UNIPROT:P04040 - FACTA Search

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Query: UNIPROT:P04040 (Catalase)
3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Environmental tobacco smoke (ETS) is a pervasive contaminant in the workplace. Our objective was to determine the oxidative stress effects of ETS on employees who are exposed. The results provide information that is useful to the resolution of risk assessment questions associated with ETS. We analyzed two blood draws from volunteers in our control and exposed groups. The level of exposure to ETS was determined through plasma cotinine measurements, which showed a 65% increase from the control group to the exposed group. Exposure to ETS resulted in a statistically significant increase of 63% of the oxidative DNA mutagen 8-hydroxy-2'-deoxyguanosine in the blood of exposed subjects. This oxidative DNA damage has been linked to an increased risk of developing several degenerative chronic diseases, including coronary heart disease and cancer. The exposed subjects also had increased levels of superoxide dismutase, catalase, glutathione peroxidase (GPOX), and glutathione reductase. However, these increases were only statistically significant in catalase and GPOX. Catalase levels were 13% higher in the exposed group, and GPOX levels were 37% higher in exposed volunteers. The biochemical evidence suggests that exposure to ETS causes oxidative stress, resulting in DNA damage that may increase the risk of certain diseases.
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PMID:Environmental tobacco smoke in the workplace induces oxidative stress in employees, including increased production of 8-hydroxy-2'-deoxyguanosine. 948 89

Antioxidant enzyme activities were measured following exposure to hypericin +/- irradiation in EMT6 cells. CuZnSOD and catalase activities peaked within 0.5 h following irradiation for nontoxic 0.5 microM hypericin and toxic 1.0 microM hypericin. Catalase remained elevated up to 3 h for 1.0 microM hypericin + light. MnSOD activity was elevated immediately following irradiation for both doses. These levels returned to control by 1 h for 0.5 microM hypericin, but were depressed after 1 h for 1.0 microM hypericin. This suggests that mitochondria impairment may be a critical factor in hypericin phototoxicity. Glutathione reductase was inhibited immediately following irradiation with 1.0 microM hypericin, suggesting that an altered status of the glutathione pool contributed to cytotoxicity. Glutathione peroxidase activities were elevated following irradiation but returned to control levels within 0.5 h for both doses, implicating hydroperoxide formation as an early event in hypericin phototoxicity. Inhibition by hypericin in the dark was demonstrated for purified CuZnSOD, Se-dependent glutathione peroxidase, glutathione S-transferase, and glutathione reductase activities in vitro. Irradiation did not potentiate hypericin-mediated glutathione reductase inhibition and decrease inhibition for the other enzymes. Collectively, these data demonstrate an antioxidant enzyme response to hypericin photoactivation and confirm a role for oxygen in hypericin phototoxicity.
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PMID:Antioxidant enzyme response to hypericin in EMT6 mouse mammary carcinoma cells. 958 12

In the framework of an INTAS project, arctic populations of the clam Macoma balthica were collected from seven stations (Mezen, Khaypudyr, Pechora 3, Pechora 5, Dvina, Keret 1, and Keret 2) in the White Sea and Pechora Sea. The main objectives of this research were to define baseline concentrations of trace metals (As, Cd, Cr, Cu, Fe, Mn, Pb, Zn) in M. balthica and to evaluate antioxidant responses as biomarkers of anthropogenic stress in these organisms. The antioxidant parameters examined included the levels of glutathione and the activities of several glutathione-dependent and antioxidant enzymes: glyoxalase I and glyoxalase II (EC 4.4.1.5 and EC 3.1.2.6), glutathione S-transferases (EC 2.5.1.18), glutathione reductase (EC 1.6.4.2), glutathione peroxidases (EC1.11.1.9 and EC 2.5.1.18, respectively, for Se-dependent and Se-independent forms), superoxide dismutase (SOD, EC 1.15.1.1), and catalase (EC 1.11.1.6). Organisms revealed enhanced concentrations of lead in both Keret stations, Khaypudyr, and Mezen, and high levels of copper in Keret and cadmium in Khaypudyr. At the biochemical level, organisms from Pechora 3, Pechora 5, and Dvina were not statistically different, whereas those from Mezen and Khaypudyr exhibited higher activities of superoxide dismutase, glutathione peroxidase, and glyoxalase II. Catalase levels were lower in Mezen and Khaypudyr. More heterogeneous were the responses of glyoxalase I and glutathione S-transferases, while no significant differences among the stations were observed for glutathione reductase. Multiple regression analyses revealed significant positive relationships between the main antioxidant enzymes (glutathione peroxidases, superoxide dismutase, glyoxalase I, and glyoxalase II), and confirmed the exception of catalase, which, when significant, was negatively correlated with the other parameters. The results support the suitability of antioxidant responses as biomarkers of pollutant exposure and/or toxicity for arctic biomonitoring programs even though only moderately polluted sites were sampled.
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PMID:Trace metals and variations of antioxidant enzymes in Arctic bivalve populations. 977 77

