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 activities of catalase (Cat), superoxide dismutase (SOD), glutathione peroxidase (GSHPx), glutathione transferase (GST), glucose-6-phosphate dehydrogenase (G6PD) and glyceraldehyde3-phosphate dehydrogenase (G3PD) were studied in tissue and hemolymph of susceptible (S) (EgBS(2)) and resistant (R) (EgBR(2)) Biomphalaria alexandrina snails. The results showed that CAT and GST were higher in the hemolymph of snails susceptible to Schistosoma mansoni than in that of snails resistant to infestation, while SOD and G3PD were lower in the susceptible snails. The role of these enzymes as free radical scavengers was traced 1 and 24 h after infection of the two snail lines with S. mansoni. Moreover, the activities of SOD and G3PD were also measured 2 and 4 weeks post infection. The results revealed that the overall enzymatic activities were higher in susceptible than in resistant snail tissues. After 1 h of infection, all enzymes were increased in R and S snails except GST and G6PD which decreased in S snails. After 24 h of infection, GST increased in S snails and G3PD decreased in both S and R snails while other enzymes reached normal levels.
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PMID:Free radical scavengers in susceptible/resistant Biomphalaria alexandrina snails before and after infection. 1553 60

This study investigates the effects of acute exposure to organophosphate insecticide malathion (250 mg/kg, i.p.) and/or ZnCl2 (5 mg/kg, i.p.), with the following parameters: lipid peroxidation and the activity of acetylcholinesterase (AChE), glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PDH), and the levels of total glutathione (GSH-t) in the hippocampus and cerebral cortex of female rats. Malathion exposure elicited lipid peroxidation and reduced AChE activity in the cerebral cortex and hippocampus. It also reduced the activity of GR and GST, and increased G6PDH activity in the cerebral cortex, without changing the levels of GSH-t and GPx activity. ZnCl2 exposure reduced AChE activity and caused a mild pro-oxidative effect, since lipid peroxidation was increased in the hippocampus. ZnCl2, individually or in combination with malathion, caused a reduction in GR and GST activity in the cerebral cortex. Malathion and/or ZnCl2 did not change the GSH-t levels. Moreover, ZnCl2 prevented the increase in G6PDH activity caused by malathion. It showed that ZnCl2 had little effect against the changes induced by malathion. In fact, zinc itself produced pro-oxidant action, such as the reduction in the activity of the antioxidant enzymes GR and GST.
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PMID:Antioxidant defenses and lipid peroxidation in the cerebral cortex and hippocampus following acute exposure to malathion and/or zinc chloride. 1559 58

We investigated the regulation of free radical metabolism in Helix aspersa snails during a cycle of 20-day estivation and 24-h arousal in summer in comparison with estivation/arousal in winter-snails. In winter-snails (J. Exp. Biol. 206, 675-685, 2003), we had already observed an increase in the selenium-dependent glutathione-peroxidase (Se-GPX) activity in foot muscle and hepatopancreas and in the contents of hepatopancreas GSH-equivalents (GSH-eq=GSH+2 GSSG) during estivation compared with 24-h aroused snails. Summer-estivation prompted a 3.6-fold increase in Se-GPX activity in hepatopancreas, though not in foot muscle. Total-superoxide dismutase and catalase activities in hepatopancreas decreased (by 30-40%) during summer-estivation; however, no changes occurred in the activities of glutathione reductase, glutathione S-transferase and glucose-6-phosphate dehydrogenase in the two organs. GSH-eq levels were increased (by 54%) in foot muscle during estivation, but were unchanged in hepatopancreas. In contrast with winter-snails, oxidative stress markers (lipid peroxidation, carbonyl protein, and the GSSG/GSH-eq ratio) were unaltered during estivation/arousal in summer. These results demonstrate that seasonality modulates not only the absolute activities/levels of antioxidants (enzymes and GSH-eq) in H. aspersa, but also the regulatory process that controls the snail's antioxidant capacity during estivation/arousal. These results suggest that H. aspersa has an "internal clock" controlling the regulation of free radical metabolism in the different seasons.
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PMID:Seasonal modulation of free radical metabolism in estivating land snails Helix aspersa. 1590 62

