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 known to play a protective role for cell membranes against free-radical attacks. Vitamin E deficiency causes a rapid macroscopic ageing of rats. On the other hand, during normal ageing, cell membranes undergo functional alterations resulting in an increased intracellular potassium concentration in brain and liver cells. Therefore, is was of interest to study whether vitamin E deficiency produces similar alterations in young rats. Female Wistar rats were fed with a vitamin E deficient diet from 1 month of age for 10 months. The parietal brain cortex and the liver were analyzed by means of a quantitative energy dispersive X-ray microanalytic method using a JEOL JSM-35C-EDAX-711-NOVA-3 system. Monovalent electrolyte contents as well as the water content of the cells were determined in 5 treated and 5 control animals. Water content was measured by analyzing the potassium content in aqueous, frozen state, and again in the dry mass of the cells. On the basis of these data, a computer program calculated the water proportions. Average values for 200 or more cells of each organ per group revealed a significant increase in the intracellular potassium content of the brain cells, whereas the sodium and chloride contents increased to a much lower extent. There was a 2.6% loss of intracellular water in the brain cells in the vitamin E deficient group. The liver monovalent ions and water content remained unchanged. The results obtained are discussed in terms of the membrane hypothesis of ageing.
 ...
PMID:In vivo effects of vitamin E deficiency on the intracellular monovalent electrolyte concentrations in brain and liver of rat. An energy dispersive X-ray microanalytic study. 726 78

Vitamin E levels were measured in the plasma of infants and children with various neuromuscular disorders. Seven of 8 infants with Werdnig-Hoffmann disease (WHD) had a significantly lower plasma vitamin E level (p less than 0.01) than age-matched normal controls, children with congenital myopathies, or children with muscular dystrophy. Vitamin E deficiency in WHD is not caused by malabsorption. A therapeutic trial of vitamin E in 3 patients with WHD did not change the natural course of the disease. Vitamin E deficiency may play a role in the pathogenesis of WHD.
 ...
PMID:Vitamin E deficiency in Werdnig-Hoffmann disease. 729 34

We report a 44-year-old woman in whom intestinal bypass for obesity at age 23 resulted in chronic malabsorption. After hysterectomy for menorrhagia due to atypical endometrial hyperplasia, the finding of myometrial lipofuscinosis led to a demonstration of vitamin E deficiency. Vitamin E supplementation led to an unexpected improvement in the unsteadiness of gait and slurring of speech of which she had also complained. We suggest that supplementation with vitamin E should be routine in all patients with persistent severe steatorrhoea.
 ...
PMID:Symptomatic vitamin E deficiency diagnosed after histological recognition of myometrial lipofuscinosis. 765 82

Vitamin E and selenium statuses were studied in thalassemic children in comparison with 16 normal controls. Twelve Hb H disease, 46 beta-thal/Hb E and 7 beta-thal major patients had lower plasma vitamin E level than controls but plasma vitamin E/total lipids ratio of Hb H disease subjects was not different from normal. Twelve Hb H disease and 33 beta-thal/Hb E patients had normal RBC Se but increased RBC GSH-Px activity. Ten vitamin E-deficient thalassemic subjects had been supplemented with 200 mg of oral vitamin E for 4-8 weeks. After supplementation, their plasma vitamin E increased and H2O2 hemolysis decreased to normal values. Their RBC GSH-Px activity also decreased but hematocrit did not change significantly. The results demonstrate that some types of thalassemic patients have vitamin E deficiency and support that vitamin E and selenium have related functions in the prevention of RBC oxidation. Vitamin E supplementation increased RBC resistance to oxidative damage.
 ...
PMID:Vitamin E status, glutathione peroxidase activity and the effect of vitamin E supplementation in children with thalassemia. 782 84

