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

A progressive neurological syndrome with cerebellar signs, abnormal proprioception, areflexia and Babinski response was observed in a child with chronic intestinal malabsorption. There was no ophtalmoplegia or retinitis pigmentosa. Electromyography and biopsy showed no axonopathy or myopathy. Two other members of the family were also affected. The serum Vitamin E corrected the serum Vitamin E levels within a few months and led to secondary neurological improvement. The authors underline the importance of searching for Vitamin E deficiency and its cause in patients, especially children, with signs of spino cerebellar degeneration. Substitative therapy may have a favorable influence on the neurological condition even when administered late.
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PMID:[Neurological manifestations in relation to vitamin E deficiency, caused by a defect of biliary acid synthesis]. 320 25

Vitamin E was discovered by Evans and Bishop in 1922. Work in the 1930s revealed the chemical structure and the biological function of alpha-tocopherol. In the 1940s Filer and others demonstrated that vitamin E protects tissue unsaturated fatty acids against oxidation. The 1940s and the 1950s marked the beginning of interest in the role of vitamin E in infant nutrition. During this period, investigators examined the intestinal absorption of vitamin E in infants and its use for the prevention of hemolysis, retrolental fibroplasia, intracranial hemorrhage, and pulmonary oxygen toxicity. These studies were the forerunners of more recent studies examining possible benefits of vitamin E therapy in premature infants. Recent studies confirmed earlier reports indicating that enteral administration of vitamin E is the safest and most effective route in infants. Although preventing vitamin E deficiency is clearly necessary, neither earlier nor more recent work has shown any benefit from high-dose vitamin E therapy (greater than 20 IU X kg-1 X d-1) for premature infants.
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PMID:History of vitamin E in infant nutrition. 330 Feb 57

Vitamin E and linoleate, both of which are found in high concentrations in sunflower seed oil, were examined independently for their influence on general and blood-vascular parameters in vitamin E-deficient common marmosets. A vitamin E-deficient diet (-E, 4 micrograms/g) was supplemented with either 40 micrograms/g vitamin E (+E), vitamin E stripped sunflower oil (+10% SSO-E), or SSO (+10% SSO w/w) in a 2 x 2 factorial designed experiment, and the diets fed for 9 months to 4 even groups of common marmosets. Vitamin E deficiency was associated in marmosets with a loss of skeletal muscle mass and of body weight, enhanced peroxidative haemolysis of erythrocytes, increased white blood cell counts, and in the SSO-E group a relative neutrophilia. Platelet reactivity was increased with vitamin E deficiency, and to a greater degree with the SSO-E group. Aortic prostacyclin production was significantly increased by the addition of vitamin E, linoleate and both as SSO to the deficient diet, the effects being additive. Fatty acid changes associated with the different treatments reflected the influence of high linoleate and vitamin E treatments. The platelet and aortic arachidonate value in the SSO-E group showed the lowest and most variable value, and this was associated with greatest platelet aggregability. An adequate vitamin E intake is essential for stabilising high PUFA diets and biomembranes and enhancing the protective role of prostacyclin in blood vessels against thrombogenesis.
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PMID:The influence of linoleate and vitamin E from sunflower seed oil on platelet function and prostaglandin production in the common marmoset monkey. 343 42

Weanling male Sprague Dawley rats were fed a vitamin E and C-free basal diet with or without supplementation of 100 IU vitamin E per kg diet. After 20 weeks, the vitamin E-deficient rats were divided into four groups, six in each group, and received supplemental ascorbic acid and/or vitamin E by tube feeding daily for 7 days: Group I, 30 mg ascorbic acid/100 g body wt.; Group II, 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; Group III, 30 mg ascorbic acid and 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; and Group IV, placebo. The six control rats (Group V) received placebo. The rats were sacrificed, blood and liver samples were collected for biochemical determinations. Vitamin E deficiency significantly increased erythrocyte (RBC) spontaneous hemolysis, liver thiobarbituric acid (TBA) value, activities of glutamateoxaloacetate transaminase (GOT), pyruvate kinase (PK), and creatine phosphokinase (CPK) in plasma, and significantly lowered plasma vitamin E levels and glutathione peroxidase (GPX) activities. Tube-feeding ascorbic acid for 7 days produced partial reversal effect on liver TBA values, activities of plasma PK, GOT, CPK, and plasma vitamin E levels but not on RBC hemolysis and plasma GPX activity. Tube feeding both ascorbic acid and vitamin E showed similar partial reversal effect as feeding vitamin E alone on all the parameters stated above. The results suggest that ascorbic acid may spare the metabolism of vitamin E and partially reverse the changes in some of the biochemical parameters characteristic of vitamin E deficiency.
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PMID:Effect of ascorbic acid and vitamin E on biochemical changes associated with vitamin E deficiency in rats. 344 Jul 14

