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

Vitamin E supplementation (dl-alpha-tocopheryl acetate except where noted) in excess of requirement significantly increased humoral immune response or disease resistance. Mice immunized with sheep red blood cells or tetanus toxoid and fed the supplemental vitamin demonstrated increased plaque-forming cells (PFC) and hemagglutinin (HA) titers. A vitamin E deficiency resulted in decreased PFC and little IgG which was partially corrected by N,N-diphenyl-p-phenylenediamine but not as effectively as by vitamin E. Hens immunized with Brucella abortus and fed different levels of the vitamin produced chicks with increased passive immunity; a biphasic antibody response to the level of the vitamin fed was noted. Vitamin E fed to nonimmunized hens was found to significantly increase the primary immune response of their immunized chicks. Feeding dl-alpha-tocopheryl acetate to guinea pigs immunized with Venezuelan equine encephalomyelitis virus resulted in no increased immunity. Injecting this form of the vitamin resulted in severe tissue reaction. However, injecting dl-alpha-tocopheryl significantly improved hemagglutinin inhibition titers. Chicks and turkeys infected with Escherichia coli and fed supplemental vitamin E had reduced mortality and increased HA titers. Sheep fed vitamin E and challenged with Chlamydia had improved weight gains and no detectable Chlamydia.
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PMID:Protective effects of supplemental vitamin E against infection. 37 53

Vitamin E status of Chinese population with different age groups was studied by determining plasma vitamin E levels (PE) and hydrogen peroxide-induced erythrocyte hemolysis (HPEH). The mean PE of 99 adults, ages 23 to 78, was 1.05 +/- 0.47 mg/100 ml. There was no significant difference between sexes. PE was negatively correlated with HPEH (P less than 0.01). There was a significant positive correlation (P less than 0.01) between PE and plasma cholesterol level. The mean PE of four young men of Yami tribesmen, ages 16 to 19, was 0.60 +/- 0.10 mg/100 ml. HPEH was low. After daily supplementation of 200 mg dl-alpha-tocopheryl acetate for 16 days, PE increased 54%, but the plasma cholesterol was not affected. The mean PE of 39 elementary school children ages 12 to 13, was 0.70 +/- 0.31 mg/100 ml. The mean PE of 20 newborn infants was 0.23 +/- 0.08 mg/100 ml. HPEH was as high as 56.5 +/- 31.9% indicating a state of vitamin E deficiency. PE of total population was positively correlated with age (P less than 0.01). It was concluded that the vitamin E status of Chinese population in Taiwan was comparable to that of population groups in many other parts of the world.
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PMID:Vitamin E status of Chinese population in Taiwan. 85 43

The role of vitamin E in human nutrition was studied by investigation of patients with cystic fibrosis (CF) and associated pancreatic insufficiency. Vitamin E status was assessed by measurement of the plasma concentration of the principal circulating isomer, alpha-tocopherol. Results of such determinations in 52 CF patients with pancreatogenic steatorrhea revealed that all were deficient in the vitamin. The extent of decreased plasma tocopherol varied markedly but correlated with indices of intestinal malabsorption, such as the serum carotene concentration and percentage of dietary fat absorbed. Supplementation with 5-10 times the recommended daily allowance of vitamin E in a water-miscible form increased the plasma alpha-tocopherol concentrations to normal in all 19 CF patients so evaluated. Studies on the effects of vitamin E deficiency focused on possible hematologic alterations. An improved technique was developed to measure erythrocyte hemolysis in vitro in the presence of hydrogen peroxide. While erythrocyte suspensions from control subjects demonstrated resistance to hemolysis during a 3-h incubation, all samples from tocopherol-deficient CF patients showed abnormal oxidant susceptibility, evidenced by greater than 5% hemoglobin release. The degree of peroxide-induced hemolysis was related to the plasma alpha-tocopherol concentration in an inverse, sigmoidal manner. The possibility of in vivo hemolysis was assessed by measuring the survival of (51)Cr-labeled erythrocytes in 19 vitamin-E deficient patients. A moderate but statistically significant decrease in the mean (51)Cr erythrocyte half-life value was found in this group. Measurement of erythrocyte survival before and after supplementation of 6 patients with vitamin E demonstrated that the shortened erythrocyte lifespan could be corrected to normal with this treatment. Other hematologic indices in deficient subjects, however, were normal and did not change upon supplementation with vitamin E. It is concluded that CF is invariably associated with vitamin E deficiency, provided that the patient in question has pancreatic achylia and is not taking supplementary doses of tocopherol. Concomitant hematologic effects consistent with mild hemolysis, but not anemia, occur and may be reversed with vitamin E therapy. Patients with CF should be given daily doses of a water-miscible form of vitamin E to correct the deficiency.
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PMID:The occurrence and effects of human vitamin E deficiency. A study in patients with cystic fibrosis. 87 86

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

Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanisms. Se, an essential component of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI2) production and platelet thromboxane (TX)A2 directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic PGI2 and platelet TXA2 synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se (0, 0.1, 0.2 ppm) for 2 mo. Thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, were measured by radioimmunoassay (RIA) after incubation of whole blood and aortic rings at 37 degrees C for 10 and 30 min, respectively. Vitamin E deficiency reduced plasma vitamin E to 5-17% of control-fed rats, and supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB2 and PGI2 synthesis. Se deficiency did not alter platelet TXB2 synthesis, but significantly decreased aortic PGI2 synthesis. It was necessary to supplement with both antioxidants in order to increase PGI2 synthesis. Se and vitamin E deficient groups had a higher TXB2/PGI2 ratio (0.17 +/- 0.08) compared to Se- and vitamin E-supplemented groups (0.03 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E. 137 63

