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)

To explore the effects of cadmium (Cd) exposure of tilapia (Oreochromis niloticus) on hepatic glutathione (GSH) metabolism, tilapias were exposed to 3.0 mg/L Cd for 1, 5, 10, 20, and 40 days. The contents of reduced GSH and oxidized GSH (GSSG) and the activities of enzymes involved in GSH metabolism and the GSSG-GSH ratio were investigated. The results showed that reduced GSH were depleted progressively whereas the GSSG-GSH ratio increased. The activities of selenium-dependent glutathione peroxidase, glutathione S-transferase and glucose-6-phosphate dehydrogenase, and GSSG levels increased initially and decreased subsequently but still higher than the controls. Glutathione reductase activity dropped on the 40th day. A transient increase in gamma-glutamylcysteine syntheses activity was detected on the 20th day. The findings demonstrated that the hepatic GSH pool showed different reaction patterns associated with exposure period. The homeostatic mechanism was activated by short-term Cd exposure while the response ability weakened for a longer exposure.
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PMID:Effects of waterborne Cd exposure on glutathione metabolism in Nile tilapia (Oreochromis niloticus) liver. 1679 7

Low-dose acetylsalicylic acid (ASA) treatment is a standard therapeutic approach in diabetes mellitus for prevention of long-term vascular complications. The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). Blood glucose, glycated hemoglobin, as well as plasma ALT and AST activities increased in rats with streptozotocin-induced experimental diabetes. The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. We did not observe increased accumulation of membrane lipid peroxidation products or altered levels of reduced glutathione in livers. The linear correlation between blood glucose and glycated hemoglobin in diabetic animals was distorted upon ASA treatment, which was likely due to a chemical competition between nonenzymatic protein glycosylation and protein acetylation. The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. Otherwise, some decrease in these parameters was noted in ASA-treated nondiabetic animals. Increased ASA-induced G6PDH activity was recorded in both diabetic and nondiabetic rats. While both glycation due to diabetic hyperglycemia and ASA-mediated acetylation had very similar effects on the activities of all studied enzymes but G6PDH, we conclude that non-enzymatic modification by either glucose or ASA may be a common mechanism of the observed convergence.
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PMID:Antioxidative enzyme and glutathione S-transferase activities in diabetic rats exposed to long-term ASA treatment. 1681 74

Caffeic acid (CA) and Trolox are phenolic acids that have beneficial antioxidant effect, but the underlying mechanisms involved are not fully understood. The extent to which CA and Trolox protect against sodium nitroprusside (SNP)-induced oxidative cell injury was investigated in cultured rainbow trout gill cells. The cells exposed to SNP for 24 h displayed a dose-dependent leakage of lactate dehydrogenase (LDH) and decreased cell viability as indicated by the MTT assay (mitochondrial dehydrogenase activity). Both effects were prevented by treatment with 50 microM CA or Trolox. CA or Trolox, protected against SNP-induced caspase-3 activation and DNA fragmentation, indicating a reduction of apoptosis. Thus, the results indicate that SNP induced cell death is caspase-3 related apoptosis and the treatment with CA inhibited the apoptotic pathway. In addition, we studied the effect of CA and Trolox on expression of zinc-responsive antioxidant genes such as metallothioneins (MT), glutathione-S-transferase (GST Class pi) and glucose-6-phosphate dehydrogenase (G6PD) in cultured gill cells. CA, 100 microM, increased accumulation of mRNA for MTA, MTB, GST and G6PD in cells. Thus, in addition to its ability to sequester free radicals, CA may protect against oxidative stress through expression of zinc-induced antioxidant proteins. Because of these properties we suggest that CA could be a beneficial additive to fish feeds in aquaculture.
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PMID:Dietary phenolic antioxidants, caffeic acid and Trolox, protect rainbow trout gill cells from nitric oxide-induced apoptosis. 1711 65

The effect of prefeeding dehydrated amaranth leaves (AL), at 10 and 20% levels on hexachlorocyclohexane (HCH)-induced free radical stress in rat liver was evaluated. The HCH-induced raise in malonadialdehyde (MDA), conjugated dienes and hydroperoxides was diminished by AL. The effect of AL was highly effective with respect to reduction in these cytotoxic products, especially at 20% level. AL intake resulted in a significant increase in hepatic vitamin A and glutathione (GSH). However, the AL consumption reduced hepatic tocopherols. Feeding of AL at 10% level increased the hepatic glucose-6-phosphate dehydrogenase (G-6-PDH) activity while that at 20% level increased the hepatic glutathione reductase (GSSGR) as well, in addition to G-6-PDH. Amaranth leaves at 10 and 20% levels of feeding reduced the hepatic superoxide dismutase and glutathione peroxidase (GSH-Px) activities. The pre-feeding of AL resulted in the reversal of HCH-induced alteration in GSH-Px and G-6-PDH activities. The significant reduction in the level of glutathione S-transferase brought about by HCH was restored to control level by feeding 20% AL. It is concluded that the consumption of AL at 20% level produces reduction in the HCH-induced impairment of antioxidant status in rat liver.
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PMID:Amelioration of hexachlorocyclohexane-induced oxidative stress by amaranth leaves in rats. 1712 63