This study investigates the dose- as well as time-dependent effects of ethanol ingestion on antioxidant system and lipid peroxidation in plasma of the rat. The plasma ethanol concentrations were 154+/-18, 231+/-53, and 268+/-49 mg/dl 1 h after oral ethanol doses of 2, 4, and 6 g/kg, respectively. Superoxide dismutase (SOD) (71%, 56%, and 41 % of control) and glutathione reductase (GR) (71%, 66%, and 55% of control) activity in plasma were significantly decreased in a dose-dependent manner. Catalase (CAT)/SOD and glutathione peroxidase (GSH-Px)/SOD ratios were significantly increased whereas GR/GSH-Px ratio was significantly decreased with increasing dose of ethanol. In a time course study, plasma ethanol concentrations were 177+/-9.7, 143+/-11, 99+/-17, and 26+/-11 mg/dl at 1.5, 2, 4, and 6 h after an oral dose (4 g/kg) of ethanol in rat indicating time-dependent elimination of ethanol. Plasma SOD and GSH-Px activity significantly increased 4-6 h whereas GR activity significantly decreased 2-4 h after ethanol ingestion. The ratio of GR/GSH-Px and the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) in plasma decreased at 1.5-6 h after ethanol ingestion. Plasma malondialdehyde (MDA) levels significantly elevated with respect to an increase in time after ethanol ingestion, indicating time-dependent augmentation of lipid peroxidation. The data indicate that ethanol ingestion perturbs the plasma antioxidant system in a dose- and time-dependent manner. The significant changes in the ratios of CAT/SOD, GSH-Px/SOD, GR/GSH-Px, and GSH/GSSG in plasma may be used as an index of alcohol-induced oxidative stress.
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PMID:Dose- and time-dependent effects of ethanol on plasma antioxidant system in rat. 1006 76

Using cultured human endothelial cells, we investigated the contribution of concentrations of magnesium to the antioxidant system and oxidative stress. Cells were cultured at decreasing magnesium levels (569, 380, 190 and 95 microM) for 72 h. We then measured the amount of released hydrogen peroxide (H2O2) from the cells, the consumption of exogenous H2O2, the intracellular reduced glutathione (GSH) and the oxidized glutathione (GSSG) contents and the activities of glutathione reductase and catalase. Magnesium at a level of 949 microM was used as a control. The effect of magnesium deficiency on cellular membrane permeability was determined by measurement of the amount of [14C] amino acid mixture released from the cells. The results showed that during 72 h of magnesium-deficient treatment, the H2O2 release from the cells gradually increased and consumption of exogenous H2O2 was enhanced during the first 48 h of treatment. GSH content gradually decreased but GSSG was not affected. The activity of glutathione reductase was first stimulated and then inhibited. Catalase activity was gradually reduced. [14C]Amino acid mixture release from the cells continuously increased. We suggest that magnesium deficiency affected the intracellular antioxidant system in cultured endothelial cells.
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PMID:Influence of low magnesium concentrations in the medium on the antioxidant system in cultured human arterial endothelial cells. 1019 96

