Hiroshige Y
Tohoku J Exp Med. 1980 Apr;130(4):385-402. doi: 10.1620/tjem.130.385.
In the presence of albumin, cytotoxic effects of copper on erythrocytes in vitro were reduced. The presence of o-phenanthroline, on the other hand, accelerated deleterious effects of copper on the erythrocytes resulting in a decrease in GSH level, accumulation of copper in the cell, loss of potassium and gain of sodium, cross-linking of membrane proteins mainly involving spectrin and band 3, and echinocyte formation. These changes were not reversible. Prior treatment of the cells with N-ethylmaleimide inhibited the cross-linking of membrane proteins and echinocytic transformation by copper o-phenanthroline complex (CuP or diamide to a certain extent. Treatment of the cells with vinblastine, a stomatocytogenic agent, restored biconcave disc shape of CuP-treated erythrocytes, although it did not inhibit the cross-linking of spectrin. Blocking of sulfhydryl groups was not the prerequisite for the copper to be accumulated in the erythrocyte. These results may be helpful for the understanding of the mechanism of hemolysis associated with copper intoxication in vivo.
在有白蛋白存在的情况下，铜对红细胞的体外细胞毒性作用会降低。另一方面，邻菲罗啉的存在会加速铜对红细胞的有害作用，导致谷胱甘肽水平降低、细胞内铜积累、钾流失和钠增加、膜蛋白交联（主要涉及血影蛋白和带3蛋白）以及棘红细胞形成。这些变化是不可逆的。用N - 乙基马来酰亚胺预先处理细胞可抑制铜 - 邻菲罗啉复合物（CuP）或二酰胺在一定程度上引起的膜蛋白交联和棘红细胞转化。用长春花碱（一种口形红细胞生成剂）处理细胞可恢复CuP处理的红细胞的双凹圆盘形状，尽管它并不抑制血影蛋白的交联。巯基的封闭不是铜在红细胞中积累的先决条件。这些结果可能有助于理解体内与铜中毒相关的溶血机制。
