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:1.11.1.9 (glutathione peroxidase)
22,002 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Filarial parasites, Litomosoides carinii and Setaria cervi, showed great susceptibility to the oxidants generated in vitro by the xanthine/xanthine-oxidase system. In order to counteract such injurious effects, both the filariids possessed an active antioxidant enzymes system. Superoxide dismutase, catalase and glutathione peroxidase were detected in appreciable amounts but glutathione reductase and glucose-6-phosphate dehydrogenase in very low quantities. The former three enzymes were also found to be released by the parasites into the ambient medium. The released enzymes may be responsible for scavenging the host-generated oxidants present in the immediate surroundings of the parasites and thereby enabling them to live comfortably in the host. This Institute-based antifilarial agent namely Compound 82/437 which is 2,2'-dicarbomethoxylamino-5,5'-dibenzimidazolylketone, markedly inhibited catalase and glutathione peroxidase of both L. carinii and S. cervi. The compound, therefore, appears to render the filariids prone to H2O2 toxicity leading to penultimate damage.
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PMID:Antioxidant system of Litomosoides carinii and Setaria cervi: effect of a macrofilaricidal agent. 149 6

Effect of organophosphorus insecticide, phosphomidon (250 and 500 ppm) on human erythrocyte and plasma were studied in vitro to get insight into the cellular antioxidant defence mechanism and malondialdehyde formation. The antioxidant defence system of erythrocyte was altered as evident by depression of glutathione reductase, glucose 6 phosphate dehydrogenase, whereas the level of reduced glutathione, glutathione peroxidase, glutathione-S-transferase, superoxidedismutase and catalase were stimulated. In the case of plasma fraction, glutathione reductase, glutathione peroxidase, glutathione-s-transferase, glucose-6-phosphate dehydrogenase, superoxide dismutase and levels of reduced glutathione were significantly depressed and the malondialdehyde formation and catalase activity were elevated indicating the less adaptive response of plasma to protect it from oxidative damage.
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PMID:Effects of organophosphorus insecticide phosphomidon on antioxidant defence components of human erythrocyte and plasma. 150 21

Oral administration of K2Cr2O7 to male albino rats at an acute dose of 1500 mg/kg body wt/day for 3 days brought about sharp decrease in the activities of glucose-6-phosphate dehydrogenase and glutathione reductase of kidney epithelial cells. The scavenging system of kidney epithelium is also affected as evident by the highly significant fall in the activities of glutathione peroxidase, superoxide dismutase and catalase which ultimately leads to the increase in lipid peroxidation value in kidney cortical homogenate. However, glutathione-s-transferase activity in cytosol and glutathione and total thiol content in cortical homogenate were not altered. Chronic oral administration of K2Cr2O7 (300 mg/kg body wt/day) for 30 days to rats lead to elevation in the activities of glutathione peroxidase, glutathione reductase, glutathione-s-transferase, superoxide dismutase and catalase with no change in glucose-6-phosphate dehydrogenase activity in epithelial cells. This might lead to the increase in glutathione and total thiol status and decrease in lipid peroxidation value in whole homogenate system.
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PMID:Impact of chromium on lipoperoxidative processes and subsequent operation of the glutathione cycle in rat renal system. 151 15

To investigate how alveolar macrophages adapt themselves to oxidative pollutants in the long term, rats were exposed to a strong oxidant, ozone (O3), or a weak oxidant, nitrogen dioxide (NO2), for a maximum duration of 12 wk. After exposures, alveolar macrophages were collected by pulmonary lavage. Throughout 11 wk of exposure to 0.2 ppm O3, the specific activities of glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase of the peroxidative metabolic pathway and pyruvate kinase and hexokinase of the glycolytic pathway were 40-70% elevated over the controls in alveolar macrophages. The population of alveolar macrophages was consistently 60% higher than the controls. The small-sized macrophages, immature macrophages, preferentially increased. To the contrary, the thymidine incorporation per cell was always 20-30% lower than in the controls, although the total incorporation remained unchanged. No infiltration of polymorphonuclear leukocytes occurred. By 12 wk of exposures to 1.2 and 4.0 ppm NO2, the population of alveolar macrophages increased 30% over the control. Among the enzymes examined, however, only the G6PDH activity increased 10% for 4.0 ppm NO2. No increase in the enzyme activities occurred for 1.2 ppm NO2. Based on these results, alveolar macrophages adapt themselves to the long-term exposure of O3 or NO2 by recruiting immature macrophages through an apparent influx of monocytes. During the exposure to O3, the peroxidative metabolic and glycolytic pathways are enhanced persistently in alveolar macrophages, whereas both pathways were not enhanced by the exposures to NO2.
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PMID:Long-term effects of ozone and nitrogen dioxide on the metabolism and population of alveolar macrophages. 153 82

