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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 and essential fatty acid status were examined in two groups of patients, one receiving fat-free total parenteral nutrition (TPN) with intravenous all-rac-alpha-tocopherol for vitamin E deficiency and the other receiving routine intravenous fat (Intralipid, 10%) emulsions with TPN to supply both fatty acid and vitamin E requirements. Initial evaluation of both groups revealed a 50% incidence of vitamin E deficiency, platelet hyperaggregation, or in vitro H2O2-induced hemolysis. Only platelet hyperaggregation correlated significantly with vitamin E deficiency. Supplementation with all-rac-alpha-tocopherol corrected platelet hyperaggregation and H2O2-induced hemolysis; daily dosage requirements of 25-50 mg (fat-free TPN) or more (with intravenous fat) suggest increased vitamin E requirements during TPN. Intravenous fat emulsion did not correct the platelet and red blood cell abnormalities, a result of either increased vitamin E requirements or low alpha-tocopherol-equivalent content of the emulsion. Essential fatty acid deficiency (EFAD) was observed in seven patients with an associated platelet hyperaggregation independent of vitamin E deficiency. Prolonged TPN for enterocutaneous fistulae in three patients was associated with persistent EFAD and platelet hyperaggregation despite up to 2.0 liters of intravenous fat emulsion weekly.
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PMID:Vitamin E and total parenteral nutrition. 681 20

Nitro blue tetrazolium (NBT) staining in normal rat retina was previously found to be affected by inhibition of free radical-related enzyme systems, indicating that NBT might be useful as a marker of free radicals. The aim of the present study was to investigate NBT staining in rat retina in vitamin E deficiency and after blue light exposure, and also to measure hydrogen peroxide (H2O2) production indirectly by measuring catalase activity under these conditions. Vitamin E deficiency resulted in morphological changes in the retina and increased NBT staining in the photoreceptors and in the outer plexiform layer. Light exposure caused increased staining in the inner segments of photoreceptors. The increased staining was not clearly influenced by addition of the free radical scavengers superoxide dismutase and catalase. The catalase activity was not influenced by light exposure, while it was increased in vitamin E-deficient retina compared to controls. The results indicate that reducing systems as measured by NBT were activated in the retina under these conditions. However, to what extent the reductants represent free radicals still has to be established using other methods.
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PMID:Nitro blue tetrazolium staining and hydrogen peroxide production in the rat retina in vitamin E deficiency and after light exposure. 751 60

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

Vitamin E is the primary lipophilic antioxidant in mammals. Lack of vitamin E may lead to an increase of cytotoxic phospholipid-peroxidation products (PL-Ox). However, we could previously show that alimentary vitamin E-depletion in rats did not change the concentrations of dienes, hydroperoxides, and platelet-activating factor-related oxidation products in alveolar type II cells (TII cells). We hypothesized that vitamin E deficiency increases the activity of enzymes involved in the degradation of PL-Ox. Degradation of PL-Ox may be catalyzed by phospholipase A2, PAF-acetylhydrolase, or peroxiredoxins (Prx's). Alimentary vitamin E deficiency in rats increased the expression of Prx-1 at the mRNA and protein levels and the formation of Prx-SO3, but it did not change the expression of Prx-6 or the activity of phospholipase A2 and PAF-acetylhydrolase in TII cells. H2O2-induced oxidative stress in isolated TII cells activated protein kinase Calpha (PKCalpha) and increased the expression of Prx-1 and Prx-6. Inhibition of PKCalpha in isolated TII cells by long-time incubation with PMA inhibited PKCalpha and Prx-1 but not Prx-6. We concluded that the expression of Prx-1 and -6 is selectively regulated in TII cells; PKCalpha regulates the expression of Prx-1 but not Prx-6. Prx-6 expression may be closely linked to lipid peroxidation.
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PMID:Vitamin E differentially regulates the expression of peroxiredoxin-1 and -6 in alveolar type II cells. 1585 58