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)

We investigated the ability of plasma membrane CoQ reductase (PMQR) purified from pig liver to reduce phenoxyl radicals of a vitamin E homologue, Trolox. We report that NADH-driven one-electron reduction of CoQ0 catalyzed by PMQR produced CoQ0 semiquinone radical and CoQoH2. These in turn, recycle vitamin E homologue, Trolox, via reducing its phenoxyl radical. A significant part of NADH/PMQR-catalyzed reduction of CoQ0 (and Trolox recycling) was superoxide-dependent. Overall, our results demonstrate that PMQR in the model system used can act as an antioxidant enzyme that recycles water-soluble homologues of coenzyme Q and vitamin E.
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PMID:Plasma membrane NADH-coenzyme Q0 reductase generates semiquinone radicals and recycles vitamin E homologue in a superoxide-dependent reaction. 964 71

In rats with five-sixths nephrectomy (remnant kidney), blood pressure, glomerulosclerosis, and proteinuria are significantly reduced by administration of the angiotensin-converting enzyme inhibitor enalapril, during 16 weeks after reduction of the nephron number. The activity of catalase in remnant-kidney cortex homogenate is not influenced by enalapril treatment; the activities of superoxide dismutase and glutathione peroxidase are significantly increased. Elevated lipid peroxidation in cortex homogenates, evaluated by malondialdehyde and 4-hydroxynonenal concentrations, is not changed by treatment. Supplementation of dietary vitamin E to enalapril treatment does not alter antioxidant enzyme activities when compared to enalapril monotherapy. These results show that enalapril improves the balance between reactive oxygen intermediates and antioxidant enzymes in the remnant-kidney cortex of the rat. This finding may in part explain the protective effect of angiotensin-converting enzyme inhibitors on the progression of glomerulosclerosis.
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PMID:Enalapril increases antioxidant enzyme activity in renal cortical tissue of five-sixths-nephrectomized rats. 1052 41

The effect of dietary vitamin E on plasma, red blood cells (RBC), hepatic antioxidant status, and antioxidant enzyme activities was investigated. Three groups of six Sprague-Dawley rats were fed 0, 100, or 1,500 ppm vitamin E for eight weeks. Plasma alpha-tocopherol level was increased significantly by increasing dietary vitamin E (p < 0.05). Plasma lipid peroxidation (thiobarbituric acid-reactive substances) stimulation by 1 mM t-butyl hydroperoxide was correlated with dietary vitamin E level and was significantly greater in rats fed no vitamin E than in rats fed 100 or 1,500 ppm vitamin E (p < 0.05). RBC reduced glutathione (GSH) level was positively correlated with dietary vitamin E and was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed 0 or 100 ppm vitamin E (p < 0.05). RBC oxidized glutathione was negatively correlated with dietary vitamin E. GSH redox status was expressed as the GSH-to-total GSH ratio; the ratio was also positively correlated with dietary vitamin E and was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed no vitamin E (p < 0.05). For antioxidant enzymes, superoxide dismutase activity in hepatic cytosolic fraction was significantly greater in rats fed 1,500 ppm vitamin E than in rats fed 100 ppm vitamin E. Hepatic GSH reductase activity was significantly greater in rats fed 100 ppm vitamin E than in rats fed no vitamin E (p < 0.05). Dietary vitamin E had no effect on plasma vitamin C and protein thiol levels. In the systems studied, results indicated that dietary vitamin E selectively influences plasma vitamin E level, RBC GSH status, and hepatic cytosolic superoxide dismutase and GSH reductase activities.
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PMID:Effect of dietary vitamin E on antioxidant status and antioxidant enzyme activities in Sprague-Dawley rats. 991 18

Atherosclerosis has been known for many years, yet its etiology remains unknown. Hypercholesterolemia is a major risk factor for atherosclerosis. The mechanism by which it triggers endothelial injury is not known. Since the role of the antioxidant vitamin E on experimental atherosclerosis is inconsistent, the present study was undertaken to evaluate platelet lipid peroxidation and the role of vitamin E (alpha-tocopherol) as protective factor in atherosclerosis in rhesus monkeys. A significant decrease in serum cholesterol and serum triglyceride levels was found in the group of animals which were reverted to stock diet along with vitamin E injections after 9 months of atherogenic diet feeding. Decreases in malonyldialdehyde levels and antioxidant enzyme activities were less significant in animals continued on an atherogenic diet feeding along with vitamin E as compared with animals fed a stock diet with vitamin E supplementation. The overall observations in this study suggest that antioxidant status and lipid peroxidation could be partly restored with vitamin E supplementation in experimental atherosclerosis. Damage to endothelial cells destroys their antithrombotic status and leads to fatal thrombosis. alpha-Tocopherol offers the best hope, but the question is how much of it should be administered for the prevention of atherosclerosis.
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PMID:Effect of antioxidant vitamin E as a protective factor in experimental atherosclerosis in rhesus monkeys. 1054 74

