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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

This study examined the in vivo antioxidant and/or prooxidant effect of short-term dehydroepiandrosterone (DHEA) injection and the effect of dietary vitamin E. Male Sprague-Dawley rats (4 wk old) were fed vitamin E-deficient or vitamin E-adequate (30 mg DL-alpha-tocopheryl acetate/kg) diet for 4 weeks followed by intraperitoneal injection of DHEA for 1 week. The results showed that DHEA injection caused a dose-dependent decrease in body weight, and this effect was more pronounced in vitamin E-deficient rats. In contrast, DHEA injection significantly increased liver, kidney and adrenal weights. Hepatic vitamin E content was significantly lowered by vitamin E deficiency, which led to significantly increased ex vivo and iron-induced lipid peroxidation. DHEA injection did not affect hepatic vitamin E content but significantly decreased ex vivo and iron-induced lipid peroxidation in vitamin E-deficient rats. Hepatic total sulfhydryl (SH) groups and non-protein SH contents were not affected by vitamin E but were significantly increased by DHEA injection, which at 100 mg/kg was not more effective than at 50 mg/kg. Hepatic glutathione S-transferase (GST) activity was significantly decreased by DHEA, but vitamin E alleviated such a decrease. DHEA injection significantly increased hepatic glucose 6-phosphate dehydrogenase (G6PD) activity, and the effect was dose dependent in vitamin E-deficient rats. Thus, DHEA may compensate for vitamin E deficiency in vivo, and this effect is masked when dietary vitamin E is adequate. The antioxidant effect of DHEA is accompanied by decreased body weights, enlarged (fat-laden) tissues and altered activities of hepatic GST and G6PD.
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PMID:Toxicological and antioxidant effects of short-term dehydroepiandrosterone injection in young rats fed diets deficient or adequate in vitamin E. 1045 78

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