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

In three trials pigs were fed semisynthetic diet characterized by vitamin E deficit and supplemented with lard at different degrees of oxidative rancidity. When rancid lard was used and pigs were exposed to the effects of stress factors from the 55th day of the trail, signs of affected walking and lack of appetite were observed. Pig organs were subject to histological examination on the 83rd day. Dystrophic changes of heart and skeletal muscles were revealed. The changes were accompanied by increased activities of aspartate and alanine amino transferases and lactate dehydrogenase in blood serum. The addition of 150 mg of tocopherol acetate per 1 kg of feed increased its concentration in tissues and prevented the occurrence of clinical, biochemical, and morphological signs; decreases in weight gains were also avoided. When fresh fat was used without any additional effect of stress factors, no morphological signs of vitamin E deficiency were observed. A decreased quality of lard in feed was not found to exert any influence on a higher consumption of vitamin E. The production of lipoperoxides in tissue homogenates was considerably decreased as a result of the addition of vitamin E to feed. The criteria to be used for intravital and post-mortal diagnosis of vitamin E deficiency in pigs are evaluated.
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PMID:[Effect of experimental lard diet on the incidence of vitamin E deficiency signs in pigs]. 81 48

We investigated the role of lipid peroxidation as the mechanism mediating copper toxicity in isolated rat hepatocytes and the modulating effect of vitamin E. Hepatocytes, isolated from rats fed diets containing deficient (E-), sufficient (E+), and excess (E++) amounts of vitamin E, were incubated with CuCl2 (0-2400 microM) for 150 min. Dose and time-dependent decreases in hepatocyte viability (determined by trypan blue exclusion and lactate dehydrogenase release) due to copper toxicity correlated with production of malonyldialdehyde in E- and E+ hepatocytes. However, malonyldialdehyde generation did not accompany copper toxicity in E++ cells. Copper toxicity was enhanced in E- compared to E+ and E++ hepatocytes as assessed by cell viability studies and ultrastructural plasma membrane bleb formation. In vitro vitamin E repletion of E- hepatocytes restored resistance to copper and decreased malonyldialdehyde production proportionately. Thus vitamin E deficiency appeared to increase the susceptibility of hepatocytes to copper toxicity. We conclude that lipid peroxidation may not be the mechanism by which copper is toxic to isolated hepatocytes but that the site of injury may be thiol-rich cellular proteins.
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PMID:Copper toxicity and lipid peroxidation in isolated rat hepatocytes: effect of vitamin E. 291 18

10-fold decrease of alpha-tocopherol content in blood serum, distinct increase in hemolysis of erythrocytes and activation of lactate dehydrogenase in blood plasma were found in rats kept on a vitamin E deficient diet within 2 months as compared with control. Content of alpha-tocopherol was decreased in myocardium 3.4-fold and in skeletal muscles--5.4-fold. Lipid peroxidation was activated in myocardium and skeletal muscles under conditions of vitamin E deficiency. Content of diene conjugates and Schiff bases was increased by 30-60% in these tissues; content of malonic dialdehyde--the secondary product of lipid peroxidation--was increased in myocardium by 60% and in skeletal muscles--4-fold. Activity of lysosomal enzymes was altered only slightly in myocardium, whereas in skeletal muscles unsedimented activity of acid phosphatase was distinctly increased. The activation of impairing factors observed led to deterioration of Ca2+ transport functions of membranes in myocardium by 30% and in skeletal muscles--4-fold. The data obtained suggest that heart muscle is better protected against vitamin E deficiency as compared with skeletal muscle. Physiological importance of these results is discussed.
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PMID:[Comparative evaluation of the effect of vitamin E deficiency on lipid peroxidation and Ca2+ transport in heart and skeletal muscles]. 357 50

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.
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PMID:Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence. 359 58

Three adult brown pelicans (Pelicanus occidentalis) were observed to be weak, anorexic and unresponsive to antibiotics, anti-inflammatory drugs, vitamins including vitamin E, and steroids. Blood chemistry revealed high activities of aspartate aminotransferase, creatinine kinase and lactate dehydrogenase. Radiographs of the birds' leg muscles revealed multiple opacities suggestive of calcification; the gross lesions included white streaks in the leg, wing, and heart muscles, and the microscopical lesions consisted of various degrees of degeneration and necrosis characterised by eosinophilia, variations in fibre size, loss of striations, myolysis, mineralisation, and proliferation of mononuclear cells in the skeletal muscles and the myocardium. The levels of heavy metals, selenium and vitamin E in the birds' livers were not abnormal. The level of peroxide in their diet of capelin fish was high, 69 meq/kg, (normal <20 meq/kg) consistent with rancid feed, and the level of vitamin E was very low, 0.5 iu/kg (normal 20 to 30 iu/kg). It was concluded that the myopathy was probably caused by vitamin E deficiency due to feeding the pelicans a rancid diet.
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PMID:Myopathy in brown pelicans (Pelicanus occidentalis) associated with rancid feed. 1191 85

The effects of 10 weeks of dietary selenium and/or vitamin E deficiency (< 0.03 mg Se and 1.5 mg vitamin E per kg diet) on body Se and vitamin E stores and on the down-regulation of liver cellular glutathione peroxidase (GPx1) and plasma glutathione peroxidase (GPx3) were examined in growing female New Zealand White rabbits in comparison to Se (+ 0.40 mg Se/kg diet) and/or vitamin E (+ 150 I.U./kg diet) supplemented controls. Additionally plasma lactate dehydrogenase (LDH) activity, liver thiobarbituric acid-reactive substances (TBA-RS) and liver protein carbonyls were measured to assess the development of oxidative stress during an alimentary Se and/or vitamin E deficiency. Significantly decreased concentrations of Se and vitamin E in plasma (Se: - 70%; vitamin E: - 87%) and liver (Se: - 90%; vitamin E: - 95%) indicated an efficacious Se and vitamin E depletion of the rabbits within 10 weeks. GPx1 messenger RNA levels (GPx1 mRNA) in the livers of Se-depleted rabbits were down-regulated to 1/3-1/8 of the Se supplemented controls. GPx1 enzyme activity in the livers of Se-deficient rabbits declined to 10% of the Se-supplied control rabbits. A significantly elevated LDH activity in the blood plasma of Se- and vitamin E-deficient rabbits indicated a general impairment of tissues. Markedly increased TBA-RS concentrations and protein carbonyl contents in the livers of Se- and vitamin E-deficient rabbits gave further evidence for severe oxidative damage of cellular lipids and proteins during an alimentary Se and/or vitamin E deficiency. Both a full expresssion of GPx1 attained by dietary Se supplementation and dietary vitamin E supply effected an almost complete protection against oxidative cellular damage of the liver.
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PMID:Down-regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium-deficient rabbits. 1245 69