Ataullakhanov F I, Vitvitskiĭ V M, Zhabotinskiĭ A M, Kiiatkin A B, Pichugin A V
Biokhimiia. 1986 Sep;51(9):1562-70.
It was shown that in vitro oxidative hemolysis of human erythrocytes occurs as a result of a great increase in membrane permeability to cations leading to osmotic damage of the cells. Infusion at a steady rate with a solution of tert-butylhydroperoxide in an erythrocyte suspension resulted in a rapid fall of the reduced glutathione level down to 0, when the rate of infusion exceeded the maximal rate of pentose phosphate pathway. Under these conditions the potassium ions liberation from the erythrocytes began with the drop of the reduced glutathione level down to zero, and the hemoglobin liberation - at the moment when more than 60% of potassium ions were liberated from the erythrocytes. The kinetics of potassium ion liberation remained unchanged in anisotonic media, but hemoglobin liberation from the erythrocytes greatly increased in hypotonic media as compared with isotonic ones. The kinetics of K+ and hemoglobin liberation were correlated only with lipid peroxidation but not with the oxidation of protein SH-groups.
结果表明,人红细胞的体外氧化溶血是由于细胞膜对阳离子的通透性大幅增加,导致细胞发生渗透损伤所致。当以稳定速率向红细胞悬液中输注叔丁基过氧化氢溶液时,若输注速率超过磷酸戊糖途径的最大速率,还原型谷胱甘肽水平会迅速降至零。在这些条件下,随着还原型谷胱甘肽水平降至零,红细胞开始释放钾离子,而当超过60%的钾离子从红细胞中释放出来时,血红蛋白开始释放。在非等渗介质中,钾离子释放的动力学保持不变,但与等渗介质相比,在低渗介质中红细胞释放血红蛋白的量大幅增加。钾离子和血红蛋白释放的动力学仅与脂质过氧化相关,而与蛋白质巯基的氧化无关。