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)

The role of different antioxidant pathways in cultured rat pleural mesothelial cells was studied by exposing the cells to various hydrogen peroxide (H2O2) concentrations and by measuring H2O2 cell cytotoxicity and the capacity of the cells to scavenge H2O2. The antioxidant enzymes, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and catalase were analyzed biochemically. Catalase and CuZn superoxide dismutase were localized by immunocytochemistry. To enable investigation of the glutathione redox cycle and catalase pathways, glutathione reductase was inactivated with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and catalase was inactivated with aminotriazole. When the cells were exposed to a low, sublethal (0.030 mM) H2O2 concentration, glutathione reductase but not catalase inactivation resulted in a decreased capacity to remove H2O2 from the extracellular medium. When the cells were exposed to a high (0.25 mM) H2O2 concentration, H2O2-scavenging capacity decreased remarkably when catalase was inactivated. When the cells were exposed to 0.1 to 0.5 mM H2O2, cell cytotoxicity (lactate dehydrogenase release) increased significantly if glutathione reductase was inactivated; catalase inactivation resulted in a significant cytotoxicity only at high (greater than or equal to 0.25 mM) H2O2 concentrations. Immunocytochemical studies showed that the cells, both in situ and in vitro, contained low amounts of catalase. This suggests that the results of the catalase-inhibition studies are probably not due to a change in the characteristics of the cells in culture. 3-Aminobenzamide is a compound that is known to prevent NAD depletion through inhibition of poly(ADP-ribose) polymerase during oxidant stress. When intact cells were treated with different antioxidants and exposed to 0.5 mM H2O2, both catalase and 3-aminobenzamide protected the cells completely.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antioxidant defense mechanisms in cultured pleural mesothelial cells. 162 38

A model of liver hyperplastic noduligenesis was induced in rats in vivo by long-term administration of thioacetamide (TAM; 100 mg/kg day i.p.). Three doses of 50 mg/kg of an antitumoral rhodium(III) complex were administered at 14, 9 and 5 days before the end of TAM treatment. Blood and liver were obtained from either TAM, Rh(III) complex or TAM plus Rh(III) complex-treated rats in order to determine the interaction of both (tumoral and antitumoral) substances with the biochemical pathways related to glutathione redox cycle, enzyme activities involved in the oxidative stress coupled to the NADPH/NADP pair and enzymes related to the mono-oxygenase P450 system. The results showed that TAM induced an imbalance between the activities of glutathione-coupled enzymes. Glutathione reductase activity increased along with the intoxication, while glutathione peroxidase activity decreased. Alterations in the activity of soluble glutathione peroxidase were parallel to those of catalase. These results, together with decreased activities of enzymes related to cytochrome P450 mono-oxygenase system, NADPH cytochrome P450 reductase and NADH cytochrome b5 reductase, suggest that liver cells are not protected against the peroxidative stress produced by chronic administration of TAM. The Rh(III) complex did not produce significant changes in the parameters assayed when administered alone. When this complex was administered to TAM-treated rats, significant restoration of the following activities was observed: those of NADPH-generating enzymes (glucose-6-phosphate dehydrogenase and malic enzyme), that of glutathione reductase (NADPH-consuming enzyme), NADPH-cytochrome P450 reductase and total catalase. These results, together with others in previous studies, suggest that the altered liver function induced by chronic administration of TAM can be partially restored by this rhodium complex. The mechanisms by which this complex counteracts the TAM-induced changes have not yet been established.
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PMID:Alterations in hepatic peroxidation mechanisms in thioacetamide-induced tumors in rats. Effect of a rhodium(III) complex. 167 54

