Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of chronic ethanol administration on pulmonary antioxidant protection systems was investigated in male Sprague-Dawley rats exposed to room air or room air containing ethanol vapors for 5 weeks. Blood ethanol concentrations in ethanol-exposed rats were usually between 200 and 300 mg/dl. Glutathione, vitamin E, and malondialdehyde concentrations were measured in lung homogenates, and antioxidant enzyme activities (catalase, glutathione peroxidase, Cu/Zn-superoxide dismutase, glutathione reductase) were determined in the supernatant fractions. For comparison, the measurements were also made using liver fractions. Ethanol treatment increased the activities of catalase (117%) and Cu/Zn-superoxide dismutase (25%) in lung but not in liver. Although chronic ethanol inhalation lowered hepatic glutathione (19%) and hepatic vitamin E (33%), there was no increase in malondialdehyde content in either liver or lung of ethanol-exposed rats. The elevation of pulmonary antioxidant enzyme activities could be interpreted to mean that lung is a target for ethanol-induced oxidative stress. However, as there was no loss of pulmonary GSH or vitamin E and no increase in malondialdehyde formation, it appears that long-term ethanol exposure did not produce a significant degree of oxidative stress in rat lung.
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PMID:Antioxidant protection systems of rat lung after chronic ethanol inhalation. 208 23

In the lung of Rana perezi no differences as a function of age have been found for any of the five major antioxidant enzymes, reduced (GSH), oxidized (GSSG) or glutathione ratio (GSSG/GSH), oxygen consumption (VO2) and for in vivo or in vitro stimulated tissue peroxidation. This frog shows a moderate rate of oxygen consumption and a life span substantially longer than that of rats and mice. Chronic (2.5 months) catalase depletion in the lung did not affect survival or any additional antioxidant enzyme, GSH, GSSG or in vivo and in vitro lung peroxidation in any age group. Only the GSSG/GSH ratio and the VO2 were elevated in catalase depleted old but not young frogs. After comparison of these results with those obtained in other animal species by other authors we suggest the possibility that decreases in antioxidant capacity in old age be restricted to species with high basal metabolic rates. Nevertheless, scavenging of oxygen radicals can not be 100% effective in any species. Thus, aging can still be due to the continuous presence of small concentrations of O2 radicals in the tissues throughout the life span in animals with either high or low metabolic rates.
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PMID:Lung antioxidant enzymes, peroxidation, glutathione system and oxygen consumption in catalase inactivated young and old Rana perezi frogs. 208

The relationship between prolonged exercise, oxidative stress, and the protective capacity of the antioxidant defense system has been determined. Venous blood samples were removed from seven trained athletes before and up to 120 h after completion of a half-marathon for measurements of blood antioxidants, antioxidant enzymes, and indices of lipid peroxidation. Plasma creatine kinase (CK) activity, an index of muscle damage, increased (P less than 0.05) to a maximum 24 h after the race but this was not accompanied by changes in conjugated dienes and thiobarbituric acid reactive substances (TBARS), which are indices of lipid peroxidation. An increase (P less than 0.05) in plasma cholesterol concentration (4%) immediately after the race was similar to the change in plasma volume (6%). However, transient increases (P less than 0.05) immediately postrace in the plasma concentrations of uric acid (24%), vitamin A (18%), and vitamin C (34%) were only partly accounted for by the fluid shifts. The immediate postrace increases in alpha- and gamma-tocopherol did not attain statistical significance. Erythrocyte antioxidant enzyme activities were unaffected by the exercise but the alpha- and gamma-tocopherol concentrations progressively increased (P less than 0.001 and P less than 0.05, respectively) up to 48 h postrace. Paradoxically, 24 h after the race erythrocyte susceptibility to in vitro peroxidation was markedly elevated (P less than 0.01). This enhanced susceptibility to peroxidation was maintained even at 120 h postrace and did not correspond to changes in the age of the red cell population. A decrease (P less than 0.001) in total erythrocyte glutathione immediately after the half-marathon was mainly due to a reduction in the reduced form (GSH). The results show that when trained athletes run a comparatively short distance sufficient to result in some degree of muscle damage but which is insufficient to cause elevations in plasma indices of lipid peroxidation, significant alterations in erythrocyte antioxidant status do occur.
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PMID:Blood antioxidant status and erythrocyte lipid peroxidation following distance running. 222 20

