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

Lipid peroxidation of microsomal membranes isolated from rat liver, and Morris hepatomas 9618A (slow-growing) and 3924A (fast-growing) was induced by superoxide radicals generated by the action of xanthine oxidase on xanthine. The peroxidation, measured as malondialdehyde and lipid hydroperoxide formation, was optimized with regard to iron concentration and chelation of iron by ADP. In such conditions hepatoma microsomes catalyze lower rates of lipid peroxidation than the normal counterpart. However, while microsomes from hepatoma 3924A show a marked decrease in both the malondialdehyde and hydroperoxide production rates, microsomes from hepatoma 9618A differ moderately from the control, mainly in the long-term production of hydroperoxides. It is also reported here that the 9618A microsomes partially lack cytochrome P-450 (about 40% deficiency), but they have a fatty acid composition similar to that of control. No differences were found in the content of vitamin E between normal and hepatoma 3924A microsomes. Moreover, induction of vitamin E deficiency in hepatoma 3924A microsomes does not influence the rate of either malondialdehyde or lipid hydroperoxide production. On the basis of these results and previous data on the lipid composition of hepatoma 3924A microsomes it is proposed that the high resistance to superoxide-dependent lipid peroxidation of hepatoma 3924A microsomes is related to the low substrate availability rather than the content of membrane antioxidants; and a limitation only in the propagation phase characterizes the hepatoma 9618A microsomal lipid peroxidation and would be due to the partial deficiency of the endogenous propagating agent, cytochrome P-450.
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PMID:Superoxide-dependent lipid peroxidation and vitamin E content of microsomes from hepatomas with different growth rates. 298 56

The efficiency of alpha-tocopherol as a 7-etoxycumarine deethylase protector in rat liver microsomes damaged by phospholipase A2 at various levels of vitamin E was studied. No selective damage of cytochrome P-450 isoforms possessing a catalytic activity towards 7-etoxycumarine under vitamin E deficiency was observed. Phospholipase A2 decreased the deethylase activity of cytochrome P-450, the efficiency of the damaging action being dependent on vitamin E content in the liver. Exogenous alpha-tocopherol exerts an antiphospholipase effect and protects 7-etoxycumarine deethylase; the protective action is inversely proportional to vitamin E level in the liver. Under normal conditions the damaging effect of phospholipase A2 on cytochrome P-450 is mainly provided for by lysophospholipids, while under vitamin E deficiency both lysophospholipids and free fatty acids exert a damaging action. A possible mechanism of the stabilizing effect of alpha-tocopherol may consist in the interaction of the chromanol nucleus in the vitamin E molecyule both with lysophospholipids and with free fatty acids.
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PMID:[Non-antioxidative mechanism of cytochrome P-450 stabilization by alpha-tocopherol: the effectiveness in avitaminosis E]. 349 Feb 81

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

In order to evaluate the effects of a necrogenic dose of diethylnitrosamine (DEN) on vitamin E-deficient and vitamin E-supplemented rats, a single dose of the drug (200 mg/kg body weight) was injected intraperitoneally at the end of 10 weeks of treatment with the diets. The hepatic necrosis and lipoperoxidation provoked by DEN were evaluated 24, 48, 72 and 120 hours after the injection and were found to be more intense in the deficient group (thiobarbituric acid reactive substances (TBARS): 5.20 +/- 1.48 nmol/mg protein; necrosis volume: 68.99 +/- 8.36%; P < 0.05) during the second period. Also, in the same group and during the same period, mean plasma and hepatic vitamin E concentrations and mean liver glutathione concentration were the lowest detected, suggesting the occurrence of antioxidant consumption due to the toxic action of DEN. In contrast to vitamin E deficiency, which permitted the drug to exert stronger toxic effects, 20-fold supplementation with vitamin E did not provide additional protection against the lipoperoxidation and necrosis provoked by DEN (P < 0.05). The results suggest that other mechanisms in addition to lipoperoxidation provoked by free radicals originating from the metabolism of nitrosamines by the cytochrome P-450-dependent enzymatic system may be involved in the hepatotoxic action of these substances.
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PMID:Effect of a necrogenic dose of diethylnitrosamine on vitamin E-deficient and vitamin E-supplemented rats. 977 54