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已知某些6-磷酸葡萄糖脱氢酶(G-6-PD)突变型产生非球形细胞溶血性贫血,其慢性溶血机制未明。本文作者用聚丙烯酰胺凝胶电泳和十二烷基硫酸钠(SDS)凝胶过滤层析,对5例G-6-PD缺乏伴慢性溶血患者和4例G-6-PD缺乏不伴慢性溶血者的红细胞膜进行了研究,并以4例正常人和10例其它类型溶血性贫血和网织红细胞增多症患者(G-6-PD活性正常)作为对照。结果发现5例G-6-PD缺乏伴慢性溶血患者的红细胞膜上,均含有分子量为4.4×10~5和>50×10~6 dalton的两种多肽聚集物(Polypeptide aggregates),仅有G-6-PD缺乏者之红细胞膜,则仅含少量>50×10~6 dalton的多肽聚集物,不
Certain 6-phosphoglucose dehydrogenase (G-6-PD) mutants are known to produce non-spherical hemolytic anemia whose mechanism of chronic hemolysis is unknown. The authors used polyacrylamide gel electrophoresis and sodium dodecyl sulfate (SDS) gel filtration chromatography on 5 cases of G-6-PD deficiency with chronic hemolysis and 4 cases of G-6-PD deficiency without chronic The hemolysin erythrocyte membrane was studied, and 4 normal subjects and 10 other patients with hemolytic anemia and reticulocytosis (normal G-6-PD activity) were used as controls. The results showed that there were two kinds of Polypeptide aggregates with molecular weight of 4.4 × 10 ~ 5 and> 50 × 10 ~ 6 dalton on the erythrocyte membrane in 5 patients with G-6-PD deficiency and chronic hemolysis. Only G -6-PD deficient erythrocyte membrane, then only a small amount of> 50 × 10 ~ 6 dalton polypeptide aggregates, not