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

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

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

The hydroperoxides corresponding to the main molecular species of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were determined after lipoxygenase treatment of erythrocyte membranes from healthy children. This work was a preliminary study prior to applying this analytical procedure to erythrocyte membranes from children with diseases associated with vitamin E deficiency. The total molecular species corresponding to 20:4 and 22:6 associated with 16:0 and 18:0 were significantly higher in PE (26.94 +/- 4.70 nmol/mg protein) than in PC (20.14 +/- 6.70 nmol/mg protein); these concentrations represented 63% of the total molecular species in PE and 22% in PC. However, the concentrations of hydroperoxides produced from these polyunsaturated fatty acid molecular species were in the same order of magnitude in PC (3.98 +/- 1.56 nmol/mg protein) and in PE (3.61 +/- 1.63 nmol/mg protein). In contrast, the molecular species concentrations containing two double bonds, such as 16:0/18:2 and 18:0/18:2 and their corresponding hydroperoxides, were clearly more elevated in PC than in PE. There was a positive relationship between the concentrations of alpha-tocopherol and each hydroperoxide of PC and PE, and this association was particularly strong in PE (P < or = 0.0001). These results suggest that alpha-tocopherol exerts a stabilizing effect toward hydroperoxides, limiting their further degradation into peroxyl radicals. The protective effect of alpha-tocopherol could be more effective in PE because more polyunsaturated fatty acids were present.
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PMID:Hydroperoxides of erythrocyte phospholipid molecular species formed by lipoxygenase correlate with alpha-tocopherol levels. 882 92

alpha-Tocopherol (alpha-TOH), generally regarded as the most important lipid-soluble, chain-breaking antioxidant in human plasma, can also be a pro-oxidant in isolated low-density lipoprotein (LDL) (Bowry V. W.; Stocker R. J. Am. Chem. Soc. 115:6029-6044; 1993). Here we examined whether this pro-oxidant activity of alpha-TOH is of more general relevance. We compared the oxidizability of lipid hydroperoxide-free, in vivo or in vitro alpha-TOH-depleted LDL and high-density lipoprotein (HDL), as well as plasma reconstituted with alpha-TOH-depleted lipoproteins, with that of the corresponding native and alpha-TOH-supplemented samples, using water- and lipid-soluble peroxyl radicals (ROO.), hydroxyl radicals (.OH), Cu2+, the transition metal-containing Ham's F-10 medium, soybean 15-lipoxygenase, and horseradish peroxidase as oxidants. Lipoprotein and plasma oxidizability was assessed by the loss of cholesteryl esters and alpha-TOH and the accumulation of hydroperoxides of cholesteryl esters and phospholipids. Compared to native LDL, HDL, and plasma, the in vivo and in vitro alpha-TOH-depleted counterparts were highly resistant to peroxidation initiation by all oxidants when used at mild radical flux conditions. Wherever tested, the oxidizability of isolated LDL decreased proportionally with decreasing alpha-TOH content. Initiation of LDL lipid oxidation by lipoxygenase and Cu2+ (even up to Cu2+:LDL ratio of 20:1) had an absolute requirement for alpha-TOH. Oxidation of reconstituted plasma with ROO. showed that in the absence of the vitamin, plasma lipids were largely resistant to oxidation, whereas bilirubin and urate oxidized more rapidly. Replenishing the in vitro depleted LDL with alpha-TOH, but not with alpha-tocopherol acetate, fully restored its original content of vitamin E and its oxidizability. Similarly, dietary supplementation with alpha-TOH restored the vitamin content and oxidizability of the in vivo alpha-TOH-depleted lipoproteins and plasma obtained from a patient with familial isolated vitamin E deficiency. Under high fluxes of ROO. and .OH, the activity of alpha-TOH in LDL switched from pro- to anti-oxidant, with the switching point for .OH observed at a lower radical flux than that for ROO.. Together, our results show that alpha-TOH generally makes lipoproteins more reactive towards radical oxidants; this can result in a pro-oxidant activity depending on the specific oxidation conditions.
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PMID:Requirement for, promotion, or inhibition by alpha-tocopherol of radical-induced initiation of plasma lipoprotein lipid peroxidation. 895 30