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

1. A vicious cycle of malabsorption and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease in infancy. Vitamin E deficiency is common in malnourished infants with protracted diarrhoea. We have studied the effects of chronic vitamin E deficiency on small-intestinal secretion and absorption in the rat. 2. Weanling rats were fed vitamin E-sufficient or -deficient diets for 21 weeks. Jejunal function was studied in vitro in an Ussing chamber after this period. 3. Steady-state isotopic flux experiments in unstimulated tissues demonstrated net Na+ and Cl- secretion in vitamin E-deficient jejuna but net Na+ and Cl- absorption in vitamin E-sufficient jejuna. 4. Basal intestinal short-circuit current was the same in both groups. 5. Cyclic nucleotide and maximal non-neuronal acetylcholine-mediated electrogenic secretion were increased in vitamin E-deficient jejuna. 6. Exogenous 5-hydroxytryptamine (serotonin) induced a smaller increment in electrogenic secretion in vitamin E-deficient jejuna. 7. Vitamin E-deficient jejuna were less responsive to exogenous noradrenaline, resulting in a smaller alpha 2-adrenergic-mediated decrease in intestinal short-circuit current. 8. Fasting for 72h produced a greater increment in intestinal short-circuit current in vitamin E-deficient jejuna. 9. Chronic vitamin E deficiency is prosecretory in the small intestine and may predispose to the perpetuation of protracted diarrhoeal diseases.
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PMID:Modulation of small-intestinal secretion and absorption in chronic vitamin E deficiency: studies in rat jejunum in vitro. 828 52

1. Vitamin A: There are very few reports on vitamin A deficiency in Japan because of the rising national status of nutrition, while vitamin A deficiency is still an important nutritional problem in developing and poorly developed countries. In the pediatric field, relationship between vitamin A nutrition and the mechanism for development of bronchopulmonary dysplasia have been discussed, since vitamin A acts as a protector from the keratinization of epithelial cells in the mucosal layer and the skin. The changes in the lung tissues with inadequately supplied vitamin A, probably cause the chronic lung disease resulting from mechanical ventilation in neonates, in whom the plasma vitamin A and retinol binding protein levels are usually low. 2. Vitamin E: In keeping with the view that newborn infants and especially premature infants suffer from vitamin E deficiency. On the basis of recent findings of the vitamin E content in the neonatal cells, the previous concept would agree, as an existing marginal deficiency in neonates. The neurologic deficits manifested in a beta-lipoproteinemia is confirmed to be vitamin deficiency in humans. It has also become clear that similar neurologic impairment occurs in other chronic fat malabsorptive states, such as cholestatic liver diseases, extensive resection of the gut. More recently several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption in whom progression of the diseases is terminated by the vitamin E therapy (isolated vitamin E deficiency) have been reported. The above items are discussed.
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PMID:[Vitamin A and E deficiency in children, including the marginal deficiency]. 848 80

Vitamin E (alpha-tocopherol) is a known biological antioxidant able to quench the lipid peroxidation chain and to protect the cellular structures (e.g., plasma membranes) from the attack of free radicals which are reported to play a primary role in aging. To assess whether the absence of alpha-tocopherol from the diet of young laboratory animals may be considered a reliable model of precocious brain aging, intracellular ionic content of brain cortex pyramidal cells, ultrastructural features of synaptic contact zones, synaptic mitochondria and perykarial mitochondria positive to the succinic dehydrogenase (SDH) histochemical reaction with copper ferrocyanide have been investigated by X-ray microanalysis and computer-assisted morphometry in young, adult, old and 11-month-old vitamin E deficient rats. Our data document significant alterations of intracellular ionic content, synaptic contact areas and synaptic and perykarial mitochondria in aging. Vitamin E deficiency caused similar alterations in adult animals. Taking into account the known role of alpha-tocopherol in protecting the cellular membrane structure, we support that the common process underlying the changes found in aging and vitamin E deficiency is an excessive deterioration of the neuronal membrane.
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PMID:Vitamin E deficiency as a model of precocious brain aging: assessment by X-ray microanalysis and morphometry. 855 24

Children deficient in vitamin E have various neurologic symptoms. 2 cases representing different mechanisms of this vitamin deficiency are reported. A 15-year-old boy with fat malabsorption due to cystic fibrosis who was diagnosed as being vitamin E deficient (< 0.5 mg/l), had typical neuropathies. On the other hand, a 12-year-old Beduin girl had isolated vitamin E deficiency, as well as neurological symptoms suggestive of Friedrich's ataxia. Vitamin E supplementation by intramuscular injection in the first case and per os in the second led to significant improvement in neurological symptoms.
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PMID:[Neurological symptoms associated with vitamin E deficiency]. 868 50

Vitamin E deficiency in organism leads to microsome membrane phospholipid composition changes, oxidation, superoxide dismutase (SOD) activity decrease, accompanied with the disorders of lung and liver tissues functional state which is connected with regulation of membrane penetration. The negative effect of E-hypovitaminosis more affects the liver than lung, which is caused by their different functional purposes, peculiarities of metabolic processes as well as by the content of biomembrane structural components. Vitamin E protects phospholipids from oxidation, regulates AOS condition, SOD-activity and promotes in such way the tissue functional disturbances correction of the animals tested. New preparation "Calmophyl" is a phospholipid complex from marine organisms with surfactant-kind effect, which displays antioxidative properties and decreases toxic affect of CCl4, corrects functional tissue disorders, regenerates normal activity of enzymes. Preparation of natural phospholipids has been shown to be capable to stabilize cell membranes probably by means of replacing the membrane phospholipid composition and decreasing disturbances in the antioxidative system.
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PMID:[Role of phospholipids in functionally different cell membranes under conditions of antioxidant system disturbance]. 875 1

