes in oxidative stress biomarkers in rabbit erythrocytes and alleviation effect of some antioxidants. 1713 48

Oxidative stress is common in inflammatory processes of many diseases, including the Chagas' disease, which is characterized by chronic inflammation. The present study is a sequence of a related publication [Oliveira TB, Pedrosa RC, Wilhelm Filho D. Oxidative stress in chronic cardiopathy associated with Chagas' disease. Int J Cardiol in press.] on the same subjects, which showed an increase in oxidative stress associated with the progression of the severity of the disease. Components of the antioxidant system and oxidative biomarkers present in the blood were measured in the same chronic chagasic patients (n=40), before and after vitamin E (800 IU/day) and vitamin C (500 mg/day) supplementation for 6 months. Antioxidant enzymes and contents of reduced glutathione in erythrocytes and plasma TBARS contents were analyzed in four groups of patients in different stages of chronic Chagas heart disease (n=10 each group, groups I, II, III, and IV) according to the Los Andes classification. After the combined vitamin supplementation, TBARS and protein carbonyl levels were decreased in plasma, whilst red cell GSH contents were increased in group I. The vitamin E contents found in the plasma were inversely related to the severity of the disease. No differences in gamma-glutamiltransferase activities were detected but the myeloperoxidase levels were decreased in patients at the initial stages, whilst seric nitric oxide levels were increased in groups II and III. After the antioxidant supplementation, CAT activity was increased in group II, GPx activity was increased in group I, GR activity was increased in groups I and II, whilst the GST activity was decreased in groups II, III and IV. The results clearly indicate that the antioxidant supplementation was able to counteract the progressive oxidative stress associated with the disease. New perspectives for the treatment of Chagas' disease might include an antioxidant therapy in order to attenuate the consequences of oxidative insult related to this disease.
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PMID:Antioxidant therapy attenuates oxidative stress in chronic cardiopathy associated with Chagas' disease. 1732 77

The purpose of this study was to investigate whether high methionine (HM) diet may influence the development of ethanol-induced hepatotoxicity and prooxidant-antioxidant balance in the liver. Rats received drinking water containing ethanol (20% v/v) and/or methionine supplemented diet (2% w/w) for 75 days. Although prooxidant-antioxidant balance did not change in the liver of rats in HM group, ethanol treatment was observed to increase plasma transaminase activities, and malondialdehyde (MDA) and protein carbonyl (PC) levels, but not glutathione (GSH), vitamin E and vitamin C levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver of rats as compared to controls. However, ethanol plus HM diet caused further increases in plasma transaminase activities and hepatic MDA and PC levels. In addition, SOD, GSH-Px and GST activities were observed to decrease, but GSH, vitamin E and vitamin C levels remained unchanged in the liver as compared to ethanol, HM and control groups. Our results show that HM diet may augment hepatotoxicity and oxidative stress in the liver of chronically ethanol-treated rats.
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PMID:Methionine-supplemented diet augments hepatotoxicity and prooxidant status in chronically ethanol-treated rats. 1749 36

The aim of the study was to evaluate the effect of exogenous mouse leptin on ethanol-induced cardiac toxicity in mice. Administering ethanol (6.32 g/kg body weight p.o.) to 4-week-old healthy mice for 45 days resulted in significantly elevated plasma levels of leptin, lactate dehydrogenase (LDH), cardiac lipid hydroperoxides (LOOH) and thiobarbituric acid reactive substances (TBARS) and significantly decreased cardiac superoxide dismutase, catalase, vitamin C, vitamin E, reduced glutathione and glutathione-dependent enzyme levels (glutathione peroxidase and glutathione S-transferase). Subsequent to the experimental induction of toxicity (i.e., after the initial period of 30 days) exogenous leptin was administered (230 microg/kg body weight i.p.) every alternate day for 15 days along with the daily dose of ethanol. Leptin administration to ethanol-treated mice significantly elevated the levels of plasma leptin, LDH and cardiac LOOH, TBARS, whereas the activity of antioxidant enzymes and the concentrations of vitamins C and E were further decreased significantly. These findings were consistent with our histological observations, confirming that leptin enhances cardiac toxicity in ethanol-supplemented mice.
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PMID:Effect of leptin on peroxidation and antioxidant defense in ethanol-supplemented Mus musculus heart. 1752 Dec 93