Antioxidant enzyme activities, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and total glutathione concentration were determined in guinea pig lung and liver over the final period of gestation (days 50-68) and at several ages post-partum. Pulmonary antioxidant capacity increased markedly over the final days of gestation, individual changes ranging from 29% (glutathione) to 198% (GSH-Px). Liver antioxidant capacity was always 4-fold to 10-fold greater than that of the lung and exhibited very similar developmental profiles to those observed in the lung. From day 60 gestation to term (68 days), activity of the liver antioxidants increased, ranging from 246% (CAT) to 610% (glutathione). A number of antioxidants in both lung and liver exhibited either immediate pre- or post-birth decreases in activity. These falls could not be attributed to the way in which the results were expressed: i.e. they were similar, expressed per unit DNA, per unit protein, or per g wet wt. Following birth, liver antioxidant capacity increased such that the highest enzyme activities or glutathione concentration were recorded at 66 days post-partum. In lung, only Mn-SOD and glutathione exhibited higher levels at 66 days postpartum than at birth. In combination, these results of pulmonary and hepatic antioxidant enzyme activity indicate that the lung is not unique in acquiring increased antioxidant protection in the final period of gestation. They also suggest that a tissue's antioxidant requirement is dictated more by metabolic rate (hence free radical production) than incident partial pressure of oxygen.
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PMID:Developmental expression of antioxidant enzymes in guinea pig lung and liver. 235 Oct 72

The resistance of human pulmonary fibroblasts (WI-38) and human umbilical vein endothelial cells to oxygen toxicity (1 atm O2) was compared. Endothelial cells were more sensitive than fibroblasts. They contained also less antioxidant enzymes except for SOD: respectively 132%, 96%, 70%, 59%, and 21% of the SOD, GSH peroxidase, GSH reductase, catalase, and G6PD content of fibroblasts. However, they contained 1.81-fold more GSH than fibroblasts. Their lower content of antioxidant enzymes can explain their higher sensitivity to oxygen. The efficiency of natural antioxidant molecules and enzymes in the protection of cells incubated 3 days under 1 atm O2 was studied. alpha-tocopherol added in the culture medium led to a significant protection, contrary to the result for ascorbic acid. Microinjection of catalase, SOD, and GSH peroxidase directly into the cells was also tested: the protection was concentration dependent for both types of cells but SOD did not protect the endothelial cells. Lower activities of the other enzymes were needed to achieve protection of the endothelial cells, compared to fibroblasts. Since endothelial cells were also shown to display lower antioxidant enzyme activities, it can be hypothesized that their content is optimized for survival in physiological conditions.
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PMID:Comparative study of oxygen toxicity in human fibroblasts and endothelial cells. 238 Feb 55

Nitrogen dioxide (NO2), a major oxidant constituent of vehicle emissions, is toxic to lung cells including endothelial cells. Since NO2 is a reactive free radical, one of the postulated mechanisms of NO2-induced pulmonary injury involves the peroxidation of membrane lipids. Therefore, this study evaluated the dose- and time-dependent effects of nitrogen dioxide exposure by measuring the biochemical and biophysical parameters, as well as the metabolic function, in porcine pulmonary artery and aortic endothelial cells in monolayer cultures. To evaluate the biochemical changes, the antioxidant enzyme GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities, as well as the lipid peroxide formation, glutathione (GSH) content, and lactate dehydrogenase (LDH) release were measured. Biophysical changes were measured by monitoring lipid fluidity in both the hydrophobic and hydrophilic regions of the plasma membrane. The uptake of 5-hydroxytryptamine (5-HT) was measured as a metabolic function of endothelial cells. Confluent porcine pulmonary artery and aortic endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 hours. After 3-, 6-, or 12-hour exposures to 3 or 5 ppm NO2, the GSH-red and G6PDH activities, as well as the lipid peroxide formation and LDH release, were not different from those of controls in both pulmonary artery and aortic endothelial cells. Exposure of the cells to 3 or 5 ppm NO2 for 24 hours resulted in significant increases in GSH-red (p less than 0.05) and G6PDH (p less than 0.001) activities in both cell types. Exposure to 5 ppm NO2 for 24 hours significantly (p less than 0.05) increased lipid peroxide formation and increased (p less than 0.01) LDH release in both the pulmonary artery and aortic endothelial cells. GSH-per activity and GSH content in NO2-exposed pulmonary artery and aortic endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. Fluorescence spectroscopy was used to measure the membrane lipid fluidity. Membrane fluidity in the hydrophobic region was measured by 1,6-diphenyl-1, 3, 5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical and metabolic response to nitrogen dioxide-induced endothelial injury. 247 62

