Kaplay S S
Biochem Med. 1984 Jun;31(3):371-7. doi: 10.1016/0006-2944(84)90093-0.
Erythrocytes from protein-energy malnourished children have been shown to have increased resistance to osmotic lysis (4). Osmotic fragility studies were carried out in protein-energy malnourished rats and A23187-induced changes in osmotic fragility were studied in rat and human erythrocytes. Rat erythrocytes were found to be much more sensitive to A23187 effect on osmotic fragility as compared to the human erythrocytes. Erythrocytes from protein-deficient rats but not from the energy-restricted rats showed increased resistance to osmotic lysis. A23187 (+ Ca)-induced changes in osmotic fragility were not different between control and experimental erythrocytes, either for humans or rats. There was, however, a difference in the extent to which Na accumulation and K depletion occurred in erythrocytes from control and experimental animals after A23187 + Ca2+ treatment.
蛋白质-能量营养不良儿童的红细胞已被证明对渗透性溶血的抵抗力增强(4)。对蛋白质-能量营养不良的大鼠进行了渗透脆性研究,并研究了A23187诱导的大鼠和人类红细胞渗透脆性变化。结果发现,与人类红细胞相比,大鼠红细胞对A23187对渗透脆性的影响更为敏感。蛋白质缺乏大鼠的红细胞对渗透性溶血的抵抗力增强,而能量限制大鼠的红细胞则没有。无论是人类还是大鼠,对照和实验红细胞之间,A23187(+Ca)诱导的渗透脆性变化没有差异。然而,在A23187 + Ca2+处理后,对照和实验动物红细胞中钠积累和钾消耗的程度存在差异。