Northern leopard frogs Rana pipiens exposed to PCB 126 (3,3',4,4',5-pentachlorobiphenyl) were examined for hepatic oxidative stress. In a dose-response study, northern leopard frogs were injected intraperitoneally with either PCB 126 in corn oil (0.2, 0.7, 2.3, or 7.8 mg/kg body weight) or corn oil alone. In a time-course study, frogs received 7.8 mg/kg or corn oil alone, and were examined at 1, 2, 3, and 4 wk after dosing. Hepatic concentrations of reduced glutathione (GSH), thiobarbituric acid-reactive substances (TBARS), and total sulfhydryls (total SH), as well as activities of glutathione peroxidase (GSH-P), GSSG reductase (GSSG-R), glucose-6-phosphate dehydrogenase (G-6-PDH), and glutathione S-transferase (GSH-S-T) were measured. In the dose-response experiment, few effects were apparent 1 wk after dosing. In the time-course experiment, significant changes were observed in the 7.8-mg/kg group at 2 wk or more posttreatment. Hepatic concentrations of GSH and TBARS were higher than in corresponding controls at wk 3 and 4; the activities of GSSG-R and GSH-S-T were higher than in controls at wk 2 and 4; and the activity of G-6-PDH was increased at wk 2 and 4. These data collectively indicate that altered glutathione metabolism and oxidative stress occurred and were indicative of both toxicity and induction of protective mechanisms in frogs exposed to PCB. A similar delay in response was reported in fish and may relate to lower metabolic rate and physiological reactions in ectothermic vertebrates.
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PMID:Oxidative stress induced in PCB 126-exposed northern leopard frogs, Rana pipiens. 1736 21

Our objective was to elucidate a temporal profile of expression of antioxidant enzymes (AOEs) and glutathione redox status in rat liver under the influence of thyroid hormone (T3). The key AOEs, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx-1) and glutathione reductase (GR) were characterized at transcriptional, translational and biochemical levels after 24 h, 72 h and 120 h of treatment. In general, catalase and GPx-1 showed opposite responses in both transcription and translation. T3 treatment caused tightly coordinated downregulation of catalase. However, transcriptional changes of other AOEs over the different durations of treatment were not always reflected in their respective protein and/or activity levels. Discordance among transcripts, proteins and biological activities of AOEs suggested differential regulation by T3 at multiple levels. Reduced and oxidized glutathione were depleted in hyperthyroid rats. Though T3 exerted a positive stimulatory effect on glucose-6-phosphate dehydrogenase, it was not sufficient to compensate for massive glutathione depletion and impaired activities of GPx-1, GR and GST, disturbing the cellular redox status in the process. Apparently, while transcriptional induction of AOEs might be adaptive responses in conditions of oxidative stress, yet post-transcriptional regulation appeared to be the predominant mechanism of regulation of AOE expression.
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PMID:Differential expression profiles of antioxidant enzymes and glutathione redox status in hyperthyroid rats: a temporal analysis. 1756 43

The effect of prefeeding of dehydrated E. officinalis (amla) powder at 5 and 10% levels on hexachlorocyclohexane (HCH)-induced changes in multicomponent antioxidant system and lipid peroxides in rat liver was studied. HCH induced significant elevation in hepatic malondialdehyde, conjugated dienes and hydroperoxides. The prefeeding of amla at 10% level could decrease the formation of these lipid peroxides significantly. The HCH abuse resulted in a significant reduction in hepatic glutathione S-transferase (GST), glucose-6-phosphate dehydrogenase (G-6-PDH) and superoxide dismutase (SOD) activities with an elevation in the activities of glutathione peroxidase and gamma-glutamyl transpeptidase (GGT). On the other hand, the HCH-induced impairment in hepatic catalase, G-6-PDH and SOD activities were modulated by amla at the 10% level of intake. Prefeeding of amla at 5 and 10% levels appeared to reduce the HCH-induced raise in renal GGT activity. The results show the elevation of hepatic antioxidant system and reduction of cytotoxic products as a result of prefeeding of amla, which were otherwise affected by the HCH administration.
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PMID:Reduction of hexachlorocyclohexane-induced oxidative stress and cytotoxicity in rat liver by Emblica officinalis gaertn. 1756 87