Preconditioning the heart with 5 min of ischemia renders the heart very resistant to infarction from subsequent ischemia by an unknown mechanism. We investigated whether the protective effect of preconditioning might be related to an increase in rabbit heart antioxidant defenses. The antioxidant activities of catalase, glutathione peroxidase, Mn superoxide dismutase, Cu,Zn superoxide dismutase, glucose-6-phosphate dehydrogenase, glutathione reductase, and total glutathione were measured in ischemic and normal regions from both control and preconditioned rabbit hearts. All hearts experienced 30 min regional ischemia and 5 min reperfusion. None of the antioxidant enzymes changed in activity when comparing nonischemic and postischemic zones in either nonpreconditioned or preconditioned hearts. Total glutathione, however, was reduced in reperfused zones and showed better preservation in preconditioned hearts. To determine whether this preservation resulted from a higher value at the onset of reperfusion or slower washout during reperfusion, we analyzed a second group of nonreperfused hearts after 30 min ischemia. The hearts had normal glutathione content in both ischemic and nonischemic zones of either preconditioned or control hearts. The most likely explanation is that preconditioned hearts experienced less washout of glutathione simply because they were less injured. We therefore conclude that enhancement of antioxidant defenses is not the mechanism of preconditioning.
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PMID:Protection from reperfusion injury by preconditioning hearts does not involve increased antioxidant defenses. 153 19

The c14CoS/c14CoS mouse has a homozygous deletion of about 1.2 cM on chromosome 7 that includes the albino (c) locus. The untreated 14CoS/14CoS newborn has been reported to exhibit a marked transcriptional activation of the hepatic NAD(P)H:menadione oxidoreductase (Nmo-1; DT diaphorase; quinone reductase; azo dye reductase) gene, as well as elevated UDP glucuronosyl-transferase (UGT1*06) and glutathione transferase (GT1) activities, when compared with the cch/cch wild-type and the cch/c14CoS heterozygote. We show here that the newborn hepatic activities of seven enzymes that play a role in the oxidative stress response--NMO1, UGT1*06, GT1, copper-zinc superoxide dismutase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase--are increased 1.5- to 25-fold in 14CoS/14CoS, as compared with ch/ch and ch/14CoS mice. The activities of four additional enzymes having no known association with the oxidative stress response--benzo[a]pyrene hydroxylase (CYP1A1, cytochrome P(1)450), acetanilide 4-hydroxylase (CYP1A2, cytochrome P(3)450), lactate dehydrogenase (LDH), and NADPH-cytochrome c reductase--are not significantly different among the three genotypes. These data suggest that there exists an "oxidative stress" response in the untreated 14CoS/14CoS newborn. We postulate that a chromosome 7 regulatory gene, which we have named Nmo-1n, might encode a trans-acting negative effector of the Nmo-1 gene, and genes corresponding to the other elevated enzymic activities described above. When both copies of Nmo-1n are deleted, as is the case in 14CoS/14CoS mice, a battery of genes involved in oxidative stress is released from negative control and becomes activated--despite the absence of any apparent oxidative insult by foreign chemicals.
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PMID:"Oxidative stress" response in liver of an untreated newborn mouse having a 1.2-centimorgan deletion on chromosome 7. 154 Jan 61

To investigate the effects of dietary protein and polyunsaturated fat levels on tissue lipid peroxidation and antioxidative enzymes, Long-Evans male weanling rats were fed either an 8% lactalbumin diet containing 2% (L2), 5% (L5), 10% (L10), 15% (L15) or 20% (L20) soybean oil or a 20% lactalbumin diet containing 5% (N5) or 20% (N20) soybean oil for 8 weeks. The tissue thiobarbituric acid-reactive substances (TBARS) concentrations of the L2 group were similar to those of the N5 group except in plasma in which they were higher. The L5 group generally showed tissue TBARS concentrations comparable to the N20 group. Gradually increasing the dietary soybean oil level in the low protein diet further increased the tissue TBARS concentrations. The L20 group had significantly higher TBARS in RBC, liver, heart, kidney and muscle than the N20 group. The low protein-fed groups had lower activities of glutathione peroxidase (EC 1.11.1.9), superoxide dismutase (EC 1.15.1.1) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49) in liver and catalase (EC 1.11.1.6) in RBC than the N5 group. Compared with the N5 group, the N20 group also showed higher TBARS concentrations and lower activities of certain antioxidative enzymes in some tissues. The antioxidative enzyme activities decreased more drastically with the increasing dietary soybean oil level in the low protein-fed groups than in those fed a normal level of protein. Supplementation of 150 mg/kg of all-rac-alpha-tocopheryl acetate to the L15 diet slightly decreased the TBARS in plasma, heart and liver and restored the depressed activities of RBC superoxide dismutase and catalase. The results indicated that insufficiency of dietary protein aggravates the enhanced production of TBARS and the reduced activities of antioxidant enzyme in rats fed a high soybean oil diet.
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PMID:Protein insufficiency aggravates the enhanced lipid peroxidation and reduced activities of antioxidative enzymes in rats fed diets high in polyunsaturated fat. 156 72