alpha-Tocopherol concentrations in brain were reduced to 3% of control levels in rats fed a vitamin E deficient diet for 52 weeks. Vitamin E deficiency resulted in a 19-33% loss of tyrosine hydroxylase (TH) immunopositive neurones in the substantia nigra, but not in the adjacent ventral tegmental area, compared with controls. Vitamin E deficiency, however, did not reduce striatal dopamine concentrations or turnover. When antioxidant defence mechanisms are defective, as in chronic vitamin E deficiency, the nigrostriatal pathway may be affected by oxidative damage and this may have implications for Parkinson's disease.
 ...
PMID:Nigral dopaminergic cell loss in vitamin E deficient rats. 782 29

alpha-Tocopherol transfer protein (alpha TTP), which specifically binds this vitamin and enhances its transfer between separate membranes, was previously isolated from rat liver cytosol. In the current study we demonstrated the presence of alpha TTP in human liver by isolating its cDNA from a human liver cDNA library. The cDNA for human alpha TTP predicts 278 amino acids with a calculated molecular mass of 31,749, and the sequence exhibits 94% similarity with rat alpha TTP at the amino acid level. The recombinant human alpha TTP expressed in Escherichia coli exhibits both alpha-tocopherol transfer activity in an in vitro assay and cross-reactivity to the anti-(rat alpha TTP) monoclonal antibody. Northern blot analysis revealed that human alpha TTP is expressed in the liver like rat alpha TTP. The human and rat alpha TTPs show structural similarity with other apparently unrelated lipid-binding/transfer proteins, i.e. retinaldehyde-binding protein present in retina, and yeast SEC14 protein, which possesses phosphatidylinositol/phosphatidylcholine transfer activity. Both Southern-blot hybridization of human-hamster somatic cell hybrid lines and fluorescence in situ hybridization revealed a single alpha TTP gene corresponding to the 8q13.1-13.3 region of chromosome 8, which is identical to the locus of a recently described clinical disorder, ataxia with selective vitamin E deficiency (AVED). The relationship between alpha TTP and AVED will be discussed.
 ...
PMID:Human alpha-tocopherol transfer protein: cDNA cloning, expression and chromosomal localization. 788 97

A kinetic model of vitamin E transport in humans is described using data from our studies with deuterium-labeled stereoisomers of alpha-tocopherol (RRR- and SRR-). In normal subjects, both alpha-tocopherols are present at similar concentrations in chylomicrons, but by 24 hr, RRR-alpha-tocopherol is at higher plasma concentrations because RRR-alpha-tocopherol is preferentially incorporated into very low density lipoproteins, which are then secreted into plasma. In three nondiscriminator patients with familial isolated vitamin E deficiency, the fractional disappearance rates (mean +/- SD) of deuterium-labeled RRR- and SRR-alpha-tocopherols in plasma were 1.4 +/- 0.6 and 1.3 +/- 0.3 pools per day, respectively (difference, 0.1 +/- 0.3). In these patients, plasma concentrations of both RRR- and SRR-alpha-tocopherols decreased similarly to SRR-alpha-tocopherol in controls. In six controls, fractional disappearance rates of deuterium-labeled RRR-alpha-tocopherol (0.4 +/- 0.1 pool per day) were significantly (P < 0.01) slower than for SRR- (1.2 +/- 0.6). The differences (0.8 +/- 0.6 pool per day) between these two rates in controls estimate the rate at which RRR-alpha-tocopherol, which had left the plasma, was returned to the plasma. Although plasma labeled RRR-alpha-tocopherol concentrations in controls appear to change slowly, these data show that both RRR- and SRR-alpha-tocopherols leave the plasma rapidly, but only RRR-alpha-tocopherol is returned to the plasma, likely in nascent very low density lipoproteins. This recycling of RRR-alpha-tocopherol accounts for nearly 1 pool of alpha-tocopherol per day.
 ...
PMID:Human plasma vitamin E kinetics demonstrate rapid recycling of plasma RRR-alpha-tocopherol. 793 27