The ability of zinc to mobilize defense against reactive oxygen species (ROS) and H2O2-induced apoptosis was studied using a primary culture of rainbow trout gill cells. Gill cells were pretreated for 24 h with 100 microM ZnSO4 followed by 24-h exposure to 100 or 200 microM H2O2, or were subjected to 100 microM ZnSO4 together with 100 or 200 microM H2O2. Metallothionein-A (MTA) and metallothionein-B (MTB) mRNA levels were increased after treatment with zinc or H2O2, separately or in combination. Similarly, mRNA for glutathione S-transferase (GST) and glucose 6-phosphate dehydrogenase (G6PD) were increased in response to either zinc or H2O2, or after sequential treatments with zinc followed by H2O2. The stimulatory effects of zinc or H2O2 on MTA, MTB, GST, and G6PD mRNA levels could be blocked by addition of the membrane permeable zinc chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), suggesting that H2O2-induced upregulation of these genes is zinc-dependent. Pretreatment with zinc protected the cells from subsequent cell damage and apoptosis, as assessed by lactate dehydrogenase leakage, mitochondrial dehydrogenase activity (MTT assay), caspase-3 activity, and DNA fragmentation. In contrast, when gill cells were coincubated with zinc and H2O2 at the same time, H2O2 toxicity was higher than after treatment with H2O2 alone. It is concluded that zinc had a direct pro-oxidant effect when administered together with H2O2, but that pretreatment of zinc inhibited cytotoxicity and apoptosis through an indirect antioxidant action. We propose that the antioxidant action is manifested through zinc-dependent expression of several genes encoding antioxidant proteins (e.g., MTA, MTB, G6PD, and GST). Furthermore, the apparent zinc-dependency of H2O2-induced expression of antioxidant genes suggests that zinc might act as a physiological signal to mediate the response to oxidative stress.
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PMID:ZINC-mediated gene expression offers protection against H2O2-induced cytotoxicity. 1592 8

Dimethoate, an organophosphate pesticide, is used in controlling the pests of a variety of crops. The study was carried out to understand the role of dimethoate in inducing oxidative stress leading to generation of free radicals and alterations in antioxidant enzymes and scavengers of oxygen free radicals. The effects of subchronic exposure of dimethoate in the production of oxidative stress were evaluated in male Wistar rats in the present study. Dimethoate was administered orally at doses 0.6, 6, and 30 mg/kg for 30 days in these rats. The results indicated an increase in levels of hepatic Cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver and brain at doses 6 and 30 mg/kg. There were no significant changes in the level of glucose-6-phosphate dehydrogenase activity except in liver at 30 mg/kg. A decrease in glutathione was observed at 30 and 6 mg/kg in both liver and brain. Glutathione-S-transferase increased at 30 and 6 mg/kg in liver and 30 mg/kg in brain. Erythrocyte acetylcholinesterase was inhibited at 30 and 6 mg/kg doses. Dose-dependent histopathological changes were seen in both liver and brain. This study concludes that oxidative stress due to dimethoate may be ascribed to induction of Cytochrome P450, inhibition of AChE and disturbance in activities of GSH and GST enzymes causing lipid peroxidation and histological and electron microscopic changes in liver and brain.
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PMID:Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure. 1611 89

Crassostrea rhizophorae is a euryhaline oyster that inhabits mangrove areas, which are widely distributed along the Brazilian coast. The aim of this study was to investigate the effects of salinity (9, 15, 25, and 35ppt) on the activities of glutathione S-transferase (GST), glucose 6-phosphate dehydrogenase (G6PDH), catalase (CAT), and acetylcholinesterase (AChE) in the digestive gland of this species after exposure to diesel oil for 7 days at nominal concentrations of 0.01, 0.1, and 1mlL(-1) and after depuration for 24h and 7 days. GST activity increased in a diesel oil concentration-dependent manner at salinities 25 and 15ppt and remained slightly elevated even after depuration periods of 24h and 7 days. No changes were observed in the activities of G6PDH, CAT, and AChE in the oysters exposed to diesel and depurated. Based on these results, GST activity in the digestive gland of C. rhizophorae might be used as a biomarker of exposure to diesel oil in sites where the salinity is between 15 and 25ppt, values usually observed in mangrove ecosystems.
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PMID:Effects of salinity on biomarker responses in Crassostrea rhizophorae (Mollusca, Bivalvia) exposed to diesel oil. 1621 31

The purpose of this study was to investigate effects of some antibiotics on glucose-6-phosphate dehydrogenase (G6PD), antioxidant enzymes, and malondialdehyde (MDA). Initially, for in vitro studies, G6PD was purified from human erythrocyte, 9811-fold in a yield of 42.4% by using ammonium sulfate precipitation and 2',5' ADP-Sepharose 4B affinity gel. The purified enzyme showed a single band on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The effects of four different antibiotics (isepamicin sulfate, meropenem, chloramphenicol, and thiamphenicol glisinat hydrochloride) were investigated on the purified enzyme. K(i) value and type of inhibition were determined by means of Lineweaver-Burk graphs and regression analysis graphs. Isepamicin sulfate inhibited the enzyme activity (I(50) value, 2.1 mM; K(i) value, 1.7 mM), whereas thiamphenicol glisinat hydrochloride activated the G6PD dose dependently. Other drugs showed no inhibition and activation effect. In addition, the effects of isepamicin sulfate on the activities of G6PD, glutathione reductase (GR), superoxide dismutases (SOD), glutathione peroxidase (GPx), catalase (CAT), and glutathione S-transferase (GST) and MDA concentrations were examined in Sprague-Dawley rat erythrocytes in vivo. A marked alteration in the activities of these enzymes and MDA levels may be the result of oxidative stress in the rats receiving isepamicin sulfate.
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PMID:Effects of some antibiotics on activity of glucose-6-phosphate dehydrogenase from human erythrocytes in vitro and effect of isepamicin sulfate on activities of antioxidant enzymes in rat erythrocytes. 1629 74

