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

It is found that the amount of saturated fatty acids grows, while that of unsaturated--falls in the erythrocyte membranes of rats maintained on a diet without vitamin E. In this case transmembrane calcium transport catalyzed by Ca2(+)-ATPase (EC 3.6.1.3) is not broken and activity of antioxidant enzyme superoxide dismutase (EC 1.15.1.11) in lysate of erythrocytes falls. The found shifts are corrected with administration of antioxidant preparations.
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PMID:[Indices of structure and function of erythrocyte membranes in rats with vitamin E deficiency and their correction with antioxidant drugs]. 196 70

Antioxidant micronutrients are one of the body's primary defenses against free radicals and reactive oxygen molecules. Carotenoids, vitamin C, and vitamin E trap these molecules, and selenium is an essential component of an antioxidant enzyme. There is considerable support from animal studies for a protective effect of antioxidant micronutrients on cancer. However, the role of these micronutrients in cancer prevention in humans is less clear. Diet studies suggest protective effects of fruits and vegetables on risk of cancer at several sites. Inverse associations between dietary carotenoids and serum beta-carotene and lung cancer have been observed repeatedly. Vitamin C has also been consistently inversely associated with risk of oral and esophageal cancer in diet studies and with stomach cancer in both diet and plasma studies. It remains unknown, however, whether carotenoids and vitamin C or some other component of fruits and vegetables, the primary sources of these micronutrients, prevent cancer in humans. Selenium has been inversely correlated with cancers at numerous sites in ecologic studies, but observational studies do not provide strong support for a protective effect of selenium on cancer at any site. There also is not strong support for a protective effect of vitamin E on cancer in humans. Results of studies on the association of antioxidant micronutrients with cancer at many sites are inconsistent. This could be due to lack of a true protective effect or could be related to methodologic problems in assessing dietary intake in epidemiologic studies.
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PMID:Antioxidant micronutrients in cancer prevention. 202 68

Information about age-related factors that influence sensitivity to hepatotoxic injury is important to geriatric medicine and environmental health. The purpose of the present study was to determine whether age-associated changes occur in hepatic antioxidant defense mechanisms of male and female Fischer 344 rats. Liver homogenates and post-mitochondrial supernatant fractions from rats aged 4, 14, 24 and 29 months were analyzed for antioxidant enzyme activities and for vitamin E and malondialdehyde content. Age-associated changes in catalase and glutathione reductase activities were observed that could be described as sex-determined differences that disappeared in old age. Cytosolic superoxide dismutase and glutathione peroxidase activities displayed sex-dependent variations in activity but were unaffected by aging. Hepatic vitamin E concentrations were lower in male rats than in female malondialdehyde concentrations also were lower in males than in females; malondialdehyde content increased in old males and decreased in old females. The results indicate that age-associated changes in enzymatic and nonenzymatic antioxidant defense mechanisms of rat liver are sex-dependent. In addition, comparison with findings from other studies in rats suggests that the effects of aging may also depend on the strain of rat.
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PMID:Sex-dependent differences in the effects of aging on antioxidant defense mechanisms of rat liver. 204 71

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

Longitudinal studies were carried out over 55 weeks in vitamin E deficient and control rats. It was shown that neurological tissues (brain, cord and nerve) retained a greater percentage of vitamin E (alpha-tocopherol) than other tissues (serum, liver and adipose tissue), and that there was no evidence for compensation by other antioxidant enzyme systems (superoxide dismutase and glutathione peroxidase). An increased uptake of alpha-[3H]tocopherol (150% of controls) was observed in peripheral nerve of deficient animals from 11 weeks, whereas similar increases were not found in brain and cord until 36 weeks. These results were correlated with tests of neurological function which included electrophysiological studies and measurement of axonal transport. Recordings of somatosensory evoked potentials showed a significant delay (P less than 0.001) of central conduction velocity after 40 weeks of deficiency, whereas peripheral conduction was unchanged. After 40 weeks of deficiency, abnormal electromyographic activity of the hind limbs was obtained which was suggestive of chronic partial denervation. By 52 weeks there were significant reductions of both fast anterograde (P less than 0.02) and retrograde (P less than 0.05) transport of acetylcholinesterase in the deficient rats.
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PMID:Longitudinal studies of the neurobiology of vitamin E and other antioxidant systems, and neurological function in the vitamin E deficient rat. 246 31