The effects of intraperitoneal injection of diethyldithiocarbamate (DDC) on free radical processes were examined in brain, liver and kidney of goldfish (Carassius auratus). Levels of oxidatively modified lipids and proteins as well as the activities of antioxidant and associated enzymes were measured. Intraperitoneal injection of DDC at a concentration of 0.01 mg/g wet mass decreased SOD activities by about 30-50% after 48 and 168 h compared to corresponding sham-injected values. This treatment resulted in transient oxidative stress. Lipid peroxide content increased after DDC injection at all time points in the kidney, after 48 h in the liver and was elevated in most experimental groups in the brain. Thiobarbituric-acid reactive substances (end products of lipid peroxidation) rose within the first 48 h after injection, but returned to initial levels after 168 h. Two other indices of oxidative stress were also transiently modified: protein carbonyl levels in the brain and kidney increased 24h post-injection, and the low-molecular mass thiol content was reduced over the same period in all tissues examined. Activities of catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase showed differential responses to DDC treatment that rebounded by 168 h post-injection. Glutathione peroxidase activities were reduced by 60, 45 and 65% in the brain, liver and kidney, respectively, after 24h but rebounded thereafter. After 48 h post-injection with DDC significant decreases were also seen in liver and kidney catalase, GST activities in all three tissues, and kidney GR and G6PDH activities. In some cases, catalase, GST, GR and G6PDH activities transiently increased after 24 h. It was concluded that DDC injection depleted SOD and simultaneously stimulated lipid peroxidation, but did not require compensatory enhancement of other enzymatic defenses. Different actions of the superoxide anion in cellular metabolism and possible consequences of the impairment of superoxide dismutase are discussed.
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PMID:Diethyldithiocarbamate injection induces transient oxidative stress in goldfish tissues. 1766 2

Brain preconditioning refers to a wide range of treatments that induce a neuronal tolerance state where neuronal tissue become more resistant to a subsequent lethal insult. The mechanisms underlying the preconditioning-induced brain tolerance are not fully understood, but up-regulation of antioxidant enzymes activity has been suggested to play an important role. In order to test this hypothesis, evaluation of glutathione (GSH) scavenger system was carried out in mice showing the neuroprotective effect of NMDA preconditioning against quinolinic acid (QA)-induced seizures. NMDA is known to prevent seizures in 53% of the animals and completely prevent neural damage against QA. Mice were preconditioned by a non-convulsant NMDA dose (75 mg/kg, 10 ml/kg i.p.) 24 h before QA infusion (4 microl, 9.2 mM i.c.v.). GSH content and enzymatic activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) and glucose-6-phosphate dehydrogenase (G6PDH) were evaluated in the cerebral cortex and hippocampus 24 h after QA infusion. NMDA preconditioning and QA infusion did not alter GSH content, GR and G6PDH activities, however, an increase in GST activity was observed in the cerebral cortex from mice. Moreover, NMDA pretreatment was able to prevent the QA-induced decrease in hippocampal GPx activity, but it was not effective against the decreased cortical GPx activity. These results indicate that, although NMDA preconditioning and QA toxicity modulate the activity of some GSH related enzymes, GSH metabolism is not directly linked to the neuroprotective effect induced by NMDA preconditioning.
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PMID:Evaluation of glutathione metabolism in NMDA preconditioning against quinolinic acid-induced seizures in mice cerebral cortex and hippocampus. 1798 Mar 54

Bee's wax produced by honeybees is rich in polyphenols. As the polyphenols are thought to protect cell constituents against oxidative damage through scavenging of free radicals, the present work was undertaken to evaluate the effects of polyphenols extracted from bees wax on the oxidative stress induced by carbon tetrachloride (CCl4) in rats. The polyphenols extracted by 80% methanol from bee wax (PBW) were fed to Wistar rats at 100 mg/kg body weight and 200 mg/kg body weight for 14 days in order to study its antioxidative and antihepatotoxic effects against CCl4 (1.5 ml/kg body weight)-induced stress. On 15th day all the rats were sacrificed, blood was collected for serum and organs/tissues were excised for biochemical analysis. The results showed a significant decrease in hepatic antioxidant enzyme activities viz. catalase, glucose-6-phosphate dehydrogenase (G-6-PDH), glutathione peroxidase (GSH-Px), glutathione reductase, superoxide dismutase (SOD) and a significant increase in glutathione S-transferase (GST) and gamma-glutamyl transpeptidase (GGT) by CCl4, probably due to the peroxidative effects. The prophylactic use of PBW at 200 mg/kg level resulted in a significant increase in CCl4-induced reduction in catalase, G-6-PDH, GSSGR and SOD. The hepatic levels of lipid peroxides viz. malondialdehyde, conjugated dienes and lipid hydroperoxides, enhanced by the administration of CCl4 were brought down by the ingestion of PBW at a level of 200 mg/kg. The hepatotoxicity caused by the administration of CCl4 was reduced significantly. Hence, it is concluded that the polyphenols from bees wax exhibit hepatoprotective and antioxidative properties in
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PMID:Bees wax polyphenols as suppressor of CC1--induced oxidative stress in rats. 1847 90


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