The effect of hyperthyroidism on liver glutathione (GSH) metabolism was studied in fed rats after the administration of 0.1 mg T3/kg body wt, for 1-3 consecutive days. T3-calorigenesis resulted in elevated rates of O2 consumption by the liver, together with higher lipid peroxidative processes and GSH depletion, compared to the euthyroid state. The study of the enzymes related to GSH metabolism revealed no significant changes in the activity of glutathione peroxidase and glutathione reductase, with decreases (27-41%) in the activity of glutathione-S-transferases and marked elevation (133%) in that of gamma-glutamyl transferase, 3 days after T3 treatment. At this experimental time, the activity of the NADPH generating enzyme glucose-6-phosphate dehydrogenase was enhanced by 84% in the liver of T3-treated rats, compared to that in the controls. In these conditions, the canalicular efflux of GSH was not altered by T3, whereas net and fractional rates of sinusoidal GSH efflux were enhanced by 86% and 288%, respectively. The latter effect of hyperthyroidism was found in parallel with an enhancement in sinusoidal lactate dehydrogenase and protein release, suggesting that loss of GSH might be related to a permeabilization of the hepatocyte plasma membrane. Liver GSH turnover assessed after a pulse of [35S]cysteine resulted in a 209% increase in the fractional turnover rate in hyperthyroid rats over controls, under steady state conditions for both hepatic GSH pools, leading to a 62% enhancement in the respective turnover flux. Data suggest that the elevation in the sinusoidal GSH efflux from the liver and in the hepatic capacity to degrade the tripeptide are major mechanisms leading to GSH depletion in the liver of T3-treated rats. As the increased GSH use is not balanced by the elevation in GSH synthesis, a lower steady state level of GSH is attained in the liver.
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PMID:Effects of hyperthyroidism on rat liver glutathione metabolism: related enzymes' activities, efflux, and turnover. 167 89

Rats treated with diets containing 20 ppm of alpha- or gamma-hexachlorocyclohexane (HCH) for 15 or 30 days showed increased levels of liver cytochrome P-450 followed by increased production of both thiobarbituric acid reactants by liver homogenates and microsomes and superoxide anion production by liver microsomes. In these animals superoxide dismutase (SOD) activity was also increased. In consequence, the ratio between SOD activity and microsomal superoxide radical (O2-.) production showed a slight increase after 15 days of treatment. However, after 30 days, there was a tendency for this ratio to decrease. Other parameters studied were liver glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase and catalase (CAT) activities. Among them, only CAT activity showed a 26% and 38% increase after 15 or 30 days of treatment with the alpha-isomer. It is suggested that when lipid peroxidation is involved in the mechanism of toxicity of a xenobiotic, this parameter can be used to determine the no-observed-effect level.
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PMID:Liver lipid peroxidation-related parameters after short-term administration of hexachlorocyclohexane isomers to rats. 170 74

The concentration of reduced glutathione in the erythrocytes of rats was significantly decreased 24-72 hr after the rats were treated with 300 mg commercial hexachlorocyclohexane/kg body weight (one-third of the LD50), given ip. The activities of glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase were also significantly decreased 24 hr after treatment but there was no change in glutathione peroxidase activity. The results suggest that hexachlorocyclohexane produces significant changes in the glutathione redox system of rat erythrocytes leading to oxidative membrane damage.
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PMID:Oxidative damage and changes in the glutathione redox system in erythrocytes from rats treated with hexachlorocyclohexane. 171 6

The influence of intratracheally instilled bleomycin (10 mg x kg-1) on antioxidant enzyme activity as well as on lipid peroxidation product levels after 7 and 14 days from drug administration in rat lungs was investigated. The 200-400% increase in superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase and glucose-6-phosphate dehydrogenase activities were observed, as compared to control group. The levels of malondialdehyde, conjugated dienes and lipid hydroperoxides in lung tissue of bleomycin-treated rats were also higher than those in control group. These phenomena are the signs of adaptative mechanisms induction in lungs, protecting the tissue from dangerous effect of bleomycin-generated free radicals.
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PMID:[The influence of intratracheal bleomycin instillation on peroxidative processes in rat lung tissue]. 172 38

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial beta-oxidation was unaffected and peroxisomal beta-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC 1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and glutathione peroxidase (EC 1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC 3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.
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PMID:Metabolic effects of coconut, safflower, or menhaden oil feeding in lean and obese Zucker rats. 176 Apr 46

