Frelin C, Vigne P, Breittmayer J P
Institut de Pharmacologie Moléculaire et Cellulaire, UPR 411 CNRS, Valbonne, France.
Mol Pharmacol. 1990 Dec;38(6):904-9.
Palytoxin (PTX) is a non-12-O-tetradecanoylphorbol-13-acetate-type tumor promoter that has potent cardiotoxic properties. In embryonic chick ventricular cells, PTX increased [Ca2+]i (K0.5 = 5 nM) in a manner that was dependent on the presence of extracellular Ca2+. The action of PTX was not consequent to its depolarizing action, to the opening of voltage-dependent Ca2+ channels, to an intracellular Na+ load, or to intracellular acidification. Flow cytometric analysis of the [Ca2+]i distribution in PTX-treated cells showed that only the largest ventricular cells responded to the toxin. All ventricular cells responded to PTX by intracellar acidification. PTX also increased 22Na+ uptake by cardiac cells (K0.5 = 100 nM) via a pathway that was sensitive to 3,4-dichlorobenzamil (K0.5 = 8 microM), suggesting a possible involvement of the Na+/Ca2+ antiporter. We conclude that the action of PTX in chick cardiac cells is distinct from that in erythrocytes or in fibroblasts and that it likely involves several distinct mechanisms. A primary action of PTX could be to open a Ca2+ uptake pathway in the plasma membrane, which would then trigger 22Na+ uptake by the Na+/Ca2+ antiporter.
刺尾鱼毒素（PTX）是一种非12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯型肿瘤促进剂，具有强大的心脏毒性。在胚胎鸡心室细胞中，PTX以依赖细胞外Ca2 +存在的方式增加了[Ca2 +]i（K0.5 = 5 nM）。PTX的作用并非因其去极化作用、电压依赖性Ca2 +通道的开放、细胞内Na +负荷或细胞内酸化所致。对PTX处理细胞中[Ca2 +]i分布的流式细胞术分析表明，只有最大的心室细胞对该毒素有反应。所有心室细胞都通过细胞内酸化对PTX产生反应。PTX还通过对3,4 - 二氯苯甲酰胺敏感的途径（K0.5 = 8 microM）增加了心脏细胞对22Na +的摄取，提示Na +/Ca2 +反向转运体可能参与其中。我们得出结论，PTX在鸡心脏细胞中的作用不同于其在红细胞或成纤维细胞中的作用，并且可能涉及几种不同的机制。PTX的主要作用可能是打开质膜中的Ca2 +摄取途径，进而触发Na +/Ca2 +反向转运体对22Na +的摄取。
