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)

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.
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PMID:Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine. 146 9

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

Feeding diets depleted of vitamin E and Se to cattle can induce a disease known as nutritional degenerative myopathy. It is believed that an increased peroxidative challenge in muscle is involved in the pathogenesis of this disease. A number of species can up-regulate the activity of some antioxidant enzymes, including glutathione reductase (EC 1.6.4.2), glutathione transferase (EC 2.5.1.18), glucose-6-phosphate dehydrogenase (EC 1.1.1.49), catalase (EC 1.11.1.6), and superoxide dismutase (EC 1.15.1.1), in an attempt to mitigate the effects of a peroxidative challenge. A 2 x 2 factorial study was set up to examine possible changes in the activities of these antioxidant enzymes in muscles of ruminant calves fed on diets low in either vitamin E or Se. Four groups of four calves each were fed on a basal diet of NaOH-treated barley which was supplemented with alpha-tocopherol or Se or both for a total of 50 weeks. Calves fed on diets depleted of vitamin E, but not those fed on diets low in Se, developed subclinical myopathy, as judged by increases in the activity of plasma creatinine kinase (EC 2.7.3.2), and had increased muscle concentrations of two indices of lipid peroxidation, namely thiobarbituric acid-reactive substances, with and without ascorbate activation. Feeding diets depleted of vitamin E and diets low in Se both increased muscle activities of glucose-6-phosphate dehydrogenase in heart, biceps and supraspinatus. This change may have occurred in an attempt to maintain intracellular pools of reduced glutathione. No other changes in antioxidant enzyme activity were observed.
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PMID:Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both. 826 Apr 86

The effect of intermittent sprint cycle training on the level of muscle antioxidant enzyme protection was investigated. Resting muscle biopsies, obtained before and after 6 wk of training and 3, 24, and 72 h after the final session of an additional 1 wk of more frequent training, were analyzed for activities of the antioxidant enzymes glutathione peroxidase (GPX), glutathione reductase (GR), and superoxide dismutase (SOD). Activities of several muscle metabolic enzymes were determined to assess the effectiveness of the training. After the first 6-wk training period, no change in GPX, GR, or SOD was observed, but after the 7th week of training there was an increase in GPX from 120 +/- 12 (SE) to 164 +/- 24 mumol.min-1.g dry wt-1 (P < 0.05) and in GR from 10.8 +/- 0.8 to 16.8 +/- 2.4 mumol.min-1.g dry wt-1 (P < 0.05). There was no significant change in SOD. Sprint cycle training induced a significant (P < 0.05) elevation in the activity of phosphofructokinase and creatine kinase, implying an enhanced anaerobic capacity in the trained muscle. The present study demonstrates that intermittent sprint cycle training that induces an enhanced capacity for anaerobic energy generation also improves the level of antioxidant protection in the muscle.
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PMID:Effect of sprint cycle training on activities of antioxidant enzymes in human skeletal muscle. 890 57

We investigated the effect of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzyme activity [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX)] and malondialdehyde (MDA) concentration in anesthetized dogs to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned into three groups: I (sham), 4 h duration; II (S + R), 2 h of shock followed by reinfusion for 2 h; III (SOD + S + R), as II but pretreated with PEG-SOD. Hemorrhagic shock was produced by withdrawal of blood to maintain the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK, CK-MB and lactate increased during shock. Following reinfusion after 2 h of shock hemodynamic parameters and plasma lactate tended to return towards control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total-, Mn- and CuZn-SOD activity increased while LV-CL decreased. In spite of the increase in the antioxidant reserve, there was oxidative damage. Pretreatment with SOD attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, and CK-MB, PMNL-CL, cardiac MDA, SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals may partly be involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.
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PMID:Cardiac depression and cellular injury in hemorrhagic shock and reinfusion: role of free radicals. 940 75

Mechanism of amyloid beta-peptide (A beta) toxicity in cultured neurons involves the development of oxidative stress in the affected cells. A significant increase in protein carbonyl formation was detected in cultured hippocampal neurons soon after the addition of preaggregated A beta(1-40), indicating oxidative damage of proteins. We report that neurons, subjected to A beta(1-40), respond to A beta oxidative impact by activation of antioxidant defense mechanisms and alternative ATP-regenerating pathway. The study demonstrates an increase of Mn SOD gene expression and the restoration of Cu, Zn SOD gene expression to a normal level after temporary suppression. Partial loss of creatine kinase (CK) BB activity, which is the key enzyme for functioning of the creatine/phosphocreatine shuttle, was compensated in neurons surviving the A beta oxidative attack by increased production of the enzyme. As soon as the oxidative attack triggered by the addition of preaggregated A beta (1-40) to rat hippocampal cell cultures has been extinguished, CK BB expression and SOD isoenzyme-specific mRNA levels in surviving neurons return to normal. We propose that the maintenance of a constant level of CK function by increased CK BB production together with the induction of antioxidant enzyme gene expression in A beta-treated hippocampal neurons accounts for at least part of their adaptation to A beta toxicity.
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PMID:Amyloid beta-peptide (1-40)-mediated oxidative stress in cultured hippocampal neurons. Protein carbonyl formation, CK BB expression, and the level of Cu, Zn, and Mn SOD mRNA. 977 Jun 41

