Wang X, Horisberger J D
Institute of Pharmacology and Toxicology, University de Lausanne, Switzerland.
FEBS Lett. 1997 Jun 16;409(3):391-5. doi: 10.1016/s0014-5793(97)00559-0.
Palytoxin (PTX) is known to bind to Na,K-ATPase, to inhibit its activity, and to induce cation conductance, but the mechanism of these effects is still poorly understood. In Xenopus oocytes, PTX induced a large cation conductance, an effect that could be prevented or reversed by ouabain for oocytes expressing Xenopus Na,K-pumps but not with those expressing Bufo Na,K-pumps. In both cases patch-clamp experiments demonstrated a 7-8 pS channel in the presence of PTX. A large PTX-induced conductance could be observed with minimal Na,K-pump inhibition. From the single PTX-induced channel and macroscopic whole oocyte conductance, and the number of Na,K-pumps, we can conclude that PTX-induced conductance occurs through a direct interaction of PTX with a small number of Na,K-pumps.
已知刺尾鱼毒素（PTX）可与钠钾ATP酶结合，抑制其活性，并诱导阳离子电导，但这些效应的机制仍知之甚少。在非洲爪蟾卵母细胞中，PTX诱导了较大的阳离子电导，对于表达非洲爪蟾钠钾泵的卵母细胞，哇巴因可阻止或逆转这种效应，但对于表达蟾蜍钠钾泵的卵母细胞则不然。在这两种情况下，膜片钳实验均表明在存在PTX时会出现一个7 - 8皮安的通道。在钠钾泵抑制作用最小的情况下，也能观察到PTX诱导的较大电导。从单个PTX诱导的通道、宏观的整个卵母细胞电导以及钠钾泵的数量来看，我们可以得出结论，PTX诱导的电导是通过PTX与少量钠钾泵的直接相互作用而发生的。
