Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin E is the general term for all tocopherols and tocotrienols, of which alpha-tocopherol is the natural and biologically most active form. Although gamma-tocopherol makes a significant contribution to the vitamin E CONTENT in foods, it is less effective in animal and human tissues, where alpha-tocopherol is the most effective chain-breaking lipid-soluble antioxidant. The antioxidant function of vitamin E is critical for the prevention of oxidation of tissue PUFA. Animal experiments have shown that increasing the degree of dietary fatty acid unsaturation increases the peroxidizability of the lipids and reduces the time required to develop symptoms of vitamin E deficiency. From these experiments, relative amounts of vitamin E required to protect the various fatty acids from being peroxidized, could be estimated. Since systematic studies on the vitamin E requirement in relation to PUFA consumption have not been performed in man, recommendations for vitamin E intake are based on animal experiments and human food intake data. An intake of 0.6 mg alpha-tocopherol equivalents per gram linoleic acid is generally seen as adequate for human adults. The minimum vitamin E requirement at consumption of fatty acids with a higher degree of unsaturation can be calculated by a formula, which takes into account the peroxidizability of unsaturated fatty acids and is based on the results of animal experiments. There are, however, no clear data on the vitamin E requirement of humans consuming the more unsaturated fatty acids as for instance EPA (20:5, n-3) and DHA (22:6, n-3). Studies investigating the effects of EPA and DHA supplementation have shown an increase in lipid peroxidation, although amounts of vitamin E were present that are considered adequate in relation to the calculated oxidative potential of these fatty acids. Furthermore, a calculation of the vitamin E requirement, using recent nutritional intake data, shows that a reduction in total fat intake with a concomitant increase in PUFA consumption, including EPA and DHA, will result in an increased amount of vitamin E required. In addition, the methods used in previous studies investigating vitamin E requirement and PUFA consumption (for instance erythrocyte hemolysis), and the techniques used to assess lipid peroxidation (e.g. MDA analysis), may be unsuitable to establish a quantitative relation between vitamin E intake and consumption of highly unsaturated fatty acids. Therefore, further studies are required to establish the vitamin E requirement when the intake of longer-chain, more-unsaturated fatty acids is increased. For this purpose it is necessary to use functional techniques based on the measurement of lipid peroxidation in vivo. Until these data are available, the widely used ratio of at least 0.6 mg alpha-TE/g PUFA is suggested. Higher levels may be necessary, however, for fats that are rich in fatty acids containing more than two double bonds.
 ...
PMID:Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review. 1080 54

One of the most dramatic and consequence-bearing age-related phenomena is the decline of the immune function with old age. Age-related T cell-mediated immunity dysfunction has been implicated in the etiology of many of the chronic degenerative diseases of the elderly, including arthritis, cancer, autoimmune diseases and increased susceptibility to infectious diseases. T cells from aged individuals are impaired in their response to mitogens and in their cytokine production. In recent years, several studies have emphasized the importance of intracellular anti-oxidant levels for preserving the immune function. Recent progress in understanding the mechanisms of action of anti-oxidants on cellular metabolism, have shown that anti-oxidants may modulate signal transduction and gene expression in immune cells. Vitamin E is widely recognized as a major lipid-soluble chain-breaking anti-oxidant in the biological membrane, where it scavenges free radicals, inhibiting the initiation and chain propagation of lipid peroxidation and protecting cellular structures against oxidative stress damage. Experimental studies have provided evidences for a role of vitamin E in protecting the immune system of elderly subjects. This article reviews the studies concerning the effect of both vitamin E deficiency and supplementation on T cell-mediated immune function in aging. Following a chronological pathway, the present article will also discuss the knowledge regarding the underlying mechanism of action of vitamin E.
 ...
PMID:Dietary vitamin E and T cell-mediated function in the elderly: effectiveness and mechanism of action. 1081 23

An improved understanding of its physiology has led to better therapeutic use of vitamin E in recent years. It is a physiological membrane bound antioxidant, protecting cell membrane lipids from oxidant damage by free redicals. Cholestatic liver disease, abetalipoproteinemia and ataxia with vitamin E deficiency are the common deficiency states where vitamin E is of definite therapeutic value, while reports of unproven benefits abound in literature. Vitamin E status of the body can be assessed by serum levels and various functional studies. The new water soluble form, tocopherol polyethylene glycol succinate (TPGS), is therapeutically superior to the standard oral forms available. Details of physiology and therapeutic application of the vitamin are discussed.
 ...
PMID:Vitamin E updated. 1082 96

