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 influences of food deprivation and refeeding on glutathione (GSH) status, antioxidant enzyme activity and lipid peroxidation in response to an acute bout of exercise were investigated in the liver and skeletal muscles of male Sprague-Dawley rats randomly divided into three groups: starved for 48 h without refeeding; starved for 48 h and refed for 24 or 48 h. Half of each group of rats was exercised on a treadmill until exhaustion and killed immediately, whereas the other half group was killed at rest. Food-deprived rats had significantly lower liver GSH concentration and GSH:glutathione disulfide (GSSG) ratio. Malondialdehyde concentrations in the liver and skeletal muscle were both higher in the starved than in the refed rats (P < 0.05). Refed rats had significantly greater liver GSH level, gamma-glutamylcysteine synthetase and glucose 6-phosphate dehydrogenase activities and plasma insulin concentration than unfed rats. Exercised 24- and 48-h refed rats had 27% and 31 % lower liver GSH (P < 0.05), respectively, and a 21 % lower GSH:GSSG ratio (P < 0.05) than their rested counterparts. Plasma insulin concentrations were significantly lower, whereas glucagon concentrations were greater in the exercised than in the rested rats. Muscle GSH concentration was significantly lower in the food-deprived than in the refed rats (P < 0.05) but was unaffected by exercise. Exercised 24-h refed rats had significantly elevated muscle GSSG concentration compared with rested rats, along with a higher GSH peroxidase and a lower gamma-glutamyltranspeptidase activity (P < 0.05). These data indicate that both food deprivation-refeeding and exhaustive exercise influence liver and skeletal muscle glutathione status and that these changes may be controlled by hepatic glutathione synthesis and release due to hormonal stimulation.
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PMID:Alteration of glutathione and antioxidant status with exercise in unfed and refed rats. 868 45

The present study used male Sprague-Dawley rats to investigate changes in glutathione [reduced (GSH) and oxidized GSH (GSSG)]. lipid peroxidation (as indicated by tissue levels of malonaldehyde and 4-hydroxyalkenals), and the activity of the antioxidant enzyme glutathione peroxidase after a bout of swimming (30 min.) with or without melatonin (N-acetyl-5-methoxytryptamine) treatment. In muscle, the concentration of GSH and the GSH/GSSG ratio were decreased following 30 min. of swimming: these changes are indicative of enhanced oxidative stress. Pretreatment with melatonin prevented these effects. In liver, swimming increased significantly both GSH and GSSG, and decreased the GSH/GSSG ratio. When animals were treated with melatonin, concentrations of GSH and GSSG were also increased after swimming: however, the reduction in the GSH/GSSG ratio was prevented by melatonin. Brain GSH/GSSG ratio was not affected by exercise or by melatonin. Swimming enhanced the levels of lipid peroxidation products is muscle: this was prevented in animals treated with melatonin. Glutathione peroxidase activity was significantly elevated after swimming in both liver and brain with the change not being influenced by concurrent melatonin treatment. It is concluded that swimming imposes an oxidative stress on liver and skeletal muscle and the results show that melatonin confers partial protection against oxidative toxicity, especially in muscle.
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PMID:Tissue changes in glutathione metabolism and lipid peroxidation induced by swimming are partially prevented by melatonin. 873 65

Increased exposure to oxidant-derived free radicals or inadequate systems for antioxidant defense could alter cellular response at critical points in development. We measured 5 antioxidant enzymes, glutathione peroxidase (GSH-Px), glutathione reductase, glutathione-S-transferase, catalase and superoxide dismutase in erythrocytes and their plasma cofactor trace elements (Se, Zn, Cu) in 37 children with myelomeningocele and in 37 age-matched controls. We placed the patients into 3 groups according to motor level of the lesion at birth. We found significantly lower GSH-Px activities (p = 0.007) in children with myelomeningocele. For paired comparisons among the 3 patient groups and controls, there were significant differences (p < 0.05) between controls and both high (thoracic) and raid (lumbar) level embryologic lesions. The finding of antioxidant enzyme variations in our patients with myelomeningocele may indicate a role for abnormal oxidative metabolism in the development of this defect. The contribution of oxidative stress to human birth defects warrants investigation. We discuss potential relationships between oxidative stress and energy metabolism during primary neurulation.
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PMID:Comparison of erythrocyte antioxidant enzyme activities and embryologic level of neural tube defects. 877 May 69

