Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was aimed at determining the effect of exercise and vitamin E on age-associated changes in the superoxide dismutase (SOD), lipid (LPO) and protein oxidations (PO) in the cerebral cortex (CC), cerebellum (CB) and hippocampus (HC) of rat brain. For this, male Wistar albino rats of 4- (adult), 12- (middle-age) and 18-month (old) of age were orally supplemented with vitamin E and swim trained at 3% intensity for 30 min/day, 5 days/week, and for a period of 30 days. Reduced total SOD was evident with age in the CC while it was highest in the HC of old rats. Vitamin E elevated SOD in the old trainees. Mn-SOD increased in the middle-age and old trainees and Cu Zn-SOD increased in the supplemented and trained adults. Age-related and region-specific increase in protein carbonyl (PrC) content with decreased sulphydryl (P-SH) was seen. Vitamin E reduced PrC and advanced oxidation of protein products (AOPP) in all ages, and appreciably in the HC and CB. Our study emphasizes a correlation between mitochondrial H(2)O(2) generation, Mn-SOD activity and MDA level, and reveals in part an age-related increase in lipid peroxidation and protein oxidation, and that may occur under conditions such as vitamin E deficiency.
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PMID:Modification by vitamin E and exercise of oxidative stress in regions of aging rat brain: studies on superoxide dismutase isoenzymes and protein oxidation status. 1684 30

The role of dietary Cu and Mn in maintaining tissue integrity, through the effects of these metals on activity of the superoxide dismutase (SOD) enzyme, and their interactions in peroxidative pathways involving Se and vitamin E was investigated. Weanling rats were fed diets deficient in Mn, Cu, Se, and/or vitamin E for 35 days, in a factorial experimental design. Dietary effects on peroxidation, measured in mitochondrial fractions prepared from liver and heart tissue, were compared with changes in the activities of glutathione peroxidase and the Cu and MnSOD enzymes.Decreased heart MnSOD and CuSOD activities, resulting from dietary Mn and Cu deficiencies, were both associated with increased peroxidation. Adequate Se (and glutathione peroxidase activity) prevented the peroxidation associated with either of these deficiencies, but was ineffective with a combined Cu-Mn deficiency. These effects of Se were only observed in tissue lacking glutathione transferase activity. Effects of Cu, Mn, and Se on peroxidation appeared to be present at both levels of vitamin E, although in both tissues, vitamin E deficiency greatly increased the overall peroxidation. Comparison of these in vitro peroxidation results with the deficiency associated lesions observed in vivo indicates that changes in SOD activities and peroxidation pathways may be the dominant cause of these lesions in only some cases. In others, the roles of Cu and Mn in different metabolic pathways appear to be of greater importance.
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PMID:The role of dietary copper, manganese, selenium, and vitamin E in lipid peroxidation in tissues of the rat. 2427 94