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)

The influence of oleic, linoleic (LIN), and eicosapentaenoic (EPA) acids incorporated into cellular lipids on susceptibility to O2-induced toxicity was evaluated in Chinese hamster fibroblasts (HA1) using a clonogenic cell survival assay. Fatty acid incorporation was achieved by incubating HA1 cells in 21% O2 for 72 h in the presence or absence of media supplemented with 25 microM oleic acid, 25 microM LIN, or 2, 4, and 25 microM EPA. This fatty acid incorporation period increased the percentage of composition in phospholipids 2-fold for oleic acid, 6-fold for LIN, and 6- to 20-fold for EPA. Vitamin E, total glutathione, superoxide dismutase activity, glutathione transferase activity, and catalase activity were unchanged, relative to control, in the 25-microM EPA-treated group, and only total glutathione was elevated in the LIN-treated group. After the incorporation period, the cells were placed in non-fatty acid supplemented media and exposed to 95% O2, and clonogenic survival responses were evaluated at time intervals up to 100 h. Sensitization to O2 toxicity in EPA-treated cells was apparent after 24 h of O2 exposure, whereas LIN-treated cells were significantly (p less than 0.05) sensitized to hyperoxia after 54 h of exposure, indicating that EPA was a more potent sensitizer for O2 injury. Furthermore, cells supplemented with 4 and 25 microM EPA were more sensitive to O2 toxicity than cells supplemented with 2 microM EPA. In contrast, cells treated with 25 microM oleic acid were significantly more resistant to O2 toxicity at 51, 72, and 98 h of O2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of monosaturated and polyunsaturated fatty acids on oxygen toxicity in cultured cells. 140 77

The combination of 1,2-dibromoethane (DBE) with carbon tetrachloride (CCl4) in the isolated rat hepatocyte model produces a significant potentiation of both lipid peroxidation and plasma membrane damage induced by the latter compound. The increase in malondialdehyde production precedes the hepatocyte damage, evaluated in terms both of lactate dehydrogenase leakage and trypan blue exclusion. When hepatocytes are isolated from vitamin E pretreated rats, both the prooxidant and the cytotoxic effects of CCl4 are prevented. Also the synergism between CCl4 and DBE on lipid peroxidation disappears completely while that on cell damage is strongly reduced. The increased lipid peroxidation appears to be one of the mechanisms of the observed synergism between CCl4 and DBE on hepatocyte damage. Regarding the antioxidant status of the hepatocyte challenged with CCl4 and DBE, an early and significant consumption of vitamin E is observed only in the presence of the mixture of these xenobiotics. Total nonprotein thiol content is not significantly modified by CCl4 poisoning while DBE, alone and in association with CCl4, markedly decreases it. Vitamin E supplementation does not prevent but moderately delays total nonprotein thiol depletion due to DBE or to the mixture. Finally, glutathione transferase activity is significantly reduced by CCl4 treatment and not by DBE, and vitamin E supplementation totally prevents such inhibition. The increased prooxidant effect of CCl4 plus DBE compared to CCl4 alone seems related to the shift in DBE metabolism consequent to the CCl4-dependent inactivation of glutathione transferase.
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PMID:Lipid peroxidation and irreversible cell damage: synergism between carbon tetrachloride and 1,2-dibromoethane in isolated rat hepatocytes. 189 69

In the companion paper we demonstrated that hepatic vitamin E in rats becomes depleted and extrahepatic pools of vitamin E are altered by treatment with 1,2-dibromoethane (DBE). Vitamin E depletion may be dependent upon initial steps of DBE metabolism that are either oxidative (cytochrome P450 dependent) or conjugative (glutathione transferase dependent). That the liver content of glutathione (GSH) and vitamin E, the plasma concentration of vitamin E, and the serum activities of AST and ALT may be influenced by cytosolic metabolism of DBE was assessed by comparison of findings from rats treated with either 1,2-dichloroethane (DCE) or 1-bromo-2-chloroethane (BCE). The extent of oxidative metabolism was diminished by the use of tetradeutero-DBE (d4-DBE), and the availability of GSH for conjugative metabolism was diminished by pretreatment of rats with L-buthionine-S,R-sulfoximine (BSO) prior to treatment with DBE. Our results indicate that neither DCE nor BCE provokes a liver vitamin E depletion in rats, that d4-DBE treatment hastens but does not enhance the observed hepatic vitamin E depletion by comparison to animals treated with an equimolar dose of DBE, and that BSO pretreatment prevented the hepatic vitamin E depletion observed from animals treated with DBE alone. These results indicate that hepatic vitamin E depletion is the unique sequelae to conjugation of GSH with DBE, and we suggest the reactive episulfonium ion intermediate or a macromolecular adduct of this ion derived from DBE may play a role in liver vitamin E depletion associated with exposure to DBE.
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PMID:Modification of hepatic vitamin E stores in vivo. III. Vitamin E depletion by 1,2-dibromoethane may be related to initial conjugation with glutathione. 189 41