BACKGROUND: Cardiac dysfunction and tissue injury during endotoxemia may be caused by increased levels of oxygen free radicals. METHODS AND RESULTS: We therefore investigated the effects of endotoxic shock on cardiac function and contractility, plasma creatine kinase (CK) activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL) and white blood corpuscles, antioxidant reserve (cardiac chemiluminescence [LV-CL]), antioxidant enzyme activity (superoxide dismutase, catalase, glutathione peroxidase), cardiac malondialdehyde (MDA) concentration, a lipid peroxidation product, and hemodynamics in the absence or presence of flaxseed treatment in anesthetized dogs. Flaxseed contains lignans that have antioxidant activites and inhibit platelet-activating factor (PAF). The dogs were assigned to three groups: group I, sham control; group II, endotoxin (ET) treated (5 mg/kg intravenously); group III, ET + flaxseed (2 gm/kg/day orally) for 6 days. ET produced a decrease in cardiac function and contractility and antioxidant enzyme levels, and an increase in cardiac MDA and LV-CL, PMNL-CL, and plasma CK and lactate. Pretreatment with flaxseed attenuated the ET-induced cardiac dysfunction and cellular damage. Protection was incomplete for cardiovascular function, plasma CK, and lactate. CONCLUSIONS: These results suggest that oxyradicals and/or PAF may be involved in the deterioration of cardiovascular function and cellular integrity during ET shock and that antioxidant and anti-PAF agents may be effective in the treatment of ET shock.
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PMID:Oxygen Free Radicals and Endotoxic Shock: Effect of Flaxseed. 1068 13

The study was undertaken to evaluate the role of free oxygen radicals in asphyxiated neonates. Thirty term neonates appropriate for gestational age and with severe birth asphyxia (Apgar score of 3 or less at 1 minute of life) formed the study subjects. The levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), creatine phosphokinase (CPK) and lipid peroxidase (LPO) in the CSF of these neonates were estimated between 12 and 48 hrs of life. Enzyme estimation was performed by standard methods and the results were analysed statistically using Multivariate Logistic Regression analysis and non parametric tests namely Kruskal Wallis test and Wilcoxon's rank sum test. Out of the thirty babies, 14 were observed to be neurologically normal, 9 had significant morbidity and 7 died. The SOD levels ranged from 12.4 to 140 units/ml, GPx from 128 to 1933 nmol/min/dl, CPK from 2 to 2098 IU/dl and LPO from 5.4 to 30.8 umol/hr/dl. The SOD and GPx levels had an inverse relationship whereas rise in LPO and CPK levels were directly proportional to the extent of neurological damage and ultimate clinical outcome. CPK levels higher than 140 IU/ml were lethal and associated with 100% mortality whereas all normal neonates had CPK below 37 IU/ml. The levels of antioxidant enzymes can reliably and significantly predict mortality and morbidity whereas level of an enzyme cannot confidently confer normalcy. Hence antioxidant enzyme levels with a cut off value can be a useful marker and serve as a prognostic indicator in times to come.
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PMID:Free oxygen radicals--predictors of neonatal outcome following perinatal asphyxia. 1077 93

There has been no investigation to determine if the widely used over-the-counter, water-soluble antioxidants vitamin C and N-acetyl-cysteine (NAC) could act as pro-oxidants in humans during inflammatory conditions. We induced an acute-phase inflammatory response by an eccentric arm muscle injury. The inflammation was characterized by edema, swelling, pain, and increases in plasma inflammatory indicators, myeloperoxidase and interleukin-6. Immediately following the injury, subjects consumed a placebo or vitamin C (12.5 mg/kg body weight) and NAC (10 mg/kg body weight) for 7 d. The resulting muscle injury caused increased levels of serum bleomycin-detectable iron and the amount of iron was higher in the vitamin C and NAC group. The concentrations of lactate dehydrogenase (LDH), creatine kinase (CK), and myoglobin were significantly elevated 2, 3, and 4 d postinjury and returned to baseline levels by day 7. In addition, LDH and CK activities were elevated to a greater extent in the vitamin C and NAC group. Levels of markers for oxidative stress (lipid hydroperoxides and 8-iso prostaglandin F2alpha; 8-Iso-PGF2alpha) and antioxidant enzyme activities were also elevated post-injury. The subjects receiving vitamin C and NAC had higher levels of lipid hydroperoxides and 8-Iso-PGF2alpha 2 d after the exercise. This acute human inflammatory model strongly suggests that vitamin C and NAC supplementation immediately post-injury, transiently increases tissue damage and oxidative stress.
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PMID:Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise. 1155 12

We have determined the effects of maximal and submaximal cycloergometer tests on the antioxidant enzyme defences of neutrophils and lymphocytes. We also compared the neutrophil and lymphocyte basal enzyme antioxidant activities. A total of 17 well-trained amateur athletes, runners, and cyclists participated in this study. Two tests were performed on an electromagnetic reduction cycloergometer: the maximal exercise test, and the submaximal prolonged exercise test. Blood samples were taken before and after the tests. Basal enzyme activity of superoxide dismutase was higher in lymphocytes but neutrophils presented higher activities of catalase and glutathione peroxidase. The maximal test increased the circulating number of lymphocytes and the activities of catalase and glutathione peroxidase. No changes were observed in lymphocyte number or in lymphocyte antioxidant enzyme activities after the submaximal test. The circulating number of neutrophils increased significantly after the submaximal test. Maximal and submaximal tests decreased the activities of neutrophil glutathione dependent antioxidant enzymes (glutathione peroxidase and glutathione reductase), but no changes were observed in catalase or superoxide dismutase activities after either test. Neither the maximal nor submaximal test produced increases in serum activities of lactate dehydrogenase and creatine kinase (CK).
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PMID:Different effects of exercise tests on the antioxidant enzyme activities in lymphocytes and neutrophils. 1530 83


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