EFFECT OF COPPER ON ERYTHROCYTE DEFORMABILITY - POSSIBLE MECHANISM OF HEMOLYSIS IN ACUTE COPPER INTOXICATION
EFFECT OF COPPER ON ERYTHROCYTE DEFORMABILITY - POSSIBLE MECHANISM OF HEMOLYSIS IN ACUTE COPPER INTOXICATION
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DOI：
10.1016/0005-2736(79)90214-1
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发表时间：
1979-01-01
期刊：
影响因子：
--
通讯作者：
LINEBERGER, TH
中科院分区：
文献类型：
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作者：
ADAMS, KF;JOHNSON, G;LINEBERGER, TH
虽然溶血性贫血作为急性铜中毒的并发症的发展是有据可查的，但铜加速人体红细胞破坏的确切机制尚不清楚。正常红细胞的存活部分取决于细胞变形和通过肝脏特别是脾脏中微循环狭窄区域的能力。毒性浓度的铜迅速和显着降低红细胞变形能力。这种细胞变形能力的降低与Cu处理的细胞的膜通透性和渗透脆性的显著增加有关。尽管细胞ATP水平正常，并且细胞明显没有氧化损伤，但变形能力下降。铜介导的红细胞膜的变化可能是负责降低细胞的灵活性。变形能力的丧失可以减少红细胞存活，从而解释与体内Cu中毒相关的溶血。
Although the development of hemolytic anemia as a complication of acute Cu intoxication is well documented, the precise mechanism by which Cu produces accelerated human erythrocyte destruction is unknown. Normal erythrocyte survival depends in part on the ability of the cell to deform and pass through narrow areas of microcirculation in the liver and especially in the spleen. Toxic concentrations of Cu rapidly and markedly reduce erythrocyte deformability. This reduction in cell deformability is associated with a marked increase in membrane permeability and osmotic fragility of Cu-treated cells. The decrease in deformability occurs despite normal levels of cell ATP and the apparent absence of oxidative damage to the cell. Cu-mediated changes in the erythrocyte membrane may be responsible for reducing the flexibility of the cell. The loss of deformability could act to reduce erythrocyte survival and thus explain the hemolysis associated with Cu intoxication in vivo.