We report here the effects of chronic ethanol consumption on the antioxidant defense system in rat kidney. Thirty-two male Wistar rats were randomly divided in two identical groups and were treated as follows: control group (water for fluid) and the ethanol-fed group (2 g/kg body weight/24 h). The animals were sacrificed after 10 weeks, and respectively 30 weeks of ethanol consumption, and the renal tissue was isolated and analyzed. Results revealed that kidney alcohol dehydrogenase activities increased significantly after ethanol administration, but the electrophoretic pattern of alcohol dehydrogenase isoforms was unmodified. The SDS polyacrylamidegel electrophoretic study of kidney proteins has revealed the appearance of two new protein bands after long-term ethanol consumption. The kidney reduced glutathione/oxidized glutathione ratio decreased, indicating an oxidative stress response due to ethanol ingestion. The malondialdehyde contents and xanthine oxidase activities were unchanged. The antioxidant enzymatic defense system showed a different response during the two periods of ethanol administration. After 10 weeks, catalase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase were activated, while superoxide dismutase, glutathione transferase, and gamma-glutamyltranspeptidase levels were stationary. After 30 weeks, superoxide dismutase and glutathione peroxidase activities were unmodified, but catalase, glutathione transferase, gamma-glutamyltranspeptidase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities were significantly increased. Remarkable changes have been registered after 30 weeks of ethanol administration for glutathione reductase and glucose-6-phosphate dehydrogenase activities, including an increase by 106 and 216' of control values, respectively. These results showed specific changes in rat kidney antioxidant system and glutathione status as a consequence of long-term ethanol administration.
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PMID:Ethanol-induced alterations of the antioxidant defense system in rat kidney. 1642 92

Active oxygen species alter the activities of the enzymes involved in the defence against free radicals and substantially influence the aging process and age-dependent neuropathology. Unilamellar liposomes were used to deliver flavonoidal antioxidant quercetin (QC) to rat brain. Antioxidant potential of QC loaded in mannosylated (QC 7.2 micromol/kg b.wt.) liposomes (50 nm) was investigated by an in vivo model of cerebral ischemia and reperfusion on Sprague Dawley young (2 months old, b.wt. 160-180 g) and aged (20 months old, b.wt. 415-440 g) rats. Animals were made ischemic for 30 min by bilateral clamping of the common carotid artery followed by a 30 min cerebral reperfusion by withdrawing the clamping. Diene level and (GSSG/GSH) ratio were found to be higher in normal aged, compared to normal young rat brain. Superoxide dismutase, catalase, glucose-6-phosphate dehydrogenase, glutathione reductase and glutathione S-transferase activities were lower in normal aged rat brain. Further reduction of these antioxidant enzymes was observed in aged rat brain by the induction of cerebral ischemia and reperfusion. Mannosylated liposomally encapsulated QC treatment resulted in a significant preservation of the activities of antioxidant enzymes and a marked inhibition of cellular edema formation in neuronal cells of young and old rats.
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PMID:Mannosylated liposomal flavonoid in combating age-related ischemia-reperfusion induced oxidative damage in rat brain. 1648 Jul 58

Cap1p, a transcription factor in Candida albicans, is thought to participate in oxidative stress tolerance, but the pathways involved are still unclear. The study was designed to reveal the possible pathways by examining changes in the transcription profile after H2O2 treatment with both the cap1-deleted strain CJD21 and its parental strain CAI4 using microarray analysis. Of the identified 89 genes differentially expressed in CAI4 after exposure to H2O2, 76 genes were in a Cap1p-dependent expression pattern. We have shown that Cap1p is involved in the oxidative stress response in C. albicans via multiple pathways, including the cellular antioxidant defense system (e.g., thioredoxin reductase, glutathione reductase, glutathione S-transferase), carbohydrate metabolism and energy metabolism (e.g., glucose-6-phosphate dehydrogenase, transaldolase, glyoxalase I, NADH-dependent flavin oxidoreductase), protein degradation (e.g., 26S proteasome regulatory subunit, ubiquitin-specific protease), ATP-dependent RNA helicase (e.g., DEAD box protein ATP-dependent RNA helicase), and resistance pathways (e.g., multidrug resistance protein, ABC transporter essential for cadmium resistance). Real-time reverse transcription-PCR analysis further confirmed the results of microarray. Collectively, this study provides new insight into the biological functions of Cap1p in oxidative stress response.
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PMID:Cap1p is involved in multiple pathways of oxidative stress response in Candida albicans. 1654 88


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