This study investigated the effect of feeding broilers with diets differing in dietary fat source (lard, sunflower oil, olive oil) and vitamin E (basal vs supplemented with 200 mg of alpha-tocopheryl acetate/kg) on meat lipid oxidative stability. The diets differed by their degree of unsaturation and included the natural antioxidant alpha-tocopherol (vitamin E). Glutathione peroxidase (GSHPx) activity was measured in raw meat and ranged from 3.62 to 8.06 nmol NADPH/min/mg protein. The enzyme activity was influenced by the degree of unsaturation of the diet. Capillary gas chromatography analyses showed that dietary alpha-tocopherol accumulated in the muscle tissue and contributed to a better oxidative stability of the raw and cooked meat. Thigh meat alpha-tocopherol levels ranged from 2.73 to 3.62 microg/g in unsupplemented chickens whereas levels from 8.69 to 13.37 microg/g were observed in the thigh meat from alpha-tocopherol supplemented animals. The inclusion of olive oil and alpha-tocopherol in the animal diet gave lower thiobarbituric acid reactive substance (TBARS) values and lower GSHPx activity. High correlations were found between the parameters studied. The results suggest that the glutathione peroxidase activity could be used as an indicator of the meat oxidative stability. A negative relationship was observed between GSHPx activity and tissue alpha-tocopherol levels, and a positive relationship was evidenced between TBARS and antioxidant enzyme activity.
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PMID:Glutathione peroxidase activity, TBARS, and alpha-tocopherol in meat from chickens fed different diets. 1055 83

The aim of this study was to better understand the effects of more or less unsaturated fat source (tallow/soy oil/rapeseed oil) and/or vitamin E dietary supplementation (200 ppm) on the antioxidant status (at day 1 post-mortem) of turkey muscles [pectoralis major (Pm) and sartorius (S)]. More particularly, when turkeys were fed tallow, supplementation was sufficient to improve significantly the vitamin E status. Feeding rapeseed oil increased the antioxidant enzyme (AOE) activities (catalase, superoxide dismutase, glutathion reductase), glutathione concentration, and value from the benzoic acid test. Dietary soy oil increased glutathione peroxidase activity, compared to other dietary fat sources. With tallow, most of AOE activities were lower than with rapeseed or soy oil. Whatever the feeding mode, vitamin E supplementation did not affect the AOE activities, glutathione concentration, or values from the benzoic acid test. AOE activities were always higher in the oxidative S muscle than in the glycolytic Pm muscle. After feeding tallow, 9 days of storage increased TBA-RS and carbonyl contents, whereas the activity of many antioxidant enzymes and the total antioxidant activity (TEAC test and benzoic acid test) decreased.
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PMID:Influence of dietary fat and vitamin E on antioxidant status of muscles of turkey. 1056 78

A disturbed embryonic antioxidant defense mechanism may play a major role in diabetes-induced teratogenesis. We therefore studied the antioxidant capacity of 10.5-day-old rat embryos and their yolk sacs after culture for 28 hr in vitro under diabetic conditions (3 mg/ml glucose, 2 mg/ml beta-hydroxybutyrate (BHOB) and 10 microg/ml of acetoacetate), as compared with control embryos in vitro. We found a high rate of congenital anomalies, decreased growth and protein content, and a decrease in the activity of both superoxide dismutase (SOD) and catalase (CAT) under diabetic conditions, as compared with controls. The reducing power, which reflects the concentration and type of water-soluble and of lipid-soluble low-molecular-weight antioxidants (LMWA), was measured by cyclic voltammetry. Generally, LMWA were reduced in the embryos and yolk sacs under diabetic conditions. In the water-soluble fraction of control embryos and yolk sacs, two peak potentials were found, indicating two major groups of LMWA, while only one peak potential was found under diabetic conditions, indicating that an entire group of LMWA is missing. HPLC studies have demonstrated a decrease in vitamin C (water-soluble fraction) and in vitamin E (lipid-soluble fraction) under diabetic culture conditions, and an increase in uric acid. Generally, the concentration of LMWA was higher in the embryos than in the yolk sac. LMWA concentration, protein content, and antioxidant enzyme activity were lower in the malformed experimental embryos than in experimental embryos without anomalies. The addition of vitamins C and E to the diabetic culture medium abolished the deleterious effects of the diabetic serum on the embryos. The disturbed antioxidant defense mechanism under diabetic conditions may be explained, at least in part, by a direct effect of diabetic metabolic factors on the activity of antioxidant enzymes and on the concentration of reducing equivalents. This, in turn, may be embryotoxic.
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PMID:Role of reactive oxygen species (ROS) in the diabetes-induced anomalies in rat embryos in vitro: reduction in antioxidant enzymes and low-molecular-weight antioxidants (LMWA) may be the causative factor for increased anomalies. 1059 Mar 99

