Weerkamp A, Geerts W, Vogels G D
Antimicrob Agents Chemother. 1977 Sep;12(3):314-21. doi: 10.1128/AAC.12.3.314.
Treatment of sensitive cells with staphylococcin 1580, a bacteriocin of Staphylococcus epidermidis, rapidly induced gross changes in the permeability of the membrane. However, only a small fraction of the cells was killed when treated cells were plated on media containing low amounts of salts. Killing was greatly enhanced by increasing the amounts of small cations incorporated in the plate medium and raising the alkalinity of the medium. The effect of cations correlated inversely with the ion radius. These conditions are shown to affect the repair mechanism of the sublethally injured cells rather than the interaction of staphylococcin 1580 with the cells. A model is proposed in which the killing effect of staphylococcin 1580 is a result of the inability of cells to maintain the protonmotive force at neutral or alkaline pH as a result of the permeation of cations. Recovery of sublethal damage appears to be a complex process requiring protein and probably also ribonucleic acid synthesis and the addition of a suitable energy source.
用表皮葡萄球菌的一种细菌素葡萄球菌素1580处理敏感细胞,会迅速引起细胞膜通透性的明显变化。然而,当将处理过的细胞接种在含盐量低的培养基上时,只有一小部分细胞被杀死。通过增加平板培养基中掺入的小阳离子量并提高培养基的碱度,杀伤力会大大增强。阳离子的作用与离子半径呈反比。结果表明,这些条件影响的是亚致死损伤细胞的修复机制,而非葡萄球菌素1580与细胞的相互作用。提出了一个模型,其中葡萄球菌素1580的杀伤作用是由于阳离子渗透导致细胞在中性或碱性pH值下无法维持质子动力势的结果。亚致死损伤的恢复似乎是一个复杂的过程,需要蛋白质,可能还需要核糖核酸合成以及添加合适的能量来源。