MECHANISM OF HEMOLYSIS INDUCED BY FERRIPROTOPORPHYRIN IX
MECHANISM OF HEMOLYSIS INDUCED BY FERRIPROTOPORPHYRIN IX
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DOI：
10.1172/jci110302
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发表时间：
1981-01-01
影响因子：
15.9
通讯作者：
FITCH, CD
中科院分区：
文献类型：
--
作者：
CHOU, AC;FITCH, CD
将0.5%洗净的正常小鼠红细胞悬浮液与铁原卟啉IX(FP)在37度孵育。C和pH 7.4可引起K的丢失、肿胀、对低渗溶解的耐受性增加和最终的溶血。在黑暗中孵育不能抑制溶血，不产生丙二醛，各种自由基清除剂对溶血没有影响。只有巯基化合物、半胱氨酸、二硫苏糖醇和硫醇对红细胞有保护作用。在暴露于5微米FP的30分钟内，K损失达90%。蔗糖(0.1M)完全阻止溶血，但不影响K的丢失。使温度从37度降至25度。C对溶血有明显的抑制作用，但对K的丢失无明显影响。FP明显损害红细胞S维持阳离子梯度的能力，并通过胶体渗透机制诱导溶血。
Incubation of a 0.5% suspension of washed, normal mouse erythrocytes with ferriprotoporphyrin IX (FP) at 37.degree. C and pH 7.4 caused K loss, swelling, increased suceptibility to hypotonic lysis and finally hemolysis. Hemolysis was not inhibited by incubation in the dark, malonyldialdehyde was not produced and various free radical scavengers had no effect on the hemolysis. Only the sulfhydryl compounds, cysteine, dithiothreitol and mercaptoethanol protected erythrocytes from FP. K loss reached 90% within 30 min of exposure to 5 .mu.M FP. This amount of FP caused > 50% hemolysis within 2.5 h. Sucrose (0.1 M) completely prevented hemolysis but had no effect on K loss. Reducing the temperature from 37-25.degree. C greatly retarded hemolysis but had no effect on K loss. FP apparently impairs the erythrocyte''s ability to maintain cation gradients and induces hemolysis by a colloid-osmotic mechanism.