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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 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

Symptoms of Vitamin E deficiency can be generally attributed to derangement of processes depending upon the integrity of cellular and subcellular membranes, following the formation of tissue-damaging products of lipid peroxidation. Antioxidants modulate also the formation of products derived from long-chain polyunsaturated fatty acids, such as arachidonic acid--which are structural components of biological membranes--through oxidative reactions involving the cyclooxygenase and lipoxygenase systems. Vitamin E inhibits the aggregatory responses of blood platelets to aggregating agents "in vitro", after a preincubation period required for the uptake of the compound by the cells. The antiaggregatory activity of alpha-tocopherol, however, does not appear to be strictly dependent upon inhibition of the formation of thromboxane, the proaggregatory compound derived from arachidonic acid through be cyclooxgenase system. The effects of Vitamin E on platelet function may be of relevance in the control of thromboembolic processes of clinical importance.
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PMID:Biological actions and possible uses of vitamin E. 675 99

The effects of dietary vitamin E-depletion and repletion on the cyclooxygenase activity was studied in the semitendinosus muscle of rabbits. The prostaglandin (PG) cyclooxygenase system in rabbit semitendinosus muscle was characterized and found to depend on reduced glutathione and 1-epinephrine as cofactors. Skeletal muscle cyclooxygenase generates PGE2 and PGF2 alpha at a ratio approximately equal to one. Weanling New Zealand white rabbits were fed a vitamin E-deficient diet for 4 to 5 weeks. Controls received 50 mg dl-alpha-tocopherol acetate twice weekly. Vitamin E deficiency caused a significant reduction in cyclooxygenase activity but did not change the PGE2/PGF2 alpha ratio. Oral supplementation of tocopherol acetate promptly returned the cyclooxygenase activity back to the control values within 48 hours. The decreased cyclooxygenase activity explains in part the increased level of arachidonic acid in skeletal muscle phospholipid previously reported in this laboratory. The possible involvement of decreased prostaglandin endoperoxides with platelet aggregation in vitamin E deficiency is discussed.
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PMID:The effects of vitamin E depletion and repletion on prostaglandin synthesis in semitendinosus muscle of young rabbits. 676 1

Preincubating platelet-rich plasma (PRP) of vitamin E-deficient rats with RRR-alpha-tocopherol prior to the aggregation induced by collagen suspension resulted in inhibition of the formation of endoperoxide metabolites derived from endogenous arachidonic acid (AA). This inhibition was not dose dependent at concentrations above the plasma level of RRR-alpha-tocopherol of vitamin E-supplemented rats. Preincubating the vitamin E-deficient PRP with RRR-alpha-tocopherol did not affect the formation of 12-hydroxyeicosatetraenoic acid, the platelet lipoxygenase product. Concentrations of endoperoxide metabolites in diluted whole blood challenged with collagen suspension were significantly greater in the vitamin E-deficient group than the supplemented group. The level of AA in platelet or plasma phospholipids was not different between the two groups. However, blood platelet counts in the deficient group were significantly greater than those of the supplemented group. Concentrations of endoperoxide metabolites in PRP samples in which platelet concentrations were equalized were still greater in vitamin E-deficient group; however, the difference was not statistically significant. There was also no difference in the degree of maximal platelet aggregation between the two groups. These results indicated that vitamin E deficiency can slightly stimulate the formation of cyclooxygenase products derived from endogenous AA, but it did not affect the formation of lipoxygenase product in rat platelets.
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PMID:In vitro and in vivo effects of vitamin E on arachidonic acid metabolism in rat platelets. 680 55

Lipid peroxides are produced during the enzymatic conversion of arachidonic acid to prostaglandins, thromboxane, prostacyclin, and leukotrienes. These peroxides include hydroperoxides of arachidonic acid formed by lipoxygenase and the prostaglandin endoperoxide intermediates produced by action of prostaglandin endoperoxide synthetase. A number of steps in the arachidonate-dependent prostaglandin pathway are vulnerable to antioxidant affects. Such points in the biosynthetic sequence include prostaglandin endoperoxide synthetase, both the cyclooxygenase and peroxidase activity, prostacyclin synthetase, thromboxane synthetase, and lipooxygenase. Antioxidants added in vitro have been shown to affect prostaglandin synthesis. The present review will stress the limited information concerning the in vivo effect of antioxidants. Studies carried out in the investigator's laboratory on prostaglandin synthesis have utilized rats deficient or replete in vitamin E or propyl gallate (an antioxidant). Differentiation of germ cells in the testis of the male rat is arrested in vitamin E deficiency. Testis microsomal prostaglandin synthesis is altered prior to any overt morphological change. The effect of exogenous antioxidant in either rat testis or mammary gland preparation depends both on the type of antioxidant and the concentration. However, the effects of in vivo and in vitro antioxidant on arachidonate turnover are not identical. The physiological effect of antioxidants on prostaglandin synthesis appear to be specific.
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PMID:Antioxidant effects on the prostaglandin endoperoxide synthetase product profile. 746 Nov 42