The biopesticide Spinosad causes a drop in cell viability in two mammalian cellular models CHO-K1 and Vero, using the neutral red incorporation assay as endpoint. Dose-response curves were assessed after 24, 48, and 72 h under different conditions i.e. presence of 10% fetal calf serum or 1% bovine serum albumin or antioxidants. The presence of antioxidant agents, viz. reduced glutathione (1 mM), vitamin C (100 microM), and vitamin E (20 microM) reduced significantly the cytotoxic effect of Spinosad, thus pointing to an oxidative damage mediated by this compound. An increase in malondialdehyde production was observed after 24-h treatment with Spinosad in both Vero and CHO-K1 cells, using fractions of NRU(50) as final concentrations. At concentrations equivalent to its NRU(20), NRU(10) and NRU(5) Spinosad caused significant alterations in the glutathione-redox cycle in the form of significant decrease in total and reduced glutathione, large increase in glutathione peroxidase activity, little induction of glutathione reductase, and significant decline of glutathione S-transferase activities.
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PMID:Alterations in the glutathione-redox balance induced by the bio-insecticide Spinosad in CHO-K1 and Vero cells. 1767 33

Environmental pollutants that disrupt endocrine system might also affect the modeling and remodeling of bone. Environmental factors, irrespective of age and sex contribute for the development of secondary osteoporosis. Polychlorinated biphenyls have adverse effects on various organs including bone. The present study was designed to investigate the effects of PCB (Aroclor 1254) on femur bone and the ameliorative role of vitamin C or E. In this regard, four groups of adult male albino rats were used as control, PCB (2mg/kgb.wt.), PCB+vitamin C (100mg/kgb.wt.) and PCB+vitamin E (50mg/kgb.wt.). The bone formation markers (ALP, Collagen), bone resorption marker (TRAP), antioxidant enzymes (SOD, GPX and GST) and lipid peroxidation in the femur were studied. Aroclor 1254 treatment decreased the ALP activity and collagen, but increased the TRAP activity and lipid peroxidation. While it decreased the SOD and GPX activity, GST was unaltered. Interestingly, simultaneous administration of vitamin C or E prevented the adverse effects of Aroclor 1254 in the femur. In conclusion, the present investigation suggests that Aroclor 1254 induced oxidative stress affects femoral bone metabolism. However, vitamin C or vitamin E protected the femur from the oxidative stress.
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PMID:Effects of Aroclor 1254 on femoral bone metabolism in adult male Wistar rats. 1788 81

The aim of the study has been to determine and compare the influence upon the kidney antioxidative system, exercised by administration of vitamin E, and vitamin E in combination with methionine, under conditions of oxidative stress induced by sodium fluoride. The experiment was carried out on Wistar FL rats (adult males) that, for 35 days, were administered water, NaF, NaF with vitamin E, or vitamin E with methionine (doses: 10 mg NaF/kg of body mass/24 h, 3 mg vitamin E per 10 microl per rat for 24 h, 2 mg methionine per rat for 24 h). The influence of administered sodium fluoride and antioxidants upon the antioxidative system in kidney was examined by analyzing the concentration of malondialdehyde (MDA) and the activity of the most important antioxidative enzymes (SOD, total and both its isoenzymes, GPX, GST, GR, and CAT). The studies carried out confirmed the disadvantageous effect of the administered dose of NaF upon the antixodiative system in rats (increase in the concentration MDA, decrease activity of all antioxidative enzymes). The administration of vitamin E increased the activity of studied enzymes with the exception of glutathione reductase GR; it also reduced the processes of lipid peroxidation. It has been found that combined doses of vitamin E and methionine were most effective in inhibiting lipid peroxidation processes. The results confirmed the antioxidative properties of methionine.
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PMID:Influence of fluoride on rat kidney antioxidant system: effects of methionine and vitamin E. 1818