The effect of chronic administration of doxorubicin on the rat heart and liver glutathione redox system was studied. Rats were administered doxorubicin, 1 mg/kg, ip., three times a week, on Monday, Wednesday and Friday. One week was skipped and then the cycle repeated for a total of one, four, seven or ten doses. It was determined that treatment in this manner had no effect on rat heart glutathione, glutathione peroxidase or glucose-6-phosphate dehydrogenase, at any of the time intervals tested. However, hepatic glutathione content was found to be moderately increased after the fourth dose and glucose-6-phosphate dehydrogenase activity was found to be markedly increased after the seventh and tenth doses. Hepatic glutathione peroxidase was not affected. These results suggest that the cardiac glutathione redox system does not respond to chronic administration of doxorubicin. In contrast, the hepatic systems do respond, which may explain the apparent resistance of this organ to doxorubicin toxicity.
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PMID:The effect of chronic administration of doxorubicin on the rat cardiac and hepatic glutathione redox system. 177 21

A concentration-response and C x T study were undertaken to determine the effect of phosgene (COCl2) inhalation on pulmonary antioxidant processes as determined by changes in endogenous glutathione (GSH) and antioxidant-associated enzymes (GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase). Rats were exposed to 0.0, 0.1, 0.25, 0.5, and 1.0 ppm phosgene for 4 hr and 0.25 ppm phosgene for 8 hr. The endpoints were assayed at 0, 1, 2, 3 and 7 days after exposure cessation. The lowest effective concentration was 0.1 ppm phosgene (increases in measured variables from 8 to 35% above control values). At all concentrations, major effects were observed 1 to 2 days after exposure (12 to 159% above control), peaking at 2 to 3 days postexposure (11 to 253% above control), and in some cases were still evident 7 days (10 to 65% above control) after exposure. The C x T study using the same dose (120 ppm-min), but different times and concentration (0.25 ppm for 8 hr and 0.5 ppm for 4 hr), showed a concentration dependence. The peak antioxidant enzyme changes observed for the higher concentration (0.5 ppm) were at least double those observed for the lower concentration (0.25 ppm). These enzyme changes were similar to those reported for the oxidants O3 and NO2. Although the suspected mechanism of initial damage between phosgene and these oxidants is different (acylation vs oxidation) the biological result is similar (i.e., damage, repair, and influx of cells), thus eliciting similar biochemical changes in response to pulmonary injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of inhaled phosgene on rat lung antioxidant systems. 177 56

While performing its functions in olfaction, modification of inspired air, and protection of the lower respiratory tract from high concentrations of potentially harmful inhalants, the nasal mucosa can be injured by a number of inhalants. In this study, F344/N male rats were exposed to filtered air or hyperoxia (85 or 87% oxygen), 24 hr/day, 7 days/week, for 1 (acute exposure) or 11 (chronic exposure) weeks. There were distinct differences between the different epithelial regions examined in replicative and morphologic responses as well as altered enzyme activities in response to oxygen exposure. Neither acute nor chronic hyperoxic exposure caused degenerative, necrotizing, or inflammatory changes in any of the nasal epithelial examined. Hyperoxia-induced hypertrophy, but not hyperplasia, of the non-ciliated cuboidal (NCC) epithelium occurred after both acute and chronic exposure. Cell replication was increased in portions of the NCC and respiratory epithelia after acute hyperoxia exposure. There were significant increases, compared to controls, in the specific activity of glucose-6-phosphate dehydrogenase in the nasal turbinates, maxilloturbinates, and lateral wall epithelium (NCC epithelium), the nasal septum (respiratory epithelium), and the ethmoturbinates (olfactory epithelium), and in the specific activity of glutathione peroxidase in the NCC epithelium and ethmoturbinates after acute hyperoxia exposure. The specific activity of cytochrome P450-dependent monooxygenase-catalyzed O-deethylation of 3-cyano-7-ethoxycoumarin was significantly decreased, compared to controls, in the NCC epithelium. These results suggest that hyperoxia exposure induces morphologic and biochemical alterations in nasal epithelia which appear to be protective responses of certain cell types to hyperoxia.
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PMID:Biochemical and morphologic responses of rat nasal epithelia to hyperoxia. 177 57


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