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.
Alcohol Clin Exp Res 1990 Dec
PMID:Antioxidant protection systems of rat lung after chronic ethanol inhalation. 208 23

Although supplemental fatty acids have been shown to alter the susceptibility of experimental animals to oxidant gases, the relationship between the degree of tissue fatty acyl unsaturation and resistance to oxidant exposure remains undefined. Because vascular endothelial cells have been demonstrated to be sensitive cellular targets in oxidant-induced lung injury, we evaluated the effects of a supplemental fatty acid on the lipid composition and oxidant susceptibility of pulmonary artery endothelial cells (PAEC) in monolayer culture. PAEC were incubated in culture medium supplemented with an ethanolic solution of 0.1 mM cis-vaccenic acid (CVA), an 18-carbon monounsaturated fatty acid, or with the ethanol vehicle alone for 3 h. Cells were then exposed to either control or oxidant (hyperoxia: 95% O2; or hydrogen peroxide: 100 microM) conditions. Oxidant-induced cell injury was assessed by phase-contrast microscopy and by measuring the release of intracellular lactate dehydrogenase. Incubation with CVA increased the CVA content of PAEC lipids and protected cells from oxidant-induced injury for up to 72 h after supplementation. CVA had no effect on nonoxidant-induced cell injury. Although the mechanism by which CVA protects cells against oxidant injury remains undefined, evidence is presented that indicates the mechanism does not involve induction of antioxidant enzyme activity, alterations in the physical state of PAEC membranes, or enhancement of PAEC nucleic acid repair mechanisms. These results define a useful model for exploring the relationship between lipid composition and oxidant susceptibility and suggest that fatty acid modifications may constitute an important strategy for protecting cells against oxidant injury.
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PMID:Fatty acid supplementation protects pulmonary artery endothelial cells from oxidant injury. 222 2

The ethanol-preferring (EP) rats have a higher level of lipid peroxidation in the brain and blood serum than the water-preferring rats. At the same time it was found that EP rats have a decreased antioxidant enzyme activity in the brain tissue (catalase and superoxide dismutase) and blood serum (ceruloplasmin and superoxide dismutase). This antioxidant status can lead to a greater sensitivity of the EP rat brain to ethanol toxicity. The increased catalase activity in blood of EP rats reflects the elevated metabolic tolerance of this group of animals to ethanol.
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PMID:[The characteristics of the enzyme status of the antioxidant protection and the level of lipid peroxidation in the brain tissue and blood of rats with differing preferences for ethanol]. 225 54

The effects of chronic intake of dietary alcohol upon left ventricular function, activities of myocardial antioxidant enzymes, reduced glutathione (GSH) content and lipoperoxidation (measured as the formation of diene conjugates and lipid-soluble fluorescence) were studied in adult domestic Nicholas turkeys. The non-invasive evaluation of left ventricular function by echocardiography revealed an impaired contractile function (the calculated fractional shortening values were 31.1 +/- 4.1% in the alcoholic group and 38.8 +/- 4.4% in the controls) and dilatation of the heart in the alcoholic birds. The changes in the non-invasive parameters of the left ventricle indicate that the adult Nicholas turkey developed congestive cardiomyopathy secondary to the ingestion of ethanol. In the hearts of normal adult turkeys, high GSH content (2.39 +/- 0.25 mumol/g wet weight) and superoxide dismutase activity were found, as compared to other animals, indicating the relatively higher development of antioxidant defence systems. Compared to the controls, significant increases were noted for all the antioxidant enzymes investigated (superoxide dismutase, catalase and glutathione peroxidase) and a moderately significant decrease in the GSH content was found in the left ventricle of alcoholic birds. The changes in GSH concentration and antioxidant enzyme activities might indirectly indicate some involvement of free radicals in the pathogenesis of ethanol-induced myocardial lesion. However, the levels of in vivo lipoperoxidation in the alcoholic birds did not significantly vary from those of control turkeys. Based on these findings, it appears that the reactive oxygen radicals may play a less important role in the pathogenesis of alcohol-induced cardiomyopathy in turkeys--probably due to the higher development of myocardial antioxidant defence systems.
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PMID:Alcohol-induced congestive cardiomyopathy in adult turkeys: effects on myocardial antioxidant defence systems. 343