Heart and red blood cell endogenous antioxidant status and plasma lipids were investigated in hypertensive, 14-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats fed a standard commercial rat chow. Specific heart and red blood cell antioxidant enzyme activities, as well as the susceptibility of tissues to H2O2-induced glutathione (GSH) depletion and lipid peroxidation, were measured. Systolic blood pressure in SHR was greater than in WKY rats at 13 weeks of age (197 +/- 12 vs. 132 +/- 14 mmHg (1 mmHg = 133.3 Pa); p < or = 0.05), confirming the presence of hypertension in SHR. Red blood cell catalase (CAT) and superoxide dismutase (SOD) activities were greater (p < or = 0.05) in SHR than WKY rats. Red blood cell CAT activity was positively correlated (r = +0.634; p = 0.026) with SOD, which in turn was correlated (r = +0.709; p = 0.049) with systolic blood pressure. Heart SOD activity was higher (p < or = 0.05) in SHR, while glutathione reductase (GSSG-Red) activity was lower (p < or = 0.05) than in WKY rats. This reduced ability to recycle GSH in the heart coincided with greater (p < or = 0.05) levels of H2O2-induced lipid oxidation products in SHR. Plasma total cholesterol and triacylglycerol levels were lower (p < or = 0.05) in SHR than WKY rats, with no visible signs of atherosclerosis in either SHR or WKY rats. In summary, hypertension in SHR was associated with alterations in antioxidant enzyme profiles of red blood cells and heart, with the latter showing an increased susceptibility to in vitro lipid oxidation. Although hypertension is a recognized factor in the development of human atherosclerosis, spontaneously hypertensive rats did not exhibit signs of aortic plaque, reflecting the resistance of this species to the development of atherosclerosis.
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PMID:Heart and red blood cell antioxidant status and plasma lipid levels in the spontaneously hypertensive and normotensive Wistar-Kyoto rat. 877 9

The effect of sulphur mustard (0.5 LD50, percutaneous) on antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)) in blood cells (erythrocytes (RBC), leucocytes (WBC) and platelets) and body tissues (liver, kidney, spleen and brain) of rats has been investigated 24 h post exposure. The SOD activity was significantly decreased in WBC, platelets, spleen and brain as compared to control. The CAT activity was significantly inhibited in RBC, WBC and spleen as compared to control. The GSH-Px activity was signficantly depressed in WBC, spleen and liver as compared to control. It is concluded that sulphur mustard at a sublethal dose inhibited antioxidant enzyme activities in WBC and spleen. Thus, antioxidant enzymes in lymphatic tissues may be used as suitable models for assessing mustard toxicity. The study suggests the formation of reactive oxygen species in sulphur mustard intoxication.
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PMID:Effect of topically applied sulphur mustard on antioxidant enzymes in blood cells and body tissues of rats. 881 65

Twenty-two hypothalamic amenorrheic patients, who were non-smokers and of normal weight, received replacement therapy for 1 month with transdermal patches containing 8 mg estradiol. No other drugs were prescribed or taken during the study. Before treatment (time 0) and 1 month after its start, blood samples were taken for assay of plasma estradiol levels, the erythrocyte antioxidant enzyme activities of superoxide dismutase, catalase, glutathione peroxidase (GSH-Px), and an age-dependent erythrocyte enzyme activity, pyruvate kinase. Plasma malondialdehyde levels, as an index of lipoperoxidation products, were also detected. The results showed no significant variations in superoxide dismutase, catalase, pyruvate kinase erythrocyte enzyme activities or plasma malondialdehyde levels. A significant increase in plasma estradiol levels (time 0, 17.33 +/- 4.12 pg/ml; 1 month, 81.25 +/- 10.45 pg/ml; means +/- SD; p < 0.0001) and in GSH-Px erythrocyte activity (time 0, 11.97 +/- 2.31 IU/g hemoglobin; 1 month, 16.88 +/- 4.38 IU/g hemoglobin; p < 0.004) was found. Plasma estradiol levels correlated significantly with GSH-Px erythrocyte activity 1 month after therapy was begun (r = 0.776, p < 0.003). We suggest that estrogens restored to physiological plasma levels, stimulate erythrocyte antioxidant GSH-Px activity, improving the antioxidant power of amenorrheic patients.
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PMID:Changes in the erythrocyte antioxidant enzyme system during transdermal estradiol therapy for secondary amenorrhea. 886 89

This study investigates the changes in renal antioxidant system after cisplatin administration and the nephroprotection with 4-methylthiobenzoic acid (MTBA). Male Wistar rats were injected with (1) vehicle control, (2) cisplatin, (3) MTBA, and (4) cisplatin plus MTBA. Rats were euthenized 3 days post-treatment and kidney was isolated and analyzed for platinum concentration, malondialdehyde (MDA), glutathione (GSH and GSSG), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Plasma creatinine increased 508% following cisplatin administration alone, which decreased to 189% with MTBA. Cisplatin-treated rats showed a depletion of renal GSH levels (53%), while cisplatin plus MTBA-injected rats had GSH values close to those of the controls. SOD, CAT, and GSH-Px activities decreased 36, 29, and 38%, respectively, and MDA levels increased 212% following cisplatin administration, which were restored to control levels after MTBA treatment. The renal platinum level depleted significantly with MTBA treatment. The data suggest that cisplatin nephrotoxicity is mediated by depletion in GSH concentration and by impaired activities of SOD, CAT, and GSH-Px, increased lipid peroxidation, and plasma creatinine levels. The protection offered by MTBA against cisplatin nephrotoxicity is related to the reduction in plasma creatinine levels, prevention of GSH depletion and lipid peroxidation, and restoring antioxidant enzyme activity in the kidneys of rats.
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PMID:4-methylthiobenzoic acid protection against cisplatin nephrotoxicity: antioxidant system. 892 31