1. A number of dietary sugars are known to mediate the effects of copper deficiency. The effects of lactose (compared with sucrose) and a dietary Cu deficiency on hepatic and cardiac antioxidant enzyme activities and tissue mineral element status were investigated in the rat. 2. Groups (n 6) of male weanling Wistar rats were provided ad lib. with deionized water and diets containing sucrose (580 g/kg) or sucrose and lactose (387 g/kg and 193 g/kg respectively) with either control (12.0 mg/kg) or deficient (1.5 mg/kg) quantities of Cu for 77 d. 3. Animals consuming the low-Cu diets exhibited significantly decreased tissue Cu levels (P less than 0.01), hepatic and cardiac cytochrome c oxidase (EC 1.9.3.1, CCO) activities (P less than 0.01 and P less than 0.001 respectively) and hepatic Cu-zinc superoxide dismutase (EC 1.15.1.1, CuZnSOD) activity (P less than 0.05). The low-Cu diets also significantly decreased cardiac manganese superoxide dismutase (EC 1.15.1.1, MnSOD), catalase (EC 1.11.1.6) and glutathione peroxidase (EC 1.11.1.9, GSH-Px) activities (P less than 0.01, P less than 0.05 and P less than 0.001 respectively). 4. Hepatic Mn was significantly increased in both lactose-fed (P less than 0.001) and Cu-deficient (P less than 0.01) animals. These increases were unrelated to hepatic MnSOD activity. Cardiac Zn was significantly (P less than 0.01) increased in Cu-deficient animals. 5. Lactose feeding resulted in significantly increased cardiac CCO activity (P less than 0.001) but significantly decreased hepatic CuZnSOD (P less than 0.05), catalase (P less than 0.01) and GSH-Px (P less than 0.001) activities. 6. The activities of lactose dehydrogenase (EC 1.1.1.27, LDH) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49, G6PDH) were found to be significantly (P less than 0.05 and P less than 0.01 respectively) increased in Cu-deficient animals and G6PDH activity was significantly (P less than 0.01) decreased as a result of lactose consumption. 7. The observed changes in antioxidant enzyme activities associated with both Cu deficieny and lactose consumption may have important implications for the development of free radical mediated cell damage. However, no significant differences in either hepatic or cardiac levels of thiobarbituric acid reactive substances, a measure of lipid peroxidation, were found.
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PMID:Effects of copper deficiency on hepatic and cardiac antioxidant enzyme activities in lactose- and sucrose-fed rats. 253 51