We carried out a study to relate the effect of the type of dietary fat and ethanol on antioxidant enzyme mRNA levels in liver in the intragastric feeding rat model. Different types of dietary fat were administered [saturated fat (SE), corn oil (CE) and fish oil (FE)] with ethanol to induce varying severities of liver injury. Ethanol-fed rats were pair-fed with dextrose-fed controls that received isocaloric amounts of dextrose. All animals were killed at 1 month and the following studies were carried out: evaluation of severity of pathologic liver injury, mRNA quantitation for catalase, glutathione peroxidase (GPx), and manganese superoxide dismutase (MnSOD), microsomal conjugated dienes, and hydrogen peroxide. SE animals had no liver injury, FE animals had severe liver injury, and CE animals had moderate liver injury. Ethanol induced GPx mRNA in all dietary groups, with the highest levels seen in the FE group. The pattern of catalase mRNA induction was similar to that of GPx mRNA. In contrast, MnSOD mRNA was decreased compared to controls in animals that developed pathologic liver injury, i.e., CE and FE groups. A positive correlation was seen between conjugated diene levels and GPx mRNA (r = 0.88, P < 0.01) and catalase mRNA. The similar slopes for the relationship between conjugated dienes and catalase in the fish oil and non-fish oil groups indicate that the same degree of lipid peroxidation increases catalase mRNA to a greater degree in fish oil-fed rats. A positive correlation was also seen between catalase mRNA and H2O2 (r = 0.95, P < 0.001).
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PMID:Effect of type of dietary fat and ethanol on antioxidant enzyme mRNA induction in rat liver. 761 20

Studies on rats treated for 15 months with ethanol (10%, w/v, solution in drinking water) revealed that the stimulation of hepatic cytochrome P-450 monooxygenases activity was accompanied by enhanced microsomal malondialdehyde formation, a lipid peroxidation index and a decreased level of the antioxidant, alpha-tocopherol. The other components of the prooxidant/antioxidant system, diene conjugates and catalase, glutathione peroxidase and superoxide dismutase activities were unaffected. Oxidative stress in blood was shown by a significant decrease in the alpha-tocopherol level whereas lipid peroxidation and antioxidant enzyme activity remained unchanged. The prooxidative effect of ethanol was catalytically promoted by an iron overload (Fe-saccharate, 100 mg Fe3+/kg body wt. intraperitoneally, 2, 5 and 7 day before test) to simulate the effect of alcoholic hemochromatosis. Thus, the level of malondialdehyde and alpha-tocopherol in the serum may be recommended as biological markers of ethanol-provoked oxidative stress, which is especially useful in the evaluation of the combined effect of ethanol and other chemicals that affect the redistribution of active iron complexes.
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PMID:Biological markers of oxidative stress induced by ethanol and iron overload in rat. 771 62

A thiol-specific antioxidant enzyme (TSA), which provides protection against the inactivation of other enzymes by the thiol/Fe(III)/oxygen system, was previously isolated and cloned. We investigated the mechanism by which TSA protects biomolecules from oxidative damage caused by the thiol-containing oxidation system using the spin trapping method with 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Thiyl radicals from dithiothreitol (.DTT) were produced by horseradish peroxidase/H2O2 under aerobic and anaerobic conditions and by the Fe(III)/oxygen system. The formation of DMPO-.DTT radical adducts were inhibited by TSA regardless of the thiyl radical-generating conditions used. The active mutant C170S also quenched the signals of the radical adduct, whereas the inactive mutant C47S did not exert any effect. It was also found that C170S has a higher rate at the initial stage of the reaction than that of the native enzyme, although C170S failed to remove DMPO-.DTT radical adducts completely. These results indicate that only active TSA can catalyze the removal of thiyl radicals, and cysteine 47 is required for this activity. In addition, thiyl radicals react with oxygen to generate unidentified thiylperoxy species. Fe.EDTA reacts with this species to generate a reactive radical that can abstract hydrogen atom from ethanol to produce a hydroxyethyl radical. This reactive thiyl-oxygen radical is believed to be responsible for causing deleterious effects on biomolecules. Together, our data indicate that TSA protects biomolecules from oxidative damage by catalyzing the removal of thiyl radicals before they generate more reactive radicals. However, presently we cannot rule out the possibility that TSA can also use other thiol-containing species as substrates.
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PMID:On the protective mechanism of the thiol-specific antioxidant enzyme against the oxidative damage of biomacromolecules. 829 8

