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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietetic microangiopathy ("mulberry heart disease") is a common disease of weaned pigs in several countries. It is characterised by sudden death and has been associated with vitamin E deficiency. We investigated whether it could be induced by depleting pigs of vitamin E with or without a mild peroxidative challenge. In a 2 x 2 experiment, the effect on pigs of depletion of alpha-tocopherol and supplementation with alpha-tocopherol-stripped corn oil were investigated. Although dietetic microangiopathy was not induced, there was evidence of lipid peroxidation, as judged by increased concentrations of Fe++(-)induced 4-hydroxynonenal (4-HNE) and decreased amounts of linolenic acid (C18:3, omega-3) in tissue. Reduced glutathione (GSH) can conjugate to 4-HNE in an attempt to detoxify this highly toxic compound. GSH concentrations were decreased in skeletal muscle, but not in heart, of pigs that were depleted of alpha-tocopherol with or without supplementation with corn oil. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was higher in heart than in skeletal muscles. It is postulated that sufficient NADPH may be produced in heart to maintain GSH concentrations at a level sufficient to conjugate the excess 4-HNE produced by alpha-tocopherol deficiency and/or oil supplementation.
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PMID:Feeding corn oil to vitamin E-deficient pigs increases lipid peroxidation and decreases tissue glutathione concentrations. 882 97

Vitamin E deficiency in rats led to a sequence of antioxidant defense adaptations in the liver. After three weeks, alpha-tocopherol concentration was 5% of control, but ascorbate and ubiquinol concentrations were 2- to 3-fold greater than control. During the early phase of adaptation no differences in markers of lipid peroxidation were observed, but the activities of both cytochrome b5 reductase and glucose-6-phosphate dehydrogenase were significantly greater in deficient livers. By nine weeks, accumulation of lipid peroxidation end products began to occur along with declining concentrations of ascorbate, and higher NQO1 activities. At twelve weeks, rat growth ceased, and both lipid peroxidation products and cytosolic calcium-independent phospholipase A2 reached maximum concentrations. Thus, in growing rats the changes progressed from increases in both ubiquinol and quinone reductases through accumulation of lipid peroxidation products and loss of endogenous antioxidants to finally induction of lipid metabolizing enzymes and cessation of rat growth.
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PMID:Adaptations to oxidative stress induced by vitamin E deficiency in rat liver. 1703 38