Hofmann J, Bosia A, Arese P, Lösche W, Pescarmona G P, Tazartes O, Till U
Acta Biol Med Ger. 1981;40(12):1707-14.
Platelets from patients with known red blood cell G-6-PD deficiency were investigated to find out whether this genetic defect is associated with changes in platelet aggregation. The enzyme defect in platelets could be verified by a decreased G-6-PD activity which was as low as 15% compared to control subjects. The decreased enzyme activity was reflected by lowered levels of NADPH and GSH and by a diminished maximum capacity of the hexose monophosphate shunt. Aggregation measurements in platelet-rich plasma from deficient patients revealed an enhanced dose response to ADP which was higher by about one order of magnitude compared to controls. The same effect was observed in a smaller degree in arachidonic acid induced aggregation.
对已知患有红细胞葡萄糖-6-磷酸脱氢酶（G-6-PD）缺乏症患者的血小板进行了研究，以确定这种基因缺陷是否与血小板聚集的变化有关。血小板中的酶缺陷可通过G-6-PD活性降低得到证实，与对照受试者相比，该活性低至15%。酶活性降低表现为还原型辅酶Ⅱ（NADPH）和谷胱甘肽（GSH）水平降低，以及磷酸己糖旁路的最大容量减小。对缺乏症患者富含血小板血浆的聚集测量显示，对二磷酸腺苷（ADP）的剂量反应增强，与对照组相比高出约一个数量级。在花生四烯酸诱导的聚集中也观察到了程度较小的相同效应。