Male and female rats were used to investigate the effects of type of dietary carbohydrate (CHO), copper, and ethanol consumption on lung antioxidant enzyme activities and levels of phosphorylated compounds in whole blood. Copper-deficient female rats exhibited a greater degree of copper deficiency than males, as assessed by hepatic copper concentration and hepatic copper superoxide dismutase (CuSOD) activity. However, copper-deficient male rats fed fructose-containing diets exhibited greater growth retardation, anemia, and heart hypertrophy than females consuming the same diets and males fed starch. In addition, one of 10 copper-deficient male rats that ate a fructose-based diet and drank water and one of 10 copper-deficient male rats that ate a starch-based diet and drank ethanol died. Copper-deficient, starch-fed males exhibited the highest activities of glutathione peroxidase (GSH-Px) and catalase as compared with fructose-fed rats. Ethanol consumption elevated the activities of GSH-Px and catalase. Copper-deficient female rats exhibited higher catalase but lower GSH-Px activities than males. It is suggested that in copper deficiency, the ability to increase antioxidant enzyme activities in rats consuming starch is greater than in rats consuming fructose. Rats fed starch are provided with a greater degree of protection against oxidative damage than rats fed fructose. In addition, polyphosphorylated compounds in blood were reduced in copper-deficient male rats that consumed fructose-based diets. This may impair supply of oxygen to tissues.
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PMID:Antioxidant defense system in lung of male and female rats: interactions with alcohol, copper, and type of dietary carbohydrate. 854 77

Recent evidence has shown that alcohol as well as exercise induces oxidative stress. However, the combination of both on the cardiac antioxidant system is not known. This study investigates the interactive effects of exercise training and chronic ethanol consumption on the antioxidant system of the rat heart. Male Fisher-344 rats were treated as follows: 1) sedentary control (SC); 2) exercise training (ET) for 6.5 weeks; 3) ethanol (2 g/kg, PO) for 6.5 weeks, and 4) ET plus ethanol for 6.5 weeks. Rats were sacrificed and hearts were isolated. Glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and lipid peroxidation (MDA) were determined in heart tissues. SOD and GSH-Px activities were significantly increased 118% and 148% of SC, respectively, due to ET. GSH level increased 118% of SC in ET rats. GSH-Px activity increased 118% of SC whereas SOD activity and CuZn-SOD protein level and GR activity decreased 87%, 71%, and 90% of SC due to chronic ethanol administration. GSH level decreased 87% of SC and lipid peroxidation increased 149% of SC due to ethanol consumption. GSH-Px activity and GSH levels increased 143% and 130% of SC due to combination of ET and ethanol. This study suggests that ET and chronic ethanol ingestion augments the antioxidant enzyme activity and GSH levels in the heart. This combination reduced the extent of ethanol-induced lipid peroxidation. The data suggest that ET may reduce the extent of the damage caused by ethanol consumption on the myocardium.
Alcohol
PMID:Response of cardiac antioxidant system to alcohol and exercise training in the rat. 916 Aug 8

The effects of chronic ethanol intoxication on the open-field behavior, on antioxidant enzyme activities, and the degree of lipid peroxidation were investigated. Rats consuming a liquid diet containing 7% ethanol for 4, 7, 14, or 21 days exhibited a significantly decreased ambulation activity, accompanied by a reduced frequency and duration of explorative rearing in an open-field task 4, 7, and 14 days after chronic ethanol ingestion, whereas presumed adaptation to the neurologic effects of ethanol was observed on day 21. Changes in the activities of glutathione peroxidase (GSH-Px): glutathione reductase (GSH-R), and catalase, and in the content of reduced glutathione (GSH) in blood samples were determined by means of biochemical methods. The degree of lipid peroxidation was measured via thiobarbituric acid assays. Chronic ethanol ingestion elicited a significant increase in GSH-Px activity (by a maximum of approximately 32% on day 14), whereas opposite alterations in GSH-R and catalase activities were recorded (49% of the control value on day 4 and 17% on day 21, respectively). Highly elevated contents of thiobarbituric acid reactive substances reflected extensive lipid peroxidation processes throughout the experiment. These changes indicate that ethanol toxicity induces profound changes in explorative behavior, mediated, at least partly, by changes in the free radical metabolism.
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PMID:Chronic ethanol ingestion-induced changes in open-field behavior and oxidative stress in the rat. 926 91


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