McClane B A
Biochim Biophys Acta. 1984 Oct 17;777(1):99-106. doi: 10.1016/0005-2736(84)90501-7.
Using a sensitive Vero (African green monkey kidney) cell model system, studies were performed to further investigate whether Clostridium perfringens enterotoxin acts via disruption of the colloid-osmotic equilibrium of sensitive cells. Enterotoxin was shown to cause a rapid loss of intracellular 86Rb+ (Mr approx. 100) with time- and dose-dependent kinetics. The enterotoxin-induced release of intracellular 86Rb+ preceded the loss of two larger labels, 51Cr label (Mr approx. 3500) and 3H-labeled nucleotides (Mr less than 1000). The osmotic stabilizers, sucrose and poly(ethylene glycol), differentially inhibited enterotoxin-induced larger label loss versus 86Rb+ loss. Further, enterotoxin was shown to cause a rapid influx of 24Na+ that was not significantly inhibited by osmotic stabilizers. Additional studies demonstrated that lysosomotropic agents were not protective against characteristic enterotoxin-induced membrane permeability alterations or morphological damage. Taken collectively, these results are consistent with an action for enterotoxin which involves a disruption of the osmotic equilibrium.
利用一种敏感的Vero（非洲绿猴肾）细胞模型系统进行研究，以进一步探究产气荚膜梭菌肠毒素是否通过破坏敏感细胞的胶体渗透平衡发挥作用。研究表明，肠毒素会导致细胞内86Rb+（相对分子质量约为100）随时间和剂量依赖性动力学迅速流失。肠毒素诱导的细胞内86Rb+释放先于另外两种较大标记物的流失，即51Cr标记物（相对分子质量约为3500）和3H标记的核苷酸（相对分子质量小于1000）。渗透稳定剂蔗糖和聚乙二醇对肠毒素诱导的较大标记物流失与86Rb+流失有不同程度的抑制作用。此外，研究表明肠毒素会导致24Na+迅速内流，而渗透稳定剂对此没有明显抑制作用。进一步的研究表明，溶酶体促渗剂对肠毒素诱导的特征性膜通透性改变或形态损伤没有保护作用。综合来看，这些结果与肠毒素通过破坏渗透平衡发挥作用的观点一致。