Lung inflammatory cells in idiopathic pulmonary fibrosis (IPF) is characterized by an increased spontaneous production of oxidants. This suggests that the oxidants may play a role in causing the epithelial cell injury in the early stage of IPF. Bleomycin (BLM) induces pulmonary fibrosis by oxidant production. We tested the hypothesis that a dietary supplement of vitamin E (VE) may protect against, and its deficiency may exacerbate, BLM-induced pulmonary fibrosis. Because the hamster is known to be the best model among animals studied mimicking human lung antioxidant enzyme activities, Syrian Golden hamsters were used in this study. In dietary VE supplement and BLM treated group (Ead.B), mean serum VE concentration increased by about 3 times that of control (C) and the BLM treated group (CB). Despite the remarkably high VE content, no significant difference was found between CB and Ead.B for pressure-volume (PV) curves and morphological data. In BLM treated with dietary VE deficient group (Ede.B), serum VE concentrations markedly decreased on all experimental days compared with other groups. Mechanical properties in P-V curves of Ede.B showed most less distensible characteristics in early stage and most distensible characteristics in later stage. These emphysematous changes observed in P-V curves in the later stage of Ede.B, coincided with the morphological observations. In the early stage of BLM treatment, lipid peroxide concentrations in the lung tissue were significantly higher in Ede.B compared with other groups. It was concluded that a dietary supplement of VE cannot protect against BLM-induced pulmonary fibrosis, and a dietary VE deficiency exacerbates BLM lung injury to produce on emphysema in the hamster.
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PMID:[Pulmonary fibrosis and antioxidant agents]. 247 76

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

It has been shown that adaptation to short-term emotional-painful stresses leads to an increase in antioxidant enzyme activities but does not change vitamin E content in the myocardium. The most labile enzyme was catalase (35% increase). During stress in nonadapted animals the enzyme activity decreased, as compared to the control, while in the group of adapted animals with subsequent stress the activity was even higher than in the control. During initiation of lipid peroxidation in the heart homogenates in vitro there was a 3-fold increase and a 1%-fold decrease in the oxidation intensity in rats exposed to stress and in adapted animals, respectively. The role of adaptation activation of cardiac antioxidant system in the prevention of stress-induced heart damage is discussed.
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PMID:[Increased enzymatic activity of antioxidant protection of the heart in the adaptation of rats to short-term stress exposure]. 367 54

This study was designed to investigate the effect of the natural bioflavonoid compound cianidanol on the blood lipid peroxide status of patients with chronic hepatitis. Nine patients had chronic active liver disease--seven of them hepatitis B virus-positive--and five had chronic alcoholic hepatitis. Besides some biochemical liver function tests (serum bilirubin, aminotransferases and gamma-glutamyl transferase), the changes in the serum level of malondialdehyde (a thiobarbituric acid reactive substance) as one of the end-products of lipid peroxidation, as well as the quantity/or activity of enzymes controlling peroxidation (superoxide dismutase (SOD), glutathione peroxidase and catalase) were measured. In addition, the serum level of the natural antioxidant vitamin E was followed-up. Cianidanol treatment (at a dose of 3.0 g/day for one month and of 1.5 g/day for two months) resulted in a slight improvement in aminotransferases and a significant fall (normalization) of high serum malondialdehyde level. After a marked transient increase, serum SOD content decreased while glutathione peroxidase and catalase activities as well as the vitamin E blood level increased during the treatment. Results suggest that (cianidanol in vivo inhibits lipid peroxidation and influences antioxidant enzyme systems and vitamin E in the blood of patients with chronic hepatitis.
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PMID:Effects of cianidanol on the blood lipid peroxide status in patients with chronic hepatitis. 409 18


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