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.