Harshman S, Sugg N
Infect Immun. 1985 Jan;47(1):37-40. doi: 10.1128/iai.47.1.37-40.1985.
Calcium in millimolar concentrations protected rabbit erythrocytes from hemolysis caused by staphylococcal alpha-toxin. This effect was maximal at 30 mM CaCl2 and required the continued presence of calcium. The protection was not absolute and could be overcome by increased concentrations of alpha-toxin. Calcium did not block the binding of alpha-toxin to erythrocytes but inhibited the alpha-toxin-induced release of small ions from the cell as measured by 86Rb release. The transient removal of calcium was sufficient to abrogate its protective effect, suggesting that its action involves a reversible alteration in the state of the membrane. The three steps of the alpha-toxin-induced hemolytic sequence are: (i) binding to specific receptors, (ii) formation of transmembrane pores, and (iii) cell lysis. We concluded that calcium acted at step ii by impeding the lateral movement of alpha-toxin necessary to form the transmembrane hexamer pores.
毫摩尔浓度的钙可保护兔红细胞免受葡萄球菌α毒素引起的溶血。此效应在30 mM氯化钙时最大,且需要钙持续存在。这种保护并非绝对的,增加α毒素的浓度可克服这种保护作用。钙不会阻断α毒素与红细胞的结合,但可抑制α毒素诱导的小离子从细胞中释放(通过