Lipid peroxide production, antioxidant contents and activities of antioxidative protective enzymes were examined in lungs of rats exposed to clean air (control group), 0.05 ppm O3, 0.05 ppm O3 + 0.04 ppm NO2 and 0.05 ppm O3 + 0.4 ppm NO2 for 22 months. The results were compared with our previous data in rats exposed to 0.04 ppm NO2, 0.4 ppm NO2 and 4 ppm NO2 for their life span (Sagai et al., Toxicol. Appl. Pharmacol., 73, (1984) 444-456). TBA values used as an index of lipid peroxidation in the lungs were increased maximally at 9 months, but were decreased below control values in animals exposed for 18 and 22 months. Nonprotein sulfhydryl (NPSH) contents were increased maximally at 9 months, and after 18 and 22 months were decreased significantly below control values. Vitamin E (VE) contents showed a similar trend. On the other hand, enzyme activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase measured by using cumene hydroperoxide (cum.OOH) substrate (GPx-cum.OOH), glutathione peroxidase measured by using H2O2 as a substrate (GPx-H2O2), glutathione S-transferase (GSH-Tase) and superoxide dismutase (SOD) did not show any significant changes during this experiment. The results show that lipid peroxidation in lungs was increased synergistically by a combination of NO2 and O3 at ambient levels, and that the time of maximum lipid peroxide production was shorter than with NO2 alone. The protective ability against lipid peroxides was higher with increased lipid peroxide levels, but the inducibility was not maintained through a life span exposure to the combined gases. Additionally, two small adenomas were observed in 2 out of 18 rats in the 0.05 ppm O3 + 0.04 ppm NO2 group and a large adenoma was observed in 1 out of 18 animals in the 0.05 ppm + 0.4 ppm NO2 group exposed for 22 months.
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PMID:Biochemical effects of combined gases of nitrogen dioxide and ozone. IV. Changes of lipid peroxidation and antioxidative protective systems in rat lungs upon life span exposure. 201 15

Vitamin E and glutathione protect against oxidative damage in vivo. In this study the relationship between these two defenses has been examined in the isolated perfused rat liver. The activities of glutathione reductase and glutathione S-transferase were unaffected by vitamin E deficiency, while glutathione peroxidase activity was decreased slightly. The glutathione redox status of vitamin E-deficient and control livers was assessed. GSSG was slightly higher in vitamin E-deficient livers (70 +/- 5 nmol GSH equivalents/g liver) than in controls (56 +/- 3 nmol GSH equivalents/g liver) under basal conditions. However, biliary GSSG release was 41% lower in vitamin E-deficient livers (0.46 +/- 0.08 nmol GSH equivalents/g liver.min) than in controls (0.78 +/- 0.23 nmol GSH equivalents/g liver.min). Inhibition of GSSG reduction by BCNU raised liver and biliary GSSG by a similar amount in vitamin E-deficient and control livers. Thus biliary GSSG efflux, a frequently used index of oxidant stress, is not increased in vitamin E-deficient perfused livers compared with control. Therefore, in the perfused rat liver model, no evidence was obtained that vitamin E deficiency activates the hepatic glutathione system.
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PMID:Tissue and biliary glutathione disulfide in the perfused vitamin E-deficient rat liver. 272 89

Lipoperoxidation has an important role in the normal processes of the cell-life. The induction is produced by oxygen-derived free radicals which attack the membrane phospholipids. Such an attack is modulated by an enzymatic protection system (superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase) and by a non-enzymatic one (vitamin C, vitamin E...). In various pathologic conditions, a dispoise takes place between radical attack and antiradical protection. The place taken by lipoperoxidation in the ageing process seems to be fundamental. We report here the results of a study carried out in aged and sick patients who were given an antioxidant medicamentous combination made from Vitamin C, Vitamin E and Rutin. Our results evidence that such a synergistic combination does modify both enzymatic protection system and lipoperoxidation, this latter showing a decrease under treatment.
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PMID:[Lipid peroxidation in aged patients. Influence of an antioxidant combination (vitamin C-vitamin E-rutin)]. 273 16