Vitamin E content of cardiac tissue has been proposed to play a major role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawley rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values +/- SEM: CON = 48.2 +/- 3.5; VE-DEF = 12.4 +/- 1.4 micrograms VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.
 ...
PMID:Vitamin E deficiency fails to affect myocardial performance during in vivo ischemia-reperfusion. 1121 54

The study was carried on 90 adult cases which were divided into 3 groups of 30 cases each. Group A consisted of 30 normal healthy controls whereas Group B and C comprised of 30 patients each of chronic stable ischaemic heart disease and of acute myocardial infarction (AMI), respectively. Patients in all the 3 groups were age and sex matched. Group C consisted of 17 cases of anterior wall myocardial infarction, 10 of inferior wall, 2 of anterolateral and 1 of antero-inferior MI and they had an average 6.96 +/- 3.39 hours of chest pain before hospitalization. Serum vitamin E in group A, B and C on day 1 was 7.90 +/- 3.23, 5.345 +/- 2.37 and 1.302 +/- 1.090 micrograms/ml, respectively and malondialdehyde (MDA) levels in these groups were 0.759 +/- 0.27, 0.780 +/- 0.334 and 3.092 +/- 1.124 nmol/ml, respectively. Vitamin E and MDA levels in group C on day 3 were 3.382 +/- 1.088 micrograms/ml and 1.492 +/- 0.849 nmol/ml, respectively. In Group C, vitamin E levels were significantly decreased (p < 0.001) as compared to controls and remained low after 2 days. MDA levels were raised more than 3 times in AMI group (p < 0.01) and decreased slightly after 2 days but were elevated compared to controls. Findings suggest that vitamin E deficiency is inversely related to lipid peroxidation and is elevated during AMI. Therefore supplementation of vitamin E in AMI would be beneficial.
 ...
PMID:Lipid peroxidation and vitamin E in ischemic heart disease. 1122 80

Neurological signs including posterior column, spinocerebellar, retinal, and peripheral nerve deficits are being increasingly recognized in vitamin E deficiency states. Children suffering from protein-energy malnutrition (PEM) revealed significantly reduced serum alpha-tocopherol levels compared to age-matched normal children, the deficient subjects also exhibited the widely recognized signs of tocopherol deficiency. In this prospective therapeutic intervention study moderate PEM subjects were administered aqueous oral vitamin E supplementation for 6 weeks and compared with control PEM subjects. The parameters studied included pre- and post-therapy serum alpha-tocopherol levels, alpha-tocopherol lipid ratio, lipid profile, creatine phosphokinase levels, and electroneurophysiological studies. Vitamin E supplementation normalized serum alpha-tocopherol levels (p < 0.001), alpha-tocopherol lipid ratio (p < 0.001), reduced creatine phosphokinase levels (p < 0.01), and reduced neurological signs in PEM subjects (p < 0.001). The observed improvement in neurological dysfunction among PEM subjects is of great interest, especially in developing countries. While larger studies are recommended, the importance of vitamin E administration in PEM is being reported.
 ...
PMID:Vitamin E administration and reversal of neurological deficits in protein-energy malnutrition. 1124 49

Vitamin E is the most important lipophilic antioxidant. Oxidative injuries are prevented or minimized by vitamin E supplementation. Various physiological and pathological situations are accompanied by vitamin E deficiency. However, it is not clear whether alimentary vitamin E deficiency in itself constitutes oxidant stress that induces appropriate responses, which, in turn, can be avoided by adequate vitamin E supplies, or whether the remaining cellular antioxidants compensate a temporary vitamin E deficiency. We studied effects of the dietary vitamin E status on cellular vitamin E levels and on the expression of heat shock proteins (HSPs) in alveolar type II cells and liver. The expression of HSPs, representing an early and very sensitive marker of cellular stress, was compared with the activity of antioxidative enzymes. Vitamin E depletion caused a substantial increase in HSP32 in alveolar type II cells, whereas in liver there was a marked increase in HSP70. The activity of the antioxidant enzymes, however, did not change significantly. A reversal of HSP expression to almost normal levels was seen after vitamin E resupplementation. These results indicate that, under normal conditions, a suboptimal supply of vitamin E to rats exposes the alveolar type II cells and the liver to reversible cellular stress.
 ...
PMID:An electrophoretic study of vitamin E status and expression of heat shock proteins in alveolar type II and liver cells. 1127 70

