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)

Selenium and vitamin E interrelationships in the nutrition of channel catfish (Ictalurus punctatus) were investigated in a 26-wk experiment. A purified basal diet alone or supplemented with 0.2 mg/kg selenium, 50 mg/kg vitamin E or both was fed to fingerling channel catfish in aquaria. Combined deficiencies of selenium and vitamin E caused suppressed growth, anemia, severe myopathy, exudative diathesis and death. Singular deficiencies of either selenium or vitamin E did not produce any of these deficiency signs. Catfish fed selenium-deficient diets with or without supplemental vitamin E had reduced glutathione peroxidase activity and elevated glutathione transferase activity in liver. Vitamin E deficiency in catfish caused elevated ascorbic acid-stimulated lipid peroxidation of hepatic microsomes, which was unaffected by selenium supplementation. The results indicate that there is a significant interaction between selenium and vitamin E in the nutrition of the channel catfish.
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PMID:Effects of singular and combined dietary deficiencies of selenium and vitamin E on fingerling channel catfish (Ictalurus punctatus). 372 1

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