Galiano S, Mareni C, Gaetani G F
Biochim Biophys Acta. 1978 Jan 11;501(1):1-9. doi: 10.1016/0005-2728(78)90090-7.
The hexose monophosphate pathway of human glucose-6-phosphate dehydrogenase (EC 1.1.1.49) - deficient erythrocytes is under a severe and unexplained restraint (Gaetani, G.D., Parker, J.C. and Kirkman, H.N. (1974) Proc. Natl. Acad. Sci. U.S. 71, 3584-3587). In this study the hexose monophosphate pathway activity and the NADPH level of normal and glucose-6-phosphate dehydrogenase-deficient erythrocytes were measured soon after haemolysis. The results indicate a prompt increase in 14CO2 evolution and a rise in MADPH levels. Since, in this study, the concentration of the haemolysate is comparable to that of intact erythrocytes, the relief of the restraint on glucose-6-phosphate dehydrogenase through dilution-dependent dissociation from inactivator or inhibitor is excluded. The possibility that the intracellular restraint may result from compartmentalization of glucose-6-phosphate dehydrogenase and substrates or from properties of the intact membrane of the erythrocytes is suggested.
人类葡萄糖-6-磷酸脱氢酶(EC 1.1.1.49)缺乏的红细胞中的磷酸己糖途径受到严重且无法解释的限制(加埃塔尼,G.D.,帕克,J.C.和柯克曼,H.N.(1974年)《美国国家科学院院刊》71,3584 - 3587)。在本研究中,溶血后不久测量了正常和葡萄糖-6-磷酸脱氢酶缺乏的红细胞的磷酸己糖途径活性及NADPH水平。结果表明14CO2释放迅速增加且MADPH水平上升。由于在本研究中,溶血产物的浓度与完整红细胞的浓度相当,因此排除了通过与灭活剂或抑制剂的稀释依赖性解离来缓解对葡萄糖-6-磷酸脱氢酶的限制的可能性。提示细胞内限制可能是由于葡萄糖-6-磷酸脱氢酶与底物的区室化或红细胞完整膜的特性所致。