Selenium (Se) and vitamin E are antioxidant micronutrients. Se functions through selenoproteins and vitamin E reacts with oxidizing molecules in membranes. The relationship of these micronutrients with the Nrf2-antioxidant response element (ARE) pathway was investigated using ARE-reporter mice and Nrf2-/- mice. Weanling males were fed Se-deficient (0 Se), vitamin E-deficient (0 E), or control diet for 16 or 22 weeks. The ARE reporter was elevated 450-fold in 0 Se liver but was not elevated in 0 E liver. Antioxidant enzymes induced by Nrf2-ARE (glutathione S-transferase (GST), NAD(P)H quinone oxidoreductase (NQOR), and heme oxygenase-1 (HO-1)) were elevated in 0 Se livers but not in 0 E livers. Deletion of Nrf2 had varying effects on the inductions, with GST induction being abolished by it but induction of NQOR and HO-1 still occurring. Thus, Se deficiency, but not vitamin E deficiency, induces a number of enzymes that protect against oxidative stress and modify xenobiotic metabolism through Nrf2-ARE and other stress-response pathways. We conclude that Se deficiency causes cytosolic oxidative stress but that vitamin E deficiency does not. This suggests that the oxidant defense mechanisms in which these antioxidant nutrients function are independent of one another.
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PMID:Selenium deficiency activates mouse liver Nrf2-ARE but vitamin E deficiency does not. 1827 78

Alcoholic liver disease is a major medical complication of drinking alcohol. Oxidative stress plays an important role in the development of alcohol liver disease. The present study was carried to evaluate the effect of grape leaf extract (GLEt) on antioxidant and lipid peroxidation states in liver and kidney alcohol induced toxicity. In vitro studies with DPPH* and ABTS*(+) (cation radical) showed that GLEt possesses antioxidant activity. In vivo administration of ethanol (7.9 g/kg bw/day) for 45 days resulted an activity of liver marker enzymes (AST, ALT, ALP and GGT), lipid peroxidation markers (TBARS, lipid hydroperoxides) in liver and kidney with significantly lower activity of SOD, CAT, GPx, GST and non-enzymatic antioxidants (vitamin E, vitamin C and GSH) in liver and kidney as compared with control rats. Administration of ethanol along with GLEt significantly decreased the activities of liver markers enzyme in serum towards near normal level. GLEt at a dose of 100 mg/kg was highly effective than 25 and 50 mg/kg body weight. In addition GLEt also significantly reduced the levels of lipid peroxidation and addition, significantly restored the enzymic and non-enzymatic antioxidants level in liver and kidney of alcohol administration rats. This observation was supplemented by histopathological examination in liver and kidney. Our data suggest that GLEt exerts its protective effect by decreased the lipid peroxidation and improving antioxidants status, thus proving itself as an effective antioxidant in alcohol induced oxidative damage in rats.
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PMID:Effect of grape (Vitis vinifera L.) leaf extract on alcohol induced oxidative stress in rats. 1828 59

The aim of this study was to investigate the effect of the changes of taurine levels in the hearts of old rats on endogenous malondialdehyde (MDA) and diene conjugate (DC) levels and ascorbic acid (AA)- and NADPH-induced lipid peroxidation as well as non-enzymatic (glutathione, vitamin E and vitamin C) and enzymatic antioxidants (superoxide dismutase, glutathione peroxidase and glutathione transferase). Two groups of old (22 mo) rats were treated with beta-alanine (3%, w/v; in drinking water), a taurine depleting agent, or taurine (2% w/v; in drinking water) for 6 wk. Significant decreases were observed in taurine contents of hearts in old rats as compared to young (5 mo) rats. We found that MDA and DC levels and AA- and NADPH-induced lipid peroxidation increased, but non-enzymatic and enzymatic antioxidants did not alter in heart homogenates of aged rats. beta-Alanine administration resulted in significant decreases in heart taurine levels of old rats. This treatment did not cause further increases in MDA or DC levels or changes in antioxidants. However, AA- and NADPH-induced lipid peroxidation was higher than that of old rats. Taurine treatment caused significant increases in heart taurine levels of old rats. This treatment was found to decrease endogenous MDA and DC levels without affecting the antioxidant system in the heart homogenates of aged rats. AA- and NADPH-induced lipid peroxidation was also reduced in old rats when given taurine, although not statistically significantly. Our results indicate that the changes in heart taurine levels may influence the susceptibility of heart tissue to lipid peroxidation in aged rats and that taurine supplementation has protective effects on age-dependent oxidative stress in heart tissue.
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PMID:Lipid peroxidation potential and antioxidants in the heart tissue of beta-alanine- or taurine-treated old rats. 1838 9


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