The specific activities of superoxide dismutase, catalase, and glutathione S-transferase (mu subtype) were significantly lower in the brains of mice with type II diabetes than in the brains of control mice. On the other hand, the specific activity of glutathione peroxidase was unaltered. The concentration of vitamin E, but not that of total glutathione and ascorbate, was increased in the brains of the type II diabetic mice. The relative amount of polyunsaturated fatty acids (as determined with soybean lipoxygenase) was increased in whole brains and crude synaptosomal membranes of the type II diabetic mice. Endogenous levels of thiobarbituric acid-positive material were decreased in both whole brain homogenates and crude synaptosomal membranes of the db/db mice. Susceptibility of lipids within whole brain homogenates and crude synaptosomal membranes of mice with type II diabetes to peroxidation with iron/ascorbate was also markedly decreased compared with that of controls. Vitamin E is known to quench lipid peroxidation. Therefore, decreased lipid peroxidation in the type II mouse brain may be due to increased vitamin E content.
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PMID:Antioxidant defense systems in the brains of type II diabetic mice. 779 Aug 73

The specific features of the action of combinations of immunostimulants (levamisole, prodigiozan, methyluracil) on a primary immune response to EB, GST and resistance to experimental infection have been studied. It has been shown that levamisole eliminates stimulation by methyluracil and prodigiozan of a primary immune response, lithium carbonate is also an antagonist of prodigiozan. Vitamin E increases the stimulating effect of prodigiozan rather than oxymethacil. The effect of vitamin A depends on the dose. Levamisole does not change the influence of prodigiozan and methyluracil on GST and, like prodigiozan, suppresses GST stimulated by lithium carbonate. The combination of prodigiozan and methyluracil to a large extent than the agent given alone increases resistance to an infection and efficiency of antibiotic therapy. The combination of methyluracil and levamisole increases only the effect of the antibiotic.
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PMID:[A combination of immunostimulants as a method for correcting secondary immunodeficiencies]. 834 38

The effect of vitamin E on gamma-glutamyl transpeptidase-positive foci, with or without phenobarbital, was investigated. Groups of six female Sprague-Dawley rats were initiated with diethylnitrosamine (15 mg/kg) at 24 hours of age. After weaning, they were fed diets with 10% (wt/wt) fish oil; the diets contained 0, 5,000 or 15,000 ppm vitamin E supplementation with or without phenobarbital (500 ppm) for six months. Phenobarbital significantly increased liver weight and liver weight as a percentage of body weight (p < 0.05), suggesting a liver hypertrophic effect of phenobarbital. Phenobarbital significantly decreased hepatic phospholipid arachidonate, eicosapentaenoate, and docosahexaenoate (p < 0.05); this may indicate that phenobarbital stimulates phospholipase A2 activity and results in the increased release of polyunsaturated fatty acids from phospholipids and the decrease of hepatic phospholipid polyunsaturated-to-saturated fat ratio. In rats fed phenobarbital, hepatic vitamin E content was lower than in rats fed no phenobarbital; this suggests that phenobarbital causes oxidative stress or induces enzymes that metabolize the vitamin. Phenobarbital exposure significantly increased hepatic prostaglandin F2 alpha and glutathione S-transferase activity (p < 0.05). Vitamin E did not influence hepatic gamma-glutamyl transpeptidase-positive foci area and number with or without phenobarbital, and phenobarbital showed a strong promoting action on enzyme-altered hepatic foci.
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PMID:No inhibition of gamma-glutamyl transpeptidase-positive foci by vitamin E with or without phenobarbital. 912 50

Hepatic cytochrome P-450 activity has been shown to be affected by various dietary factors including vitamin E. However, reports of the effect of dietary vitamin E on cytochrome P-450 activity have been inconsistent. The aim of the present study was to investigate the influence of dietary vitamin E on rat hepatic cytochrome P-450 activity. Three groups of six male weanling Sprague-Dawley rats were fed semipurified diets containing 0, 100, or 1,500 ppm vitamin E for eight weeks. Vitamin E was given in the form of alpha-tocopheryl acetate. Dietary vitamin E significantly affected liver vitamin E content (p < 0.05) but had no effect on rat hepatic total P-450 content, N-nitrosodimethylamine demethylase, and NADPH-cytochrome-P-450 reductase activities. Hepatic pentoxyresorufin O-dealkylase and glutathione S-transferase activities were significantly greater in rats fed 100 and 1,500 ppm vitamin E than in rats fed no vitamin E (p < 0.05). Dietary vitamin E induced changes in hepatic phospholipid fatty acid composition. Hepatic phospholipid linoleate was significantly greater in rats fed 0 and 1,500 ppm vitamin E than in rats fed 100 ppm vitamin E (p < 0.05). Hepatic phospholipid eicosapentaenoate was increased significantly by dietary vitamin E (p < 0.05). Hepatic thiobarbituric acid-reactive substance was significantly greater in rats fed no vitamin E than in rats fed 100 and 1,500 ppm vitamin E (p < 0.05). The results suggest that vitamin E may influence cytochrome P-450 IIB1 enzyme activity and may affect hepatic phospholipid fatty acid composition.
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PMID:Effect of vitamin E on rat hepatic cytochrome P-450 activity. 979 69


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