The study was aimed to investigate if vitamin C could exert protective effects on development of eryptosis caused by glucose-6-phosphate dehydrogenase (G6PD) deficiency and hydrogen peroxide.,Isolated erythrocytes with different G6PD activity (normal or deficient) were divided into various groups treated by either Vitamin C or H2O2. Phosphatidylserine (PS) extroversion rate was detected by Annexin V binding. The intracellular Ca2+ concentration was detected by Fluo3-fluorescence, and western blot was used to detect the expression of apoptosis factor caspase 3.,Compared with the blank group, the PS extroversion rate (P < 0.001), intracellular Ca2+ concentration (P < 0.001) and active caspase 3 expression level (P < 0.05) of erythrocytes significantly increased after treatment of 0.05% H2O2. Then the index of eryptosis significantly decreased after erythrocytes were treated with Vitamin C (1 mg/ml) for 30 min (all P < 0.05). The decline in erythrocytes with G6PD normal activity was more significant than those with G6PD deficiency.,Vitamin C could effectively inhibit the eryptosis contributed by H2O2 oxidative stress, and the suppression on eryptosis with G6PD normal activity was more effective than that with G6PD deficiency.
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