An increase in antioxidant enzyme activity after acute exercise and exercise training have been reported by many investigators including our laboratory. This study was undertaken in order to determine whether an increase in activity of superoxide dismutase (MnSOD and CuZnSOD), catalase (CAT) and glutathione peroxidase (GSH-Px) during exercise training was associated with the increased levels of respective mRNAs. Male Fisher-344 rats (age 77 weeks) were given exercise training for 9 weeks on the treadmill. Enzyme activity and mRNA's were measured in the heart tissue 23 hr after stopping exercise training. The heart tissues of exercised and sedentary control rats were used to isolate mRNAs encoding MnSOD, CuZnSOD, CAT and GSH-Px by northern blotting experiments. The intensities of mRNA bands were measured by densitometric scanning of the autoradiograms. Northern blot for tubulin was used to normalize the respective intensities. Compared to sedentary controls, the level of mRNAs of enzymes MnSOD, CAT and GSH-Px were found to increase by 126 +/- 5, 133 +/- 6, and 138 +/- 5 percent of sedentary control (mean +/- SEM) respectively, due to exercise training. Corresponding values for these enzyme activity were 153 +/- 19%, 255 +/- 7%, 133 +/- 2% of sedentary control. These results suggest that post-translational modification of these enzyme activity increased in response to exercise training more than increased transcription in aged rats.
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PMID:Comparative effects of exercise training on transcription of antioxidant enzyme and the activity in old rat heart. 895 Jan 34

The purpose of this study was to determine the antioxidant enzyme activities in renal tissues of early stage ddY mice, an animal model for primary IgA nephropathy. Eight- and 40-week-old ddY female mice and normal healthy Balb/c female mice were used in this study. The levels of Cu/Zn-SOD, Mn-SOD, and GSH-PX activities in the renal cortex were significantly higher in 40-week-old ddY mice than in Balb/c control mice of the same age; no change of catalase activity was observed. There were no significant differences in the levels of Cu/Zn-SOD, Mn-SOD, GSH-PX, and catalase activities between the ddY mice and Balb/c mice at 8 weeks of age. Urinary protein was slightly higher in 40-week-old ddY mice. IgA or C3 was deposited at low levels in the glomerular mesangial areas of 8-week-old ddY mice. Marked depositions of IgA and C3 extended from the glomerular mesangial areas to the capillary walls of 40-week-old ddY mice. Expansion of glomerular mesangial matrices and mild mesangial cell proliferation was observed in 40-week-old ddY mice. Antioxidant enzyme activities in the renal cortex were already increased in the early stage IgA nephropathy in 40-week-old ddY mice. These findings suggest that measurements of antioxidant enzyme activities in the renal cortex of 40-week-old ddY mice was useful for evaluation of the pathogenesis of renal involvement in the early stage of IgA nephropathy.
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PMID:Detection of antioxidant enzyme activities in renal tissues of early stage IgA nephropathy in ddY mice. 895 8

The changes in red blood cell (RBC) lipid peroxidation [measured via the malonyl dialdehyde (MDA) concentration], reduced (GSH), and oxidized glutathione (GSSG) levels, hemoglobin (Hb) oxidation and antioxidant enzyme [catalase (Cat), glutathione peroxidase, and superoxide dismutase (SOD)] activities were studied in 45 pediatric patients with various glomerular diseases [minimal change nephrotic syndrome (MCNS) in relapse or in remission, lupus nephropathy (SLE), poststreptococcal glomerulonephritis (APSGN), IgA nephropathy (IGA gn)], and in 20 adult patients with IGA gn and also in 15 pediatric and 14 adult controls. The in vitro effects of hydrogen peroxide [acetyl phenylhydrazine (APH) test] on the GSH and Hb metabolisms were likewise investigated. There was an increased oxidative stress in MCNS with relapse, IGA gn, SLE gn, and APSGN, which could be detected in the GSH and Hb oxidation and in the lipid peroxidation on the peripheral RBC-s. The RBC SOD and Cat activities were significantly lower in all patients than in the controls. The RBC GSSG level was significantly elevated in all patients, with the exception of MCNS in remission. This stimulated a compensatory GSH production in MCNS with relapse and in IGA gn, but not in SLE or APSGN. The regeneration of GSH from GSSG was reduced in MCNS with relapse, SLE, and IGA gn, but not in APSGN. In remission, the GSH-GSSG redox system normalizes, but in vitro the APH test stimulates an intensive Hb oxidation. In conclusion, there is a correlation between the presence of active glomerular disease and the evidence of oxidative changes in the various parameters measured in peripheral RBCs.
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PMID:Oxidative stress and antioxidant defense mechanism in glomerular diseases. 895 40


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