Over the last decade, much evidence has emerged to suggest that alterations in maternal nutrition during pregnancy may irreversibly affect aspects of physiological and biochemical functions in the fetus. This study was designed to determine the mechanisms involved in these alterations. Our hypothesis was that the type of maternal dietary fat received in early life could determine the level of lipoprotein lipase (LPL; EC 3.1.1.34) activity and gene expression which would be maintained into later life. A diet high in (n-3) polyunsaturated fatty acids was predicted to be associated with higher levels of lipoprotein lipase (LPL) activity and expression and lower levels of plasma triglyceride after a high fat meal challenge. Using a 2x2 factorial design, Wistar Albino rats were pair-fed either a fish oil diet (50 g/kg) or a mixed oil diet (50 g/kg) for the last 2 wk of gestation, during lactation and pups were fed these diets until 5 wk of age. After 5 wk, the rats were fed nonpurified diet. The rats were killed at 5 wk (young) or 10 wk (adult) of age after a mixed oil (50 g/kg) test meal. There were significant age effects on plasma triglyceride (P<0.02), cholesterol (P<0.001), glucose-dependent insulinotrophic polypeptide (GIP) (P<0.001) and liver glutathione reductase activity (P<0.05) which were all higher in the young rats compared to the adults. There were significant effects of diet on triglyceride (P<0.001), cholesterol (P<0.001) and LPL mRNA levels (P<0.001). GIP and triglyceride levels were significantly correlated (r = 0.66; P<0.001). Omental adipose tissue LPL activity as significantly higher in the fish-oil fed groups compared to the other groups (P<0.001), whereas Epididymal adipose tissue LPL mRNA was significantly higher in the mixed oil-fed adults compared to the other groups (P<0.001). The latter result suggested an imprinting effect of fatty acid composition in early life on LPL gene expression. Liver superoxide dismutase activity was affected by age and diet and was higher in the young than in the adults and higher in the fish oil-fed young than in those fed the mixed oil-fed (P<0.005). Catalase activity was also affected by age (P<0.001) and diet (P<0.001), and there was a significant interaction between age and diet (P<0.001). Catalase activity was higher in rats fed fish oils at both stages of development, suggesting that feeding fish oils to rats in early life raises oxidative stress throughout life. The majority of the significant differences shown were between the age groups and not between the two dietary groups, suggesting that postprandial handling of a standard fat meal is affected more by age than by early dietary fatty acid composition. However, the mechanisms of biological imprinting of fatty acids on LPL expression and on enzymes related to oxidative stress requires more investigation.
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PMID:Maternal and early dietary fatty acid intake: changes in lipid metabolism and liver enzymes in adult rats. 1072 Jan 61

While programmed cell death is induced by a variety of internal and external stimuli, including reactive oxygen species, the anti-apoptotic protein Bcl-2 is involved in opposing cell death and affects the antioxidant status of cells. Since the exact mechanism of its action is uncertain, in this study we examined the role of Bcl-2 using a loss of function model, Bcl-2 knockout mice. The consequence of Bcl-2 knockout was assessed in kidneys, liver and brain, using protein carbonyls and cellular levels of antioxidant enzymes as markers of oxidative stress. Kidney extracts from 8 days-old Bcl-2-knockout mice had 59% higher content of protein carbonyls relative to the wild type, but similar levels of oxidized proteins at the age of 30 days. By marked contrast, in liver and brain, levels of protein carbonyls were similar at 8 days but by 30 days the liver of knockout animals (and brains, as we have shown previously) show 36% higher protein carbonyls. Measures of glutathione reductase (GRX), glutathione transferase (GST) and catalase revealed significantly higher levels in kidneys of 8 days old Bcl-2-knockout mice compared to wild type. By 30 days activities of glutathione-related enzymes and catalase increased and abolished the differences between the knockout and wild type. At 8 days, in liver there were no significant differences in activities of all enzymes between the mice, however by 30 days, the specific activity of GRX was significantly higher in Bcl-2-knockout mice, relative to controls. From day 8 to day 30 there was an increase in liver catalase activity that resulted in significantly higher levels in Bcl-2-knockout animals. Catalase activity in brains of Bcl-2-knockout, 8 days old mice was significantly higher compared to the wild type, and significantly lowers at 30 days. Taken together our findings indicate that Bcl-2 knockout results in significant perturbations of oxidative metabolism and antioxidant status of in kidney, liver and brain. Such changes are tissue specific with respect to age, magnitude and type of enzyme affected.
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PMID:Developmental changes in antioxidant enzymes and oxidative damage in kidneys, liver and brain of bcl-2 knockout mice. 1072 70

