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

Clinical and biochemical responses were studied after taking the measures to prevent nutrition muscular dystrophy in young cattle in the given ecological conditions. Analyzing the biological material (blood, hair, feed, soil), we found the sufficiently high saturation of heifer organisms with the microelement selenium and on the contrary, vitamin E deficiency. Sensitive indicators of the break-down of muscular tissue were the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and mainly creatinine kinase (CPK): the activities of these enzymes increased significantly after the heifers had been driven to pasture. The stay of animals in the run to get them used to the physical load before going to the pasture was not found to be a sufficient measure to prevent muscular nutrition myodystrophy if the animals had not been administered vitamin E and selenium supplements. Of the one hundred heifers we examined, seven animals began to show the signs of nutrition muscular dystrophy; none of these animals had been administered vitamin E and selenium supplements.
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PMID:[Clinical and biochemical response in the prevention of nutritional myodystrophy in heifers]. 310 11

A novel creatinine metabolite, creatol (5-hydroxycreatinine), is a key precursor in the synthesis of the uremic toxin methylguanidine (MG). Creatinine is converted to creatol within the mammalian body and this conversion is mediated specifically by hydroxyl radicals. We investigated the production of creatol and MG from creatinine in rats with renal failure induced by the lipid peroxide produced as a consequence of vitamin E deficiency and depletion of the reduced form of glutathione (GSH). In addition, we examined serum levels of other guanidino compounds, namely guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA). The injury to kidneys induced by the depletion of GSH in combination with vitamin E deficiency caused markedly elevated serum levels of creatol, MG and GSA and decreased serum GAA. The molar ratio of creatol to creatinine in the serum, which should be an index of the oxygen stress mediated by hydroxyl radicals, increased with time. Therefore, the enhanced production of creatol in vitamin-E-deficient rats that have been depleted of GSH might be due to the enhanced production of oxygen radicals in this system.
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PMID:Changes in serum levels of creatol and methylguanidine in renal injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats. 904 46

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

Eight young rhesus monkeys were fed a purified diet devoid of vitamin E. After from 6 to 13 months of feeding, all the animals developed signs of vitamin E deficiency. The signs of vitamin E deficiency in the monkey include muscular dystrophy, elevated excretion of creatine, allantoin, and free amino acids and decreased excretion of creatinine. The vitamin E-deficient monkeys all developed anemia and granulocytosis. Anemia was the first sign of vitamin E deficiency which was observed. All of these signs of vitamin E deficiency were reversed by treatment with alpha-tocopherol.
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PMID:Vitamin E deficiency in the monkey. I. Muscular dystrophy, hematologic changes, and the excretion of urinary nitrogenous constituents. 1342 10