Vitamin E supplementation exhibits anti-inflammatory properties. In the lung, the beneficial effects of vitamin E supplementation on inflammation and infections are well documented, but potential consequences of alimentary vitamin E deficiency to the immunological status of lung cells are not known. It is unclear if temporary vitamin E deficiency exhibits deleterious consequences or can be compensated for by other cellular antioxidants. To address this question, the alimentary vitamin E supply to rats was modified. We then investigated the effects on major histocompatibility molecule (MHC) class II, cell adhesion molecules, interleukin (IL)10, tumor necrosis factor (TNF)alpha in various lung cells. The constitutive expression of MHC class II, intercellular adhesion molecule (ICAM)-1, L-selectin, alpha5-integrin, and CD 166, was demonstrated by flow cytometry on type II pneumocytes, alveolar macrophages, and on co-isolated lymphocytes. Vitamin E depletion increased ICAM-1 and CD166 on type II cells and macrophages, whereas the expression of L-selectin increased only on macrophages. Furthermore, the vitamin E depletion increased the cellular content and secretion of IL10 in type II cells, but decreased the content and secretion of TNFalpha. Vitamin E depletion decreased the cellular vitamin E content, but did not change the activity of antioxidant enzymes (catalase, superoxide dismutase) and the glutathion (GSH)/oxidized glutathion (GSSG) ratio in alveolar type II cells. The shift of protein kinase C (PKC) from the cytosol to membranes indicates that a PKC-dependent signaling pathway may be involved in the change of the immunological status of type II cells. All these effects were reversed by vitamin E repletion. In summary, these results are clearly compatible with the view that a temporary vitamin E deficiency induces a reversible immunological dysregulation in alveolar type II cells and lung macrophages. This deficiency might predispose the lung to develop acute or chronic inflammation.
 ...
PMID:Immunological dysregulation of lung cells in response to vitamin E deficiency. 1136 5

The Food and Nutrition Board of the Institute of Medicine recently published a comprehensive evaluation of antioxidants in human diets that includes dietary reference intakes for vitamin E. The new dietary reference intake is 15 mg (35 mol)/d for adults, which is 50% greater than the generous allowance in the 10th edition of Recommended Dietary Allowances published in 1989. Much of the data interpreted in these publications came from studies sponsored by the Committee of Nutritional Studies at Elgin State Hospital (Elgin, IL) of an earlier Food and Nutrition BOARD: The 50% increase in the recommended dietary allowances for vitamin E is not supported by any new data. It is possible that the publication of the Institute of Medicine did not take into consideration the effects of the oxidized lipids in the diets used to promote the development of vitamin E deficiency. If lipids, oxidized to remove tocopherols, had not been a part of the experimental diets, the minimum requirement for vitamin E would have been too small for possible evaluation. Studies on the different effects of saturated and oxidized lipids in the production of encephalomalacia in chicks and muscular dystrophy in rats are reviewed. The tolerable upper intake level of vitamin E supplementation is reported to be 1000 mg/d. It is possible that the universal consumption of aspirin may not have been taken into consideration when this level was determined. Vitamin E plus aspirin may increase the tendency to hemorrhage, which makes a lower upper intake level worth consideration.
 ...
PMID:Critique of the requirement for vitamin E. 1191 70

Vitamin E is a term that encompasses a group of potent, lipid-soluble, chain-breaking antioxidants. Structural analysis reveals that molecules having vitamin E activity include four isomers (alpha, beta, gamma, and delta) of both tocopherols and tocotrienols. Alpha-tocopherol has been shown to have the highest biological vitamin E activity in mammalian tissues based on fetal resorption assays, and it reverses vitamin E deficiency symptoms. Although the molecular functions fulfilled specifically by alpha-tocopherol have yet to be fully described, it is unlikely that they are limited to general antioxidant functions. Here we show the functional characterization of alpha-tocopherol associated protein, TAP, which displays significant sequence similarity to the alpha-tocopherol transfer protein. Ligand competition analysis showed that recombinant TAP binds to alpha-tocopherol but not to other isomers of tocopherols. Using GFP fusion protein expression system, we observed that TAP translocates from cytosol to nuclei in alpha-tocopherol-dependent fashion. Transient transfection experiment showed that TAP activates transcription of the reporter gene in alpha-tocopherol-dependent manner. These results suggest that the biological function of alpha-tocopherol is not only as an antioxidant but also as a transcriptional regulator of gene expression via association with a transcription factor TAP.
 ...
PMID:Tocopherol-associated protein is a ligand-dependent transcriptional activator. 1144 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>