The effect of age on the glutathione antioxidant system and its acinar distribution in rat liver was studied. GSH/GSSG ratio in blood and liver was lower in old than in young rats. Hepatic glutathione peroxidase and glutathione S-transferase activities were higher in old than in young rats, whereas hepatic gamma-glutamyl transpeptidase activity was lower in old than in young rats. Glutathione reductase and glucose-6-phosphate dehydrogenase activities did not change with age in rat liver. Total glutathione levels and glutathione peroxidase activity were higher in periportal than in perivenous areas of young rats, but this heterogeneous distribution did not occur in old rats. No change with age was found in hepatic zonation of glutathione reductase and glucose-6-phosphate dehydrogenase.
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PMID:Effect of aging on metabolic zonation in rat liver: acinar distribution of GSH metabolism. 156 87

Studies were performed to determine the effects of chronic hypoxia on enzymes that catalyze various detoxication reactions. Rats were exposed to room air or 10.5% O2 for 10 days, and microsomes and postmicrosomal supernatants were isolated from liver. Detoxication enzyme activities were measured by radiochemical and spectrophotometric assays, and immunoreactive protein amounts were measured by Western blot analysis. Total cytochrome P450, as measured by the CO-difference spectrum, and activities of superoxide dismutase (EC 1.15.1.1), epoxide hydrolase (EC 4.2.1.63), catalase (EC 1.11.1.6), glutathione disulfide reductase (EC 1.6.4.2), and glutathione (GSH) S-transferase (EC 2.5.1.18) were not affected by this extent of hypoxia. In contrast, 10 days of hypoxia decreased activities or immunoreactivities (% of aerobic) of GSH peroxidase (EC 1.11.1.9) (54%), cytochrome P450EtOH2 (42%), CYP3A1 (53%), sulfotransferase (EC 2.8.2.1) (77%) and UDP-glucuronosyltransferase (EC 2.4.1.17) (65%). Activity of glucose-6-phosphate dehydrogenase (EC 1.1.1.49), an important enzyme in NADPH production was also decreased to 56% of the aerobic value, but Western blot analysis showed that the amount of protein reactive with antibodies to glucose-6-phosphate dehydrogenase was not affected by hypoxia. Thus, hypoxia may decrease activity of enzymes by regulatory mechanisms even though the amount of immuno-detectable enzyme is unchanged. Liver cells isolated from rats exposed to hypoxia also gave lower GSH synthetic rates than cells from normoxic rats. This result, together with the effect of hypoxia on glucose-6-phosphate dehydrogenase, indicates that the GSH supply for GSH-dependent detoxication reactions may be limited due to chronic hypoxia. To test directly whether chronic hypoxia increased sensitivity to a compound normally detoxified by a GSH-dependent reaction, sensitivity to tert-butyl hydroperoxide (t-BuOOH) of hepatocytes from rats exposed to in vivo hypoxia was compared to that from normoxic rats. The results showed that the cells from the hypoxic rats were much more sensitive to injury. Taken together, these results suggest that decreases in amounts and/or activities of detoxication enzymes during chronic hypoxia may result in increased susceptibility of cells to chemical injury.
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PMID:Effect of chronic hypoxia on detoxication enzymes in rat liver. 161 Apr 6

Previous reports from our laboratory showed that rats fed a polyunsaturated fatty acid-rich diet (UC), during an acute intervals, present important changes in macrophage metabolism and function, while a saturated fatty acid diet (SC) did not induce significant changes (10). In this study, two important questions were addressed: 1. the persistence of the changes induced by the UC and 2. the effect of a SC offered during ageing. The maximal activities of hexokinase, glucose-6-phosphate dehydrogenase, glutaminase, citrate synthase and glutathione peroxidase and the total content of lipid peroxides were measured in resident and inflammatory macrophages of rats fed control chow (CC), UC or SC during 14 months. Intraperitoneal cell migration by thioglycollate injection and the phagocytosis capacity were also evaluated. The results indicate that: 1) the changes caused by UC are exacerbated during ageing, and 2) the SC, given during a prolonged period of time, also caused important alterations of macrophage metabolism and function.
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PMID:Metabolic and functional changes in macrophages of rats fed polyunsaturated or saturated fatty acid rich-diets during ageing. 162 81


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