Kitao T, Hattori K, Takeshita M
Blood. 1976 Apr;47(4):651-5.
The erythrocytes of hereditary spherocytosis (HS) demonstrate an increased inward movement of sodium ions, an alteration which has been proposed as the primary defect leading to cell destruction. Parachloromercuriphenylsulfonate (PCMBS), an agent reacting with sulfhydryl groups of the membrane, increases the cation permeability of normal red cells, but does so to a much lesser extent in the HS red cells. On the other hand, pronase that is specific for amino groups of the membrane increases cation permeability and decreases anion permeability equally in normal and HS red cells. It may be postulated that a decreased number of sulfhydryl sites or a mutation of proteins in the PCMBS-sensitive cation channels of the HS cell membrane result in this hyposensitivity to PCMBS.
遗传性球形红细胞增多症(HS)的红细胞表现出钠离子内向运动增加,这一改变被认为是导致细胞破坏的主要缺陷。对氯汞苯磺酸盐(PCMBS)是一种与膜的巯基反应的试剂,它会增加正常红细胞的阳离子通透性,但在HS红细胞中这种作用程度要小得多。另一方面,对膜氨基具有特异性的链霉蛋白酶在正常和HS红细胞中同等程度地增加阳离子通透性并降低阴离子通透性。可以推测,HS细胞膜中对PCMBS敏感的阳离子通道中巯基位点数量减少或蛋白质发生突变导致了对PCMBS的这种低敏感性。