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

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH). Rats fed a vitamin-E-supplemented diet and exposed to 3 ppm NO2 for 7 days did not exhibit increases in microsomal lipid peroxidation compared to air-breathing controls. However, increase were found in microsomes prepared from rats fed a vitamin-E-deficient diet and exposed to NO2. Lung microsomes from vitamin-E-fed rats contained almost 10 times as much vitamin E as liver microsomes when expressed in terms of polyunsaturated fatty acid content. The extent of lipid peroxidation was, in turn, considerably less in lung than in liver microsomes. Lipid peroxidation in lung microsomes from vitamin-E-deficient rats comparable to liver microsomes from vitamin-E-supplemented rats as was the content of vitamin E in these respective microsomal samples. A combination of vitamin E deficiency and NO2 exposure resulted in the greatest increases in lung and liver microsomal lipid peroxidation with the largest relative increases occurring in lung microsomes. An inverse relationship was found between the extent of lipid peroxidation and vitamin E content. Most of the peroxidation in lung microsomes appeared to proceed nonenzymatically whereas peroxidation in liver was largely enzymatic. Vitamin E appears to be assimilated by the lung during oxidant inhalation, but with dietary vitamin E deprivation, the margin for protection in lung may be less than in liver.
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PMID:Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes. 707 57

The mechanisms and consequences of Vitamin E deficiency were studied in 12 children presenting with chronic cholestasis. Preliminary results indicate that: (1) Vitamin E serum levels are lowest in children with the long-lasting cholestasis and in children in whom fat malabsorption is deepest. (2) Signs of neurologic dysfunction involving peripheral nerves, cerebellum, eye movements and retina were present in 7 children. (3) In vitro study of RBC showed increased hemolysis with oxidating agents and in physiological saline. Degree of hemolysis was inversely related to the serum level of vitamin E. (4) Increased platelet aggregation was observed in 8 patients; 6 of these also had low levels of serum Vitamin E.
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PMID:[Vitamin E and cholestasis in children]. 714 9

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.
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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.
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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.
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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.
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PMID:Vitamin E status, glutathione peroxidase activity and the effect of vitamin E supplementation in children with thalassemia. 782 84

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.
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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.
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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.
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PMID:Modulation of rat heart mitochondrial function and the production of reactive oxygen by vitamin E deficiency. 802 35

This study examines whether vitamin E deficiency has any role in the hypercoagulability of neonatal blood. Blood was collected from mothers and their full-term placental cords. Vitamin E was measured by high-pressure liquid chromatography and whole blood clotting time was measured by recalcification. Cord plasma had significantly lower vitamin E (P < 0.0001) compared with maternal plasma. Whole blood clotting time of cord blood was significantly (P < 0.002) shorter compared with the clotting time of maternal blood. There was a significant correlation between plasma vitamin E and whole blood clotting time (r = 0.54, P < 0.04) of cord blood. The addition of standard vitamin E to cord blood in vitro resulted in prolongation of whole blood clotting time. This suggests that a deficiency of plasma vitamin E can shorten whole blood clotting time in newborns, which may have a role in the disseminated intravascular coagulation frequently experienced by newborn infants.
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PMID:Vitamin E and the hypercoagulability of neonatal blood. 808 11


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