McGahan M C, Matthews D O, Bentley P J
Biochim Biophys Acta. 1986 Feb 13;855(1):63-7. doi: 10.1016/0005-2736(86)90189-6.
The bee venom melittin, 10(-6) M, on the mucosal (urinary) side of the toad urinary bladder (in vitro), markedly decreased transepithelial potential difference, short-circuit current (Isc, sodium-dependent) and resistance. However, these effects were not seen when the toxin was placed on the opposite (serosal) side of the membrane preparation. The electrical effects were accompanied by a large increase in the transepithelial permeability to 22Na. The response was not changed by meclofenamic acid (which blocks formation of prostaglandins) but it was inhibited by La3+. In the presence of amiloride, which usually inhibits active Na transport and Isc, melittin, on the mucosal side, increased the Isc. The action of melittin appears to involve an interaction with anionic sites, which mediate its effects. Such sites appear to be present on the apical plasma membranes of the toad bladder epithelial cells, but they are not as abundant or they are inaccessible on the basal plasma membrane.
10⁻⁶ M的蜂毒溶血肽作用于蟾蜍膀胱黏膜(尿道)侧(体外实验)时,可显著降低跨上皮电位差、短路电流(Isc,依赖于钠)和电阻。然而,当毒素置于膜制剂的另一侧(浆膜侧)时,未观察到这些效应。电效应伴随着跨上皮对²²Na通透性的大幅增加。该反应不受甲氯芬那酸(阻断前列腺素形成)的影响,但被La³⁺抑制。在通常抑制主动钠转运和Isc的氨氯吡咪存在的情况下,黏膜侧的溶血肽可增加Isc。溶血肽的作用似乎涉及与阴离子位点的相互作用,这些位点介导了其效应。此类位点似乎存在于蟾蜍膀胱上皮细胞的顶端质膜上,但在基底质膜上数量较少或难以接近。