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

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.
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PMID:Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs. 93 27

Rats of three age groups were fed tocopherol deficient or supplemented diets for 16 weeks or until signs of tocopherol deficiency were apparent. Erythrocyte hemolysis and liver tocopherol content were used as measurements of the tocopherol status of the rats. The following measurements were made on liver microsomal and mitochondrial fractions of all three groups; phospholipid content, lipid peroxidation, fatty acid patterns, pigment fluorescence, ANS fluorescence and the activities of several membrane bound enzymes. Eleven week-old rats displayed signs of vitamin E deficiency after consuming the diet for 7 weeks. Forty-two-week-old rats displayed borderline deficiency signs after 16 weeks of consuming the diet whereas 67-week-old rats displayed no deficiency signs. The need for dietary tocopherol, therefore, appeared to decrease with increasing animal age. Age related alterations in membrane compositional and functional parameters were not modified by either tocopherol deficient or supplemented diets. Tocopherol does not appear to stabilize microsomal membrane composition or function although mitochondrial membranes appear to be labilized by the dietary manipulation of the vitamin.
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PMID:Effect of dietary alpha tocopherol on liver microsomes and mitochondria of aging rats. 93 28

Four weanling swine fed for 4 weeks a commercial ration adequate in selenium and vitamin E, but supplemented with 0.5% silver acetate, developed lesions typical of selenium-vitamin E deficiency. Clinically, the pigs fed this high level of silver had anorexia, diarrhea, and growth depression; 3 of 4 pigs died. At necropsy, hepatic lesions of hepatosis dietetica were present in 4 of 4 silver-fed pigs, and 1 of 4 pigs had cardiac and skeletal muscle lesions characteristic of selenium-vitamin E deficiency. Development of lesions and mortality was prevented in 2 pigs fed the silver diet supplemented with alpha-tocopherol (100 IU/kg of diet), but not in 2 pigs fed the ration supplemented with selenium as selenite (1 ppm). Four pigs fed a lower dose level of silver (0.2% silver acetate) for 6 weeks failed to develop clinical or pathologic features of selenium-vitamin E deficiency. However, hepatic selenium content was significantly increased in pigs fed the silver-supplemented ration.
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PMID:Induction of lesions of selenium-vitamin E deficiency in pigs fed silver. 99 68

An experiment was conducted to study the effects of feeding a 96.8% cull pea basal ration, low in selenium (0.061 ppm) and vitamin E (7.0 IU alpha-tocopherol/kg of ration), to growing pigs with and without supplementation of selenium, vitamin E, or both. The basal ration was high in crude protein (25.2%) and contained no supplemented fat. Nine of 10 pigs fed the unsupplemented basal ration had lesions attributed to selenium-vitamin E deficiency, and 8 of these pigs died during the 160-day experiment. The deficiency was usually characterized by sudden death (with no prior signs of illness), massive hepatic necrosis, hemoglobinuric and to a lesser extent cholemic nephrosis, degenerative myopathy of cardiac and skeletal muscles, edema, icterus, and acute terminal congestion and hemorrhage. Clinical signs, deaths, or lesions attributed to selenium-vitamin E deficiency were not observed in any of the pigs fed the basal ration supplemented with as little as 0.01 ppm selenium as sodium selenite or 100 ppm alpha-tocopherol. Pigs fed the unsupplemented basal ration gained more slowly (P less than 0.01) and less efficiently and had higher serum glutamic oxalacetic transaminase (SGOT) levels (P less than 0.01) than pigs fed the basal ration supplemented with selenium, vitamin E, or both. There was no difference (P greater than 0.05) in albumin-to-globulin (A/G) ratios among dietary treatment groups. Using the criteria of this study, the minimum selenium requirement of growing pigs fed a low tocopherol cull pea diet was determined to be between 0.06 and 0.07 ppm.
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PMID:Selenium-vitamin E deficiency in swine fed peas (Pisum sativum). 111 25

1. Sheep fed on a maintenance ration of wheaten-hay chaff or of wheaten-hay chaff-lucerne-hay chaff (I : I, W/W) became deficient or incipiently deficient in vitamin E. 2. Degenerative changes were observed in bone marrow and muscle, and liver function was imparied in some animals. These abnormalities were not influenced by the vitamin B12 status of the animals or by a shortage of cobalt in the rumen. 3. Plasma ascorbic acid levels may not have been optimum, and folic may not have been fully utilized by some sheep. 4. Liver function responded faily rapidly to alpha-tocopheryl acetate, but skeletal muscle had not returned to normal after 28 weeks of treatment. A variable trend towards normal cellularity was found in bone marrow following supplementation with alpha-tocopheryl acetate. 5. A secondary deficiency or, alternatively, inefficient excretion or metabolism of a toxic material, may occur in vitamin E deficiency as a result of degenerative changes in the absorptive or excretory areas of the intestinal tract and be responsible for the bone marrow abnormality.
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PMID:An abnormality of the bone marrow associated with vitamin E deficiency in sheep. 112 67