The effects of culture duration on primary cultured mouse hepatocyte antioxidant levels (superoxide dismutase, catalase, glutathione peroxidase, vitamin E, and glutathione) and susceptibility to glucose oxidase (GO)- and hydrogen peroxide (H2O2)-induced cell killing and lipid peroxidation were examined. Membrane fatty acid composition was also evaluated. Adult male B6C3F1/CrlBR mouse hepatocytes were isolated by collagenase perfusion of the liver and cultured on 60-mm plastic dishes in Leibovitz's L-15 medium supplemented with glucose (1 mg/ml), dexamethasone (1 microM), fetal bovine serum (10%, v/v), and gentamicin sulfate (50 micrograms/ml) for 0 hr (freshly isolated cells) to 96 hr. Hepatocyte toxicity (determined by lactate dehydrogenase release and lipid peroxidation) after a 2-hr exposure to GO (0.8-80 micrograms/ml) or H2O2 (1-5 mM) decreased with increased time in culture. This decreased hepatocyte sensitivity to GO and H2O2 toxicity was not related to antioxidant enzyme activity since superoxide dismutase, catalase, and glutathione peroxidase declined during the 96-hr culture period. In contrast, glutathione and vitamin E levels in the cultured hepatocytes rose to 274.9 +/- 8.3% and 220.6 +/- 18.6% of the levels in freshly isolated cells (129.6 +/- 11.5 nmol and 0.10 +/- 0.01 nmol per 10(6) hepatocytes, respectively). The percentage of polyunsaturated fatty acids in hepatocyte phospholipids and triglycerides decreased with culture duration while the percentage of oleic acid increased in esterified and free fatty acid pools after 2 hr in culture. Total fatty acids were not affected by time in culture. These results suggest that the decreased hepatocyte susceptibility to the toxic effects of hydrogen peroxide may have been due to elevations in cellular GSH and vitamin E levels and decreases in membrane polyunsaturated fatty acids. The data also indicate that hepatocytes in primary culture undergo changes in antioxidant levels and fatty acid composition that may affect free radical toxicity at different times in culture.
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PMID:Effects of culture duration on hydrogen peroxide-induced hepatocyte toxicity. 278 69

Evidence has been obtained that implicates the generation of reactive oxygen species as an early and critical event in the promotion of neoplastic transformation in mouse JB6 cells. The time courses for specific inhibition by CuZn-superoxide dismutase (CuZn-SOD) of the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced promotion of neoplastic transformation in JB6 cells and for changes in antioxidant enzyme activities associated with TPA-exposure were examined. The antipromoting effect of CuZn-SOD was found to be critically dependent on the time of addition of CuZn-SOD relative to the start of a 14-day exposure of cells to TPA. Treatment of JB6 P+ Clone 22 and Clone 41 cells with CuZn-SOD for 18 h before, simultaneously with or up to 1 h after exposure to TPA, all inhibited promotion of transformation maximally. Delay of addition of CuZn-SOD by 2 h or more after the start of TPA treatment resulted in a marked decrease in the promotion inhibitory effect. CuZn-SOD added 24 or 48 h after TPA had no effect on promotion of transformation. Exposure of JB6 cells to 0.2- (superoxide anion radical) generated exogenously by the aerobic xanthine oxidase reaction resulted in promotion of neoplastic transformation that was prevented by concurrent addition of CuZn-SOD. Taken together these studies provide evidence that increased superoxide anion generation within the first 2 h following TPA exposure is an essential event in promotion of transformation in JB6 cells. Upon TPA exposure, JB6 Clone 41 cells exhibited time-specific activity changes in the cellular SOD, glutathione peroxidase (GSH-Px), and catalase. SOD and GSH-Px activities were reduced to 54% and 26% respectively of basal levels within 2 h of TPA treatment. GSH-Px activity recovered to basal levels within 4 h and CuZn-SOD within 48 h. Catalase activity was maximally reduced to 50% of basal within 1 h after TPA treatment and rebounded to greater than basal levels within 4 h. It is postulated that a c-kinase-dependent event induces rapid elevation of superoxide anion following TPA exposure and that this leads to reduced activity of antioxidant enzymes. Since antipromotion by exogenous CuZn-SOD is effective only during the first 2 h following TPA exposure, this suggests that the promotion-relevant 0.2- elevation is transient.
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PMID:Early superoxide dismutase-sensitive event promotes neoplastic transformation in mouse epidermal JB6 cells. 282 3

It was demonstrated that cysteine and D-penicillamine are able to replace reduced glutathione to some extent in the glutathione peroxidase reaction. An in vivo study was made of the role played by--SH compounds in the antioxidant enzyme system involved in the detoxication of the LD50 of paraquat (PQ), and hence of their role in the detoxication of PQ. The effectiveness was D-PA greater than GSH greater then Cys in the liver and GSH greater than Cys greater than D-PA in the lung.
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PMID:Effects of various thiols on paraquat toxicity. 286 90


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