alpha-Lipoic acid, an essential cofactor in mitochondrial dehydrogenases, has recently been shown to be a potent antioxidant in vitro, as well as being capable of regenerating vitamin E in vitro. In this study, using a new animal model for rapid vitamin E deficiency in adult animals and a new technique for tissue extraction of oxidized and reduced alpha-lipoic acid, we examined the antioxidant action of alpha-lipoic acid in vivo. Vitamin E-deficient adult hairless mice displayed obvious symptoms of deficiency within five weeks, but if the diet was supplemented with alpha-lipoic acid the animals were completely protected. At five weeks on a vitamin E-deficient diet animals exhibited similar decreases in tissue vitamin E levels, whether supplemented or unsupplemented with alpha-lipoic acid: vitamin E levels in liver, kidney, heart, and skin decreased 70 to 85%; levels in brain decreased only 25%. These data show that there was no effect of alpha-lipoic acid supplementation on vitamin E tissue concentrations, arguing against a role for alpha-lipoic acid in regenerating vitamin E in vivo.
 ...
PMID:Alpha-lipoic acid supplementation prevents symptoms of vitamin E deficiency. 794 98

There is a growing body of evidence implicating free radicals in a wide variety of medical diseases and conditions, especially the diseases of ageing, such as cancer and cardiovascular disease, which appear to be ultimate expressions of long-term, cumulative and sustained cellular damage. Vitamin E is an excellent lipid-soluble, chain-breaking antioxidant in the presence of other co-operative antioxidants such as vitamin C or ubiquinol, but it can act as a pro-oxidant in their absence. Epidemiological findings and animal studies support the belief that vitamin E is protective against cardiovascular disease and possibly cancer. The wide range of symptoms associated with vitamin E deficiency is consistent with a loss of antioxidant protection in those long-lived cells in which there is sufficient opportunity for accumulation of free radical damage. The cellular damage is proposed to arise from the generation of free radicals during normal aerobic metabolism. Some susceptible tissues may have enhanced levels of radicals that are produced, for example, by the action of cytochrome P-450 enzymes in steroidogenic tissues, or by the generation of NO in neural tissues.
 ...
PMID:Vitamin E: molecular and biological function. 797 39

Vitamin E, an antioxidant present in all cellular membranes, is associated with protein complexes in the inner mitochondrial membranes and may affect oxidative changes which occur in these organelles when heart tissue is subjected to hypoxia. The effect of 60 min hypoxia, after a 30 min normoxic equilibration period, on the function and the production of reactive oxygen species (ROS) by cardiac mitochondria from rats fed vitamin E sufficient or deficient diets for 9 weeks was examined. Mitochondria from the hearts of rats fed vitamin E deficient diets had 40-fold less vitamin E and were more susceptible to lipid peroxidation, as compared to heart mitochondria from rats fed vitamin E sufficient diet. Perfusion with normoxic, but not hypoxic, media significantly decreased cardiac vitamin E in deficient, but not sufficient rats. Hypoxia decreased the production of ROS by mitochondria from vitamin E sufficient hearts, compared to normoxia. A similar level of ROS production was seen after hypoxia in mitochondria from vitamin E deficient hearts. However, vitamin E deficiency alone decreased the production of ROS by mitochondria from normoxic hearts, relative to vitamin E sufficient animals. Under all conditions where the production of ROS was decreased, 1 microM calcium increased production to the maximum levels seen in vitamin E sufficient, normoxic heart mitochondria. Mitochondrial function was depressed in mitochondria from hypoxic hearts as compared to mitochondria from normoxic hearts of vitamin E sufficient rats. A similar depression of mitochondrial function was not seen in mitochondria from hypoxic hearts of vitamin E deficient rats. Compensatory changes in response to long-term vitamin E deficiency may be responsible for the differences in response to hypoxia of mitochondria from vitamin E sufficient and deficient rats.
 ...
PMID:Modulation of rat heart mitochondrial function and the production of reactive oxygen by vitamin E deficiency. 802 35


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