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

Safflower oil and its distilled methyl esters were thermally oxidized and fed to young chicks in a vitamin E deficient diet. At a dietary level of 10%, the oxidized lipids caused more severe nutritional encephalopathy (NE) than the unoxidized methyl esters, indicating that factors other than dietary linoleic acid and vitamin E affect the development of NE. A polar lipid extract from oxidized methyl esters accelerated the induction of NE, as did the synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids. Dicumarol exerted a protective action against NE. The possibility is discussed that conjugated keto-polyenoic fatty acids, provided by oxidized oils or formed endogenously in vitamin E deficiency, may play a role in causing NE.
Lipids 1979 Sep
PMID:Lipid oxidation products and chick nutritional encephalopathy. 49 61

Following sudden exposure to extreme cold, a group of 15-week-old pigs exhibited strange nervous signs which included arching the back, a high stepping gait, violent tremors of the whole body and screaming. The animals lowered themselves and once sitting, the tremors and screaming stopped. But if forced to rise, these signs recurred. When the pigs returned to a warmer environment, they rapidly recovered. An acute clinical myopathy caused by a marginal vitamin E deficiency was suspected. Other stress-induced factors, such as circulatory collapse caused by movement from a warm to a cold environment, were also thought to have contributed towards the myopathy.
Vet Rec 1979 Sep 22
PMID:Suspected acute myopathy of pigs. 51 11

Vitamin E deficiency in two species of monkeys (capuchins and cynamolgus) reduced the in vitro cholesterol esterification by plasma lecithin-cholesterol acyltransferase. The reduction was greates in the most deficient species and in animals fed a diet rich in polyunsaturated fat (safflower oil) stripped of vitamin E. The best correlate of total esterification was the plasma concentration of free cholesterol which reflected the degree of hyperlipidemia, found to be greatest in capuchins fed coconut oil. A logical explanation for the decreased LCAT activity in vitamin E deficiency would be peroxidative damage of substrate (the PUFA of lecithin) or of sulfhydryl sited on lecithin-cholesterol acyltransferase itself. However, neither case was fully supported by the data suggesting that additional information concerning the nature of the reaction and the role of vitamin E is required.
Am J Clin Nutr 1975 Sep
PMID:Depression of lecithin-cholesterol acyltransferase esterification in vitamin E-deficient monkeys. 80 56

In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene: tetraene ratio greater than 0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene: tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
Am J Clin Nutr 1976 Sep
PMID:Essential fatty acid deficiency in adults receiving total parenteral nutrition. 82 4

In 11 patients with alcohol-induced hyperlipemia, of whom 6 showed a Zieve Syndrome increased phospholipids, triglycerides and total cholesterol were found in the red cells stromal. The gasliquid chromatographic analysis of the phospholipid fatty acids showed increased contents of saturated and monounsaturated fatty acids C 16-C 18 smaller contents of longchain highly unsaturated fatty acids. The changes in the fatty acid pattern mainly occurred in patients with Zieve Syndrome and could be important for the mechanism of the hemolytic anemia. Theses findings could be in connexion with vitamin E deficiency.
Klin Wochenschr 1976 Sep 01
PMID:[Changes of erythrocyte membrane lipids in ethanol induced hyperlipidemia (Zieve's syndrome) (author's transl)]. 96 32

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.
Vet Rec 1975 Sep 06
PMID:Myopathy in young cattle associated with possible myoglobinuria. 116 61

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.
Tijdschr Diergeneeskd 1975 Sep 01
PMID:[Vitamin E and selenium in the feed of farm animals (author's transl)]. 123 79

A 33-day feeding experiment was conducted with 3-day-old broiler chicks to assess the efficacy of various flavonoid and simple phenolic antioxidants in preventing nutritional muscular dystrophy (NMD) resulting from vitamin E deficiency. None of the flavonoids or simple phenolics at a dietary concentration of 1,000 ppm completely prevented NMD but quercetin reduced (P less than .05) its incidence and quercetin, morin, and ferulic acid reduced (P less than .05) the severity of the disorder. The low-selenium, low-vitamin E diet also promoted the development of a mild exudative diathesis (ED) in many of the birds, which was inhibited (P less than .05) by the rutin and silymarin treatments, but exacerbated (P less than .05) by quercetin, morin, and ferulic acid. Changes in concentrations of vitamin E in plasma, liver, or muscle, caused by the various treatments (other than vitamin E), were not related to protection against NMD or ED.
Poult Sci 1992 Sep
PMID:Research note: efficacy of various flavonoids and simple phenolics in prevention of nutritional myopathy in the chick. 140 42

It is speculated that oxidative stress in vivo may have some influence on advanced, nonenzymatic, glycosylation end products. However, this has not been demonstrated yet. We assessed changes in collagen-linked fluorescence in the skin of nondiabetic and streptozotocin-induced diabetic rats fed three different diets for 4 weeks that could modify oxidative stress: vitamin E-deficient (D), vitamin E-supplemented (S), and control (C). The serum lipid peroxide level expressed as thiobarbituric acid (TBA) activity in diabetic rats on the S diet (9.6 +/- 1.0 [SE] nmol/L/mL) was significantly (P less than .01) lower than that in rats on the D diet (111.4 +/- 22.4), and similar to that in nondiabetic rats on the C diet (12.4 +/- 2.2). The collagen-linked fluorescence level was significantly (P less than .01) higher in diabetic rats than in nondiabetic rats, which corresponded to the serum glucose and glycosylated hemoglobin levels. However, there were no significant differences in the fluorescence levels among three groups classified by three different diets in both nondiabetic and diabetic rats (21.7 +/- 1.7 arbitrary U/mg collagen for D, 22.3 +/- 2.0 for C, and 22.8 +/- 2.5 for S in nondiabetic rats v 41.2 +/- 4.1 for D, 40.1 +/- 4.7 for C, and 39.3 +/- 3.5 for S in diabetic rats), despite significant changes in serum lipid peroxide levels. Consequently, there were no significant changes found in collagen-linked fluorescence levels in diabetic rats wherein oxidative stress was modified by vitamin E deficiency and supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)
Metabolism 1992 Sep
PMID:No significant effect of vitamin E deficiency or supplementation on collagen-linked fluorescence in skin of diabetic rats. 151 18

The requirement for vitamin E is closely related to the dietary intake of polyunsaturated fatty acids (PUFA). By the protective mechanism to prevent PUFA from being peroxidized, vitamin E is metabolically consumed. In addition, PUFA impair the intestinal absorption of vitamin E. Therefore PUFA generate an additional vitamin E requirement on the order of 0.6, 0.9, 1.2, 1.5, and 1.8 mg vitamin E (RRR-alpha-tocopherol-equivalents), respectively, for 1 g of dienoic, trienoic, tetraenoic, pentaenoic, and hexaenoic acid. For this reason, the gross vitamin E content of food containing PUFA does not allow an evaluation of this food as a source of vitamin E. A suitable measure is the net vitamin E content, i.e., gross vitamin E minus the amount needed for PUFA protection. Therefore, some food-stuffs generally considered as vitamin-E sources, as concluded from their gross vitamin E content, cause in reality a vitamin E deficiency if not sufficiently compensated by other vitamin E supplying food constituents. Examples of the net vitamin E content of some fats and oils, fish and nuts are shown. Consequences for food composition data and food labeling and the problem of meeting the vitamin-E requirements are discussed.
Z Ernahrungswiss 1991 Sep
PMID:On the problematic nature of vitamin E requirements: net vitamin E. 176 54


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