Two 10-month-old heifers from a group of 20 young stock showed symptoms closely resembling paralytic myoglobinuria. One animal died five days after the onset of the symptoms and the other recovered slowly with selenium and vitamin E therapy. Histological examination of muscle tissue from the dead animal showed a myopathy resembling that due to vitamin E deficiency.
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PMID:Myopathy in young cattle associated with possible myoglobinuria. 116 61

A 16-month-old infant with hepatic fibrosis, cholestasis, and chronic jaundice had signs of vitamin E deficiency, including mild acanthocytosis, thrombocytosis, increased peroxide haemolysis, and absent serum vitamin E. Abormal prothrombin consumption and platelet restocetin aggregation suggested the presence of defective platelet function, and correction studies indicated that this was due to a plasma defect. The abnormality was corrected by treatment with vitamin E, and the findings suggest a possible role of this vitamin in platelet reactions.
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PMID:Vitamin E deficiency and platelet functional defect in a jaundiced infant. 117 3

Weanling male rats were fed either a vitamin E-deficient Torula yeast diet or the same diet supplemented with 100 ppm vitamin E for a period of 3 months. One group of animals fed each diet received 250 ppm lead in the drinking water, whereas another group of animals fed each diet received no lead in the water. Vitamin E deficiency per se had little or no effect on hematocrit value, reticulocyte count, spleen weight, or erythrocyte mechanical fragility in rats not poisoned with lead. On the other hand, the decreased hematocrit, increased reticulocyte count, and splenic enlargement due to lead poisoning were much more pronounced in vitamin E-deficient rats than in rats supplemented with vitamin E. The resistance to mechanical trauma of red blood cells from vitamin E-deficient lead-poisoned rats was much less than that of red cells from vitamin E-adequate lead-poisoned rats. Dietary vitamin E status had no significant influence on the increased mechanical fragility of erythrocytes from nonpoisoned rats caused by exposure to lead in vitro. These results suggest that vitamin E deficiency enhances the susceptibility of animals to the in vivo hemolytic effect of lead poisoning.
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PMID:Lead poisoning in vitamin E-deficient rats. 118 84

The effect of vitamin E deficiency on three enzyme systems involved in steroidogenesis was investigated. No change was found in vitro activity of cholesterol side-chain cleavage enzyme in adrenal or testicular tissue, or of 11-beta-hydroxylase activity in adrenal tissue. Significantly less 3-beta-hydroxysteroid dehydrogenase activity was found in ovarian tissue from female rats given a diet deficient in vitamin E for 141 days, and in testicular tissue and adrenal glands from male rats given the deficient diet for 280 days. Testicular tissue from male rats given the deficient diet for 91 days showed considerably less 3-beta-hydroxysteroid dehydrogenase activity than did tissue from control rats, but the difference was not statistically significant.
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PMID:The effects of vitamin E deficiency on some enzymes of steroid hormone biosynthesis. 121 66

A survey is given of vitamin E and selenium deficiency syndromes in farm animals. Some syndromes can be attributed to the exclusive deficiency of one of the above-mentioned feed components. In some cases with practically complete lack of both componentspathological symptoms can be cured by the addition of one of them to the feed in sufficient amount. A synergistic effect of vitamin E and selenium is sometimes found to recur. The most important theory about the functioning of vitamin E is that it acts as an antioxidant. This theory presumes that, in case of a vitamin E deficiency, peroxidation of unsaturated lipids can occur everywhere in the body leading to oxidative chain reactions. The free radicals thus produced might participate in non-specific reactions with functional and structural compounds. Vitamin E is considered able to reduce lipid peroxides or scavenge free radicals from chain reactions. The pros' and cons' of this theory are discussed. The role of vitamin E has further been associated with thenium is part of the enzyme glutathione peroxidase. This enzyme catalyses the reaction of reduced glutathione with peroxides, whereby hydroxy-acids and oxidized glutathione are generated. Most probably the glutathione peroxidase has its antioxidative action in the cytosol, whereas vitamin E is mainly located in the membranes of the cell.
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PMID:[Vitamin E and selenium in the feed of farm animals (author's transl)]. 123 79


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