期刊论文详细信息
Journal of Lipid Research
Role of vitamin E in glutathione-induced oxidant stress: methemoglobin, lipid peroxidation, and hemolysis
R V Panganamala1  J J Huttner1  D G Cornwell1  N R Brownlee1 
[1] Department of Physiological Chemistry, Ohio State University, Columbus, OH 43210;
关键词: hydrogen peroxide;    superoxide;    hydroxyl radical;    catalase;    superoxide dismutase;    oxygen electrode;   
DOI  :  
来源: DOAJ
【 摘 要 】

Red blood cells (RBC) from normal and vitamin E-deficient rats were incubated in a hypertonic solution of reduced glutathione adjusted to pH 8. Methemoglobin formation occurred in intact RBC from both normal and vitamin E-deficient rats. Hemolysis was significantly greater in RBC from vitamin E-deficient rats. Experiments with catalase, superoxide dismutase, and methional showed that H2O2 was the primary extracellular source of oxidant stress. Extracellular superoxide and hydroxyl radical were not involved in oxidant stress. Experiments with dimethyl sulfoxide showed that intracellular hydroxyl radical, generated from H2O2, was the hemolytic agent. Neither methemoglobin formation nor lipid peroxidation involved hydroxyl radical. Indeed, lipid peroxidation and hemolysis in RBC from vitamin E-deficient rats were concurrent rather than consecutive events. Phase contrast microscopy showed that rigid, crenated RBC with a precipitate around the interior periphery formed during glutathione-induced oxidant stress. The precipitate dissolved slowly as the crenated RBC were converted to smooth ghosts. It appeared that protein precipitates involving mixed disulfide bonds were reduced and solubilized when extracellular glutathione penetrated the ruptured cell. Comparisons between normal RBC and vitamin E-deficient RBC suggest that vitamin E has little effect on the inward diffusion of extra-cellular H2O2. Vitamin E apparently interacts with different oxidant species derived from intracellular H2O2 in preventing lipid peroxidation and the sulfhydryl group oxidation leading to hemolysis.

【 授权许可】

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