Tsai K J, Shih L Y, Hung I J, Huang S W, Wei J S, Liu T Z, Chiu D T
Chang Gung College of Medicine, Kwei-Shan, Tao-Yuan, Taiwan.
Life Sci. 1996;59(10):867-76. doi: 10.1016/0024-3205(96)00377-3.
Glucose-6-phosphate dehydrogenase (G6PD) deficient red blood cells (RBCs) are known to be more susceptible to oxidant-induced hemolysis. Erythrocytes from G6PD-deficient individuals are significantly more susceptible to Ca(2+)-induced vesiculation than normal control cells. The enhanced susceptibility of G6PD-deficient RBCs to Ca(2+)-induced vesiculation is not due to ATP depletion. The remnant G6PD-deficient RBCs following vesiculation are more sensitive to complement-mediated hemolysis than control normal RBCs. A strong positive correlation exists between the level of Ca(2+)-induced vesiculation and the extent of complement mediated hemolysis.
已知葡萄糖-6-磷酸脱氢酶（G6PD）缺乏的红细胞（RBC）更容易受到氧化剂诱导的溶血作用。与正常对照细胞相比，G6PD缺乏个体的红细胞对Ca(2+)诱导的囊泡形成明显更敏感。G6PD缺乏的RBC对Ca(2+)诱导的囊泡形成的易感性增强并非由于ATP耗竭。囊泡形成后剩余的G6PD缺乏的RBC比对照正常RBC对补体介导的溶血更敏感。Ca(2+)诱导的囊泡形成水平与补体介导的溶血程度之间存在强正相关。