It has been over 50 years since vitamin E was originally described as a lipid-soluble dietary constituent required for normal reproduction in rats. Vitamin E is recognized as an essential vitamin required for all classes of animals functioning predominantly as an intracellular antioxidant in maintaining the integrity of biological cell membranes. Although a wealth of information has been gathered on clinical signs of vitamin E deficiency, establishing its requirements for animals has been exceedingly difficult because of interrelationships with other dietary constituents. Vitamin E requirements for animals cannot be defined in isolation. Requirements are influenced by the amount and type of fat (particularly with monogastrics) and degree of fat oxidation in the diet; the presence of antioxidants; dietary selenium (closely interrelated with vitamin E), iron, copper, and sulphur amino acids, as well as the physiological status of the animal. Other factors to be considered in assessing vitamin E needs of animals under commercial production conditions include: a) variability of vitamin E content in feedstuffs; b) poor stability of vitamin E during processing and storage of feeds; and c) management practices resulting in overstressed animals. Information on the function of or requirements for vitamin E in animals is very incomplete. Estimated dietary vitamin E requirements for most animal species are in the range of 10-40 IU/kg of diet. Of particular concern is the lack of vitamin E requirement information regarding young dairy and beef calves. Although good experimental evidence indicates a beneficial role of supplemental vitamin E above physiological levels on overall performance, enhanced immunocompetence and preservation of meat and milk products, levels of vitamin E required to produce these desired effects needs to be firmly established. Present estimated dietary requirements for vitamin E across species may need to be redefined as new information becomes available about the role this nutrient plays in growth, health and overall metabolism.
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PMID:Comparative vitamin E requirements and metabolism in livestock. 147 5

Vitamin E includes eight naturally occurring fat-soluble nutrients called tocopherols and dietary intake of vitamin E activity is essential in many species. alpha-Tocopherol has the highest biological activity and the highest molar concentration of lipid soluble antioxidant in man. Deficiency of vitamin E may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma alpha-tocopherol is found in all lipoprotein fractions, but mostly associated with apo B-containing lipoproteins in man. In rats approximately 50% of alpha-tocopherol is bound to high density lipoproteins (HDL). After intestinal absorption and transport with chylomicrons alpha-tocopherol is mostly transferred to parenchymal cells of the liver were most of the fat-soluble vitamin is stored. Little vitamin E is stored in the non-parenchymal cells (endothelial, stellate and Kupffer cells). alpha-Tocopherol is secreted in association with very low density lipoprotein (VLDL) from the liver. In the rat about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. Clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol, causing reduced tissue concentrations of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature babies and patients with malabsorption, but there is little evidence that the well balanced diet of the healthy population would be improved by supplementation with vitamin E.
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PMID:Absorption, transport and metabolism of vitamin E. 187 54

This study revealed the occurrence of vitamin E deficiency in the myocardium of 60-day-old Syrian cardiomyopathic hamsters (BIO14.6), and that this deficiency might be related to the increase in lipid peroxide. Vitamin E administration for ten days effectively restored creatininekinase activity and decreased the lipid peroxide content in the myocardium, returning these to normal control levels (F1b). These results indicate that vitamin E deficiency, possibly combined with oxidative stress in the early cardiomyopathic stage plays an important role in initiating the pathogenesis of myocardial lesions.
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PMID:Vitamin E deficiency has a pathological role in myocytolysis in cardiomyopathic Syrian hamster (BIO14.6). 195 82

The purpose of this study was to determine the prevalence of vitamin E deficiency in adults with chronic cholestatic liver disease and to quantify the association between their psychomotor performance and vitamin E status. In 42 female patients with primary biliary cirrhosis, 43.5% met two standard criteria for vitamin E deficiency. Vitamin E-deficient patients performed less well than did healthy control subjects on six of eight neuropsychologic tests of psychomotor capacity (p less than 0.01). Vitamin E-sufficient patients did not differ significantly from normal control subjects. Serum vitamin E concentrations were significantly lower in the group classified as significantly psychomotor-impaired by two independent neuropsychologists (blind to vitamin E status) whereas liver-injury measures failed to distinguish between these two groups. Patients with low serum vitamin E exhibited clinically evident neurologic abnormalities. These data suggest that vitamin E deficiency may, in part, underlie psychomotor and neurologic disturbance found in adult patients with chronic cholestatic liver disease.
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PMID:Vitamin E deficiency and psychomotor dysfunction in adults with primary biliary cirrhosis. 197 68

Chronic vitamin E deficiency results in the premature and exaggerated development of neuroaxonal dystrophy (NAD) in primary sensory axon terminals in rat medullary gracile/cuneate nuclei, sites in which NAD develops normally with age. In the current study we determined if chronic Vitamin E deprivation had a similar effect on the development of NAD in the celiac/superior mesenteric sympathetic ganglia (C/SMG), another site with age-dependent NAD. The frequency of NAD failed to increase in the SMG of the same vitamin-E deficient animals in which a marked increase in severity of NAD was found in the gracile nucleus. These findings indicate that different populations of neurons are selectively involved in vitamin E deficiency and that the distribution of axonopathy in the E-deficient C/SMG does not duplicate the pattern of experimental diabetes and aging.
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PMID:Differential effect of chronic vitamin E deficiency on the development of neuroaxonal dystrophy in rat gracile/cuneate nuclei and prevertebral sympathetic ganglia. 206 45


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