Effect of repeated oral administration of hexachlorocyclohexane (HCH) (10 and 20 mg/kg body weight/day for 7 and 30 days) on the antioxidant defense system and lipid peroxidation (LPX) of rat cerebral hemisphere (CH) was evaluated. The level of LPX was elevated after 7 days of treatment in crude homogenate (endogenous and FeSO(4)- and ascorbic acid-stimulated) and subcellular fractions except the nuclear fraction in which induction was seen after 30 days. The pesticide elicited a significant decrease in the activities of cytosolic total and CN(-)-sensitive superoxide dismutase (SOD) after 7 and 30 days of HCH treatment, but failed to evoke any change in CN(-)-resistant SOD. Catalase activity decreased throughout the treatment period. Cerebral glutathione peroxidase activity (both selenium-dependent and -independent isoenzymes) and the level of glutathione content were decreased after 7 and 30 days of treatment, respectively. Activity of glutathione reductase and content of ascorbic acid, however, were enhanced following the pesticide exposure. The results suggest that repeated HCH administration induced oxidative stress in rat CH.
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PMID:Mediation of oxidative stress in HCH-induced neurotoxicity in rat. 1079 Apr 96

Electron spin resonance (ESR) spin trapping measurements provide evidence for the generation of hydroxyl radicals (*OH) in the reduction of Cr(VI) by glutathione reductase (GSSG-R) in the presence of NADPH as a cofactor. Catalase inhibited the *OH generation, while the addition of H2O2 enhanced it, indicating that the *OH radical generation involves a Fenton-like reaction. The metal chelator, deferoxamine, inhibited the *OH generation with a concomitant generation of a deferoxamine nitroxide radical. EDTA and 1,10-phenanthroline also inhibited the *OH generation. Experiments performed under argon atmosphere decreased the yield of the *OH formation, showing that molecular oxygen plays a critical role. ESR spin trapping and measurements of fluorescence change of scopoletin in the presence of horseradish peroxidase show that reduction of Cr(VI) by GSSG-R/NADPH generates superoxide anion radicals (O2*-) as well as H2O2. It can be concluded that *OH radical is generated by the reaction of H2O2 with Cr(V), which is produced by enzymatic one-electron reduction of Cr(VI). H2O2 is produced by the reduction of molecular oxygen via O2*- as an intermediate. The *OH radicals generated by these reactions are capable of causing DNA strand breaks, which can be inhibited by catalase, formate, and experiments performed under argon.
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PMID:Role of molecular oxygen in the generation of hydroxyl and superoxide anion radicals during enzymatic Cr(VI) reduction and its implication to Cr(VI)-induced carcinogenesis. 1090 8

The distribution of antioxidants between bundle sheath and mesophyll cells of maize leaves was analysed in plants grown at 20 degrees C, 18 degrees C and 15 degrees C. The purity of the isolated bundle sheath and mesophyll fractions was determined using compartment-specific marker enzymes. In plants grown at 15 degrees C, ascorbate peroxidase, CuZn-superoxide dismutase (CuZn-SOD) and monodehydroascorbate reductase activities were increased in the bundle sheath cells, and glutathione reductase, dehydroascorbate reductase and monodehydroascorbate reductase activities were enhanced in the mesophyll cells. SOD was absent from the mesophyll of plants grown at 20 degrees C but an Fe-SOD activity was found in the mesophyll of plants grown at 15 degrees C. Foliar Mn-SOD activities were decreased at 15 degrees C compared to 20 degrees C. Catalase was undetectable in the mesophyll extracts of plants grown at 15 degrees C. Ascorbate and glutathione contents were considerably higher in the mesophyll than the bundle sheath fractions of plants grown at 20 degrees C. The ratios of reduced to oxidized forms of these antioxidants were significantly decreased in the bundle sheath, but increased in the mesophyll of leaves grown at 15 degrees C. Foliar H2O2 accumulated at 15 degrees C compared to 20 degrees C. Most of the foliar H2O2 was localized in the mesophyll tissues at all growth temperatures. The differential distribution of antioxidants between leaf bundle sheath and mesophyll tissues, observed at 20 degrees C, is even more pronounced when plants are grown at 15 degrees C and may contribute to the extreme sensitivity of maize to low temperatures.
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PMID:Low temperature-induced changes in the distribution of H2O2 and antioxidants between the bundle sheath and mesophyll cells of maize leaves. 1093 1

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