A 22-year-old man presented with progressive gait instability, tremor, and dysarthria since childhood. Electrophysiologic studies revealed a sensorimotor polyneuropathy. Laboratory studies documented vitamin E deficiency; however, no gastrointestinal, hepatic, or lipoprotein disorder could be identified. Vitamin E therapy normalized the serum level, but there was no neurologic improvement. Isolated vitamin E deficiency, in the absence of lipid malabsorption, should be considered in the evaluation of children and adults with ataxia and peripheral neuropathy.
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PMID:Isolated vitamin E deficiency. 876 Dec 74

The aims of the present study were to establish a suitable criterion for estimating the vitamin E requirement for young pigs, and to investigate the influence of dietary fats on the requirement of this nutrient. In Expt 1 weaned pigs were given a semi-purified diet supplemented with 0, 20, or 100 mg DL-alpha-tocopheryl acetate/kg. Pigs in Expt 2 were fed on diets containing 10 g sunflower oil (SO) stripped of vitamin E/kg in diets 1 and 2, 100 g SO/kg in diets 3 and 4, and 100 g tallow/kg in diet 5. Diets 2, 4 and 5 were supplemented with DL-alpha-tocopheryl acetate at 20 mg/kg for 0-28 d and 50 mg/kg for 29-56 d of the experiment respectively. Results showed that vitamin E concentrations in plasma and tissues reflected dietary levels of vitamin E. No apparent clinical signs of vitamin E deficiency were observed, but pigs fed on diets without vitamin E supplementation showed a higher (P < 0.05) lipid peroxidation status as indicated by thiobarbituric acid-reactive substances in erythrocytes, and ethane and pentane levels in exhaled gases than those fed on supplemental diets. This indicated that the former was deficient in vitamin E. Data in Expt 1 suggested that supplementation with 20 mg DL-alpha-tocopheryl acetate/kg is adequate for young pigs when the diet contains 30 g lard/kg. However, results in Expt 2 showed that this level was inadequate when the diet contains 100 g SO/kg or its equivalent to 70 mg polyunsaturated fatty acids (PUFA)/g. Vitamin E and lipid peroxidation status of pigs were affected by both dietary vitamin E and dietary PUFA. This demonstrates that the requirement for vitamin E in young pigs increases as PUFA levels in the diet increase. The present study shows that lipid peroxidation response of pigs is a suitable index to evaluate vitamin E requirements.
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PMID:Lipid peroxidation status as an index to evaluate the influence of dietary fats on vitamin E requirements of young pigs. 878 93

Unlike other vitamins, Vitamin E probably has received less attention in the past because humans are not likely to suffer from deficiency disorders. This fat soluble vitamin is available in many foods, is easily stored, and is readily reused by the body. The original research carried out in the 1920s found that a Vitamin E deficiency in rats produced problems in their reproductive capacity. The name given to the substance at that time, "tocopherol," reflects this action as it is taken from the Greek word, "tocos," meaning "to give birth."
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PMID:Vitamin E: hype or hope. 886 89

We describe 4 siblings of a consanguineous Bedouin family with Friedreich ataxia phenotype in whom low serum vitamin E levels without other indicators of fat malabsorption were detected. Although age of onset and some of the clinical features were alike in all 4 patients, the electrophysiological parameters were markedly abnormal in 2, but normal in the other 2. Erythrocytes revealed both membranous and intracellular evidence of oxidative damage. The mutations described in other families with ataxia with isolated vitamin E deficiency were not detectable, nor was an abnormal single-stranded conformation polymorphism pattern apparent in the three exons at the 3' region of the gene. Vitamin E administration in pharmacological doses improved the neurological condition in 2 patients and also corrected some of the patients' erythrocyte cell abnormalities. The finding of vitamin E deficiency in other cases of Friedreich ataxia phenotype may allow treatment at an early stage of the disease, when large dose Vitamin E therapy may reverse the neurological lesions.
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PMID:Ataxia with isolated vitamin E deficiency in four siblings. 897 36

Vitamin E is one of the most important lipid-soluble antioxidant nutrients. Severe vitamin E deficiency can have a profound effect on the central nervous system. Cystic fibrosis, chronic cholestatic liver disease, abetalipoproteinemia, short bowel syndrome, isolated vitamin E deficiency syndrome and other malabsorption syndromes all may cause varying degrees of neurologic deficits due to related vitamin deficiencies. The classic abnormalities in vitamin E deficiency progress from hyporeflexia, ataxia, limitations in upward gaze and strabismus to long-tract defects, profound muscle weakness and visual field constriction. Patients with severe, prolonged deficiency may develop complete blindness, dementia and cardiac arrhythmias. Treatment must be tailored to the underlying cause of vitamin E deficiency and may include oral or parenteral vitamin supplementation. The more advanced the deficits, the more limited the response to therapy. Therefore, a good neurologic examination and periodic serum vitamin E levels are essential in patients at risk of vitamin E deficiency.
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PMID:Neurologic findings in vitamin E deficiency. 901 78


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