| Summary: | 碩士 === 長庚大學 === 基礎醫學研究所 === 87 === Glucose-6-phosphate dehydrogenase (G6PD) deficiencies are due to diverse point mutations in G6PD gene associated with the loss of enzyme activity. A major biochemical defect in G6PD-deficient red cells is a decreased ability to generate reduced nicotinamide adenine dinucleotide phosphate (NADPH). Such an impairment in NADPH production weakens the antioxidant system of the deficient cells and renders these cells more susceptible to oxidative damage. The purposes of this study were three folds. First, to detect lipid peroxidation in intact red cells by a novel fluorescence-based flow-cytometric method recently reported by Makrigiorgos et al. (Free Radical Biology and Medicine, 22: 93-100, 1997). When red cells exposed to as low as 0.01mM H2O2 or 0.01mM cumene hydroperoxide, alterations in fluorescent intensity in intact red cells could be detected. This method is more sensitive than the conventional method of detecting thiobarbituric acid reactive substance (TBARS). Second, to compare the susceptibility of G6PD deficient red cells and normal red cells to oxidative stress. The result indicated that G6PD deficient red cells are more prone to lipid peroxidation under oxidative stress (p < 0.05). Third, the effects of oxidants on red cells membrane asymmetry were investigated. The result showed that phosphatidylserine is exposed to the outer membrane leaflet on G6PD deficient red cells after treatment with 0.5mM cumene hydroperoxide. However, similar treatment with cumene hydroperoxide did not result in abnormal exposure of phosphatidylserine in normal red cells.
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