Habermann E, Hudel M, Dauzenroth M E
Rudolf-Buchheim Institute of Pharmacology, Justus-Liebig University Giessen, F.R.G.
Toxicon. 1989;27(4):419-30. doi: 10.1016/0041-0101(89)90204-3.
Erythrocytes from four mammalian species were compared with regard to K+ loss triggered by palytoxin, to Na+, K+ -ATPase activity, and to ouabain sensitivity of both events. Palytoxin sensitivity (EC50) decreased in the order rat, man (approximately equal to 1 pM) greater than cattle (approximately equal to 500 pM) greater than dog (greater than 10 nM). Na+, K+ -ATPase activity, as measured by Rb uptake, was in the series rat greater than man greater than cattle greater than dog. The glycoside potently inhibited both palytoxin action and ATPase activity in man, cattle and dog erythrocytes, but weakly in those from rats. Ca2+ promoted the palytoxin effects on all erythrocytes. As shown for human erythrocytes, Sr2+ and Ba2+ but not Mg2+ can substitute for Ca2+, and sucrose can substitute for sodium chloride. Human HeLa and bovine adrenomedullary cells also lost their K+ within a few min when exposed to palytoxin (1-10 pM). Ouabain acted as a palytoxin antagonist on both cell types. We conclude that: (a) the ouabain binding site of Na+, K+ -ATPase is part of the palytoxin receptor in every cell type tested, (b) high palytoxin sensitivity is not necessarily accompanied by high ouabain sensitivity, and (c) active ion transport is not a precondition for the action of palytoxin or for its inhibition by ouabain.
对来自四种哺乳动物的红细胞在由岩沙海葵毒素引发的钾离子流失、钠钾 -ATP 酶活性以及这两个过程对哇巴因的敏感性方面进行了比较。岩沙海葵毒素敏感性（半数有效浓度，EC50）按大鼠、人（约 1 pM）＞牛（约 500 pM）＞狗（＞10 nM）的顺序降低。通过铷摄取测量的钠钾 -ATP 酶活性顺序为大鼠＞人＞牛＞狗。该糖苷对人、牛和狗的红细胞中的岩沙海葵毒素作用和 ATP 酶活性均有强力抑制作用，但对大鼠红细胞的抑制作用较弱。钙离子促进了岩沙海葵毒素对所有红细胞的作用。如对人红细胞所示，锶离子和钡离子而非镁离子可替代钙离子，蔗糖可替代氯化钠。人宫颈癌细胞系 HeLa 细胞和牛肾上腺髓质细胞在暴露于岩沙海葵毒素（1 - 10 pM）时，几分钟内也会失去钾离子。哇巴因对这两种细胞类型均起岩沙海葵毒素拮抗剂的作用。我们得出以下结论：(a) 在每种测试的细胞类型中，钠钾 -ATP 酶的哇巴因结合位点是岩沙海葵毒素受体的一部分；(b) 高岩沙海葵毒素敏感性不一定伴随着高哇巴因敏感性；(c) 主动离子转运不是岩沙海葵毒素作用或其被哇巴因抑制的先决条件。