We report the cases of two adult patients with cystic fibrosis affecting the pancreas and liver, who also had severe vitamin E deficiency and neurologic disease. The most prominent clinical features were abnormal eye movements, diminished reflexes, decreased vibratory and position sense, ataxia, and muscle weakness. Treatment with intramuscular injections of vitamin E partially corrected the neurologic deficits. Vitamin E absorption tests documented severe malabsorption, which was later alleviated by the addition of dessicated ox bile to the regimen of alpha-tocopheryl acetate. These studies suggest that a decreased intraluminal concentration of bile salts is an important factor in the development of severe vitamin E deficiency and in the poor response to oral replacement therapy that is seen in some patients with cystic fibrosis.
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PMID:Vitamin E deficiency and neurologic disease in adults with cystic fibrosis. 359 48

Four patients had accumulation of ceroid in smooth muscle (lipofuscinosis), which indicated severe or uncontrolled malabsorption, with confirmed vitamin E deficiency in three cases. The distribution of the pigment was systematic, and there seemed to be an association between malabsorption syndrome and vitamin E deficiency. Vitamin E supplementation seems to be indicated in such patients, and it is suggested that studies of smooth muscle function should be made in cases of heavy accumulation of ceroid.
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PMID:Accumulation of ceroid in smooth muscle indicates severe malabsorption and vitamin E deficiency. 362 1

The in vivo Rb+ uptake and release of rat brain cortical cells of 11-months-old rats fed with a vitamin E deficient diet was investigated. The animals were treated with a daily dose of 30 mg RbCl/100 g body weight for 14 days. After discontinuation of the RbCl treatment the animals were killed at intervals of 2, 4, 9 and 15 days, respectively. The intracellular Rb+ and K+ contents were analyzed by energy dispersive X-ray microanalysis, whereas concentrations of these two ions were determined by atomic absorbtion spectrophotometry in the serum and cerebrospinal fluid. Vitamin E deficient rats accumulate more Rb+ than age-matched normally fed animals at any time taken into account. Rb+-discrimination ratios calculated on the basis of Rb+ and K+ contents of both, cortical cell cytoplasm and cerebrospinal fluid, are higher in vitamin E deficient rats than in the controls (+20%), which supports the view that the enhanced membrane lipid peroxidation induced by vitamin E deficiency impairs the passive membrane permeability for Rb+ (and K+).
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PMID:Vitamin E deficiency alters the in vivo Rb+ discrimination of rat brain cortical cells. 371 68

To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18:2 omega 6 or 18:3 omega 3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18:3 omega 3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22:6 omega 3, since this fatty acid is very low in livers of the rats fed the marginal 18:2 omega 6 diet but much higher in livers of the rats fed the marginal 18:3 omega 3 diet. Brain 22:6 omega 3 values are comparable for both groups. The source of 22:6 omega 3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22:6 omega 3 in serum, liver and carcass of rats on the 18:2 omega 6--containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats.
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PMID:A relationship between essential fatty acid and vitamin E deficiency. 376 33

The effects of dietary vitamin E and high-level supplementation of ascorbic acid on iron distribution in rat tissues were studied. Weanling male Sprague-Dawley rats, fed ad libitum a vitamin E and ascorbic acid free basal diet, were divided into four groups. They were supplemented with 0 or 45 IU/kg diet of vitamin E, and O or 0.2% ascorbic acid in a 2 X 2 complete factorial design. After 12 weeks, rats were killed; blood, liver, spleen, heart and skeletal muscle were collected for analysis. Vitamin E deficiency resulted in significantly decreased plasma iron levels and total iron binding capacity. The total iron and nonheme iron contents of the liver and spleen were significantly higher in the vitamin E-deficient groups compared with control groups. Vitamin E or ascorbic acid supplementation had no effect on iron content of the heart. Non-heme iron levels on per gram tissue were highest in the skeletal muscle of the group to which no vitamin E or ascorbic acid were supplemented. It appears that vitamin E and ascorbic acid interactively affect the iron distribution in rat tissues.
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PMID:Effects of dietary vitamin E and high level of ascorbic acid on iron distribution in rat tissues. 378 49

Since the spinal cord and peripheral nerves are vulnerable to the effects of vitamin E deficiency, vitamin E concentrations in various discrete regions of these parts of the nervous system of the rat were determined. Furthermore, as acrylamide toxicity and vitamin E deficiency share some neuropathological features, tissue vitamin E concentrations in acrylamide-treated rats were also studied. Male Sprague Dawley rats (200 to 250 g body weight) were fed normal rat chow with or without 0.03% acrylamide in their drinking water. After 24 days, the animals were sacrificed and the tissues assayed for vitamin E by a liquid chromatographic method. Vitamin E concentrations decreased from cerebral cortex to spinal cord with no concentration gradients between different levels of the spinal cord. Sciatic nerve concentration of alpha tocopherol was as high as that of cerebral cortex, and the former also contained measurable amounts of gamma tocopherol. Vitamin E concentrations in the majority of nervous tissues samples remained unchanged with acrylamide treatment.
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PMID:Vitamin E concentrations in different regions of the spinal cord and sciatic nerve of the rat. 378 36


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