Till U, Petermann H, Wenz I, Frunder H
Acta Biol Med Ger. 1977;36(3-4):597-610.
Keeping constant cellular magnesium an A 23 187 mediated moderate calcium loading of human red cells causes isoosmotic cell shrinkage, potassium efflux, slight decrease of cellular pH, ATP depletion connected with an increase of AMP, ADP and Pi and enhanced lactic acid formation. The calcium loading and accompanying effects can be abolished by EGTA or by extracellular magnesium, the latter kept more than two orders of magnitude above that of calcium which was 30 micrometer. Inhibition of the (Mg2+ + Ca2+)-dependent ATPase by ruthenium red or lanthanum decreases the calcium stimulated lactic acid formation after a lag phase. However, the ATP depletion proceeds faster and is much more pronounced under these conditions. (Mg+2 + Na+ +K+)-dependent ATPase, hexokinase, phosphofructokinase and cell shrinkage are ruled out, too, as mediators of the ATP depletion. This suggests that an unknown ATP consuming reaction, apparently not being related to the calcium pump, causes the calcium induced ATP depletion.
维持细胞内镁离子浓度恒定，在A23187介导下对人红细胞进行适度钙负荷，会导致等渗性细胞皱缩、钾离子外流、细胞内pH值略有下降、ATP耗竭并伴有AMP、ADP和无机磷酸增加，以及乳酸生成增强。EGTA或细胞外镁离子可消除钙负荷及其伴随效应，后者浓度保持在30微摩尔钙浓度的两个数量级以上。钌红或镧对（Mg2+ + Ca2+）依赖性ATP酶的抑制作用，在延迟期后会降低钙刺激的乳酸生成。然而，在这些条件下，ATP耗竭进展更快且更为明显。（Mg+2 + Na+ +K+）依赖性ATP酶、己糖激酶、磷酸果糖激酶和细胞皱缩也被排除是ATP耗竭的介导因素。这表明一种未知的ATP消耗反应，显然与钙泵无关，导致了钙诱导的ATP耗竭。