This paper was designed to investigate whether phototherapy is an oxidative stress in newborn infants undergoing phototherapy. A day-light continuous phototherapy was given to jaundiced 20 term and 16 preterm newborns for 72 hours. We measured serum vitamin E and the activities of red blood cell anti-oxidation enzymes (superoxide dismutase, catalase and glutathione peroxidase) before and after 72 h of phototherapy. Serum vitamin E levels were not different before and after 72 h of phototherapy in both preterm and term infants. In several studies, antioxidant enzyme activities have been shown to increase in response to oxidative stresses. In this study, however, the antioxidant enzyme activities in the hemolysate were similar before and at the end of the phototherapy in both preterm and full term. In conclusion, the results of our in vivo study do not confirm the thesis that phototherapy is an oxidative stress in newborn infants. Therefore, phototherapy would preferably seem to be safe and efficient method of treatment for all neonates presenting with hyperbilirubinemia.
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PMID:Antioxidant defense systems in newborns undergoing phototherapy. 1079 24

Organophosphates are known primarily as neurotoxins. However, reactive oxygen species (ROS) caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study we aimed to examine how an organophosphate insecticide, chlorpyrifos-ethyl (CE) [0,0-diethyl 0 (3,5,6-trichloro-2-pyridyl) phosphorothioate], affects lipid peroxidation and the antioxidant defense system in vitro. For this purpose, four experiments were carried out. In experiment 1, erythrocyte packets obtained from six (three male, three female) volunteers were divided into six portions, and to each was added CE in both a high concentration range (0, 0.4, 2, 10, 50, 100 g/l) and a low concentration range (0, 0.01, 0.1 g/l). Additionally, each concentration group was divided into five tubes, and incubated at +4 degrees C for 0, 30, 60, 120, and 240 min. After incubation, the levels of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were determined in the erythrocytes in all tubes. In experiment 2, to examine the effect of CE (or its main metabolites) on the activity of purified, commercially available enzymes, CE at concentrations of 0. 0.01, 0.1, 0.4, and 10 g/l was incubated with purified SOD, GSH-Px and CAT at the concentrations observed in control group at the 0 CE concentration level in experiment 1 for 1 h at room temperature (25 degrees C). In experiment 3, the xanthine-xanthine oxidase system was used to determine whether the activities of SOD, GSH-Px and CAT were inactivated other than by CE, for example by superoxide radicals inducing lipid peroxidation in erythrocytes. Samples with xanthine and xanthine oxidase were mixed and incubated for 1 h at room temperature (25 degrees C). In experiment 4, to determine whether enzyme activities were still inhibited if lipid peroxidation was prevented by exogenous antioxidants, experiment 1 was repeated with the CE concentrations of 0.01, 0.1, 0.4, and 10 g/l by adding butylated hydroxytoluene and vitamin E to the medium. The MDA levels were determined spectrophotometrically. Enzymatic methods were used for the determination of SOD, GSH-Px, and CAT activities. The Friedman test and Wilcoxon's Signed Ranks test were used to compare paired groups. MDA values and GSH-Px activities increased with increasing CE concentration and incubation period (P<0.05), but SOD and CAT activities decreased with increasing CE concentration and incubation period (P<0.01). From these results, it can be concluded that in vitro administration of CE resulted in the induction of erythrocyte lipid peroxidation and significant changes in antioxidant enzyme activities, suggesting that ROS and/or free radicals may be involved in the toxic effects of CE.
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PMID:The effect of organophosphate insecticide chlorpyrifos-ethyl on lipid peroxidation and antioxidant enzymes (in vitro). 1113 Oct 33

We have investigated the protective effect of vitamin C and E together supplementation on oxidative stress and antioxidant enzyme activities in the liver of streptozotocin-induced diabetic rats, unsupplemented diabetic and control rats. We also determined the levels of both the vitamins and oxidative stress in plasma. Vitamin supplementation in diabetic rats lowered plasma and liver lipid peroxidation, normalised plasma vitamin C levels and raised vitamin E above normal levels. In liver, the activity of glutathione peroxidase was raised significantly and that of glutathione-S-transferase was normalised by vitamin supplementation in diabetic rats. The levels of lipid peroxidation products in plasma and liver of vitamin-supplemented diabetic rats and activities of antioxidant enzymes in liver suggest that these vitamins reduce lipid peroxidation by quenching free radicals.
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PMID:Protective antioxidant effect of vitamins C and E in streptozotocin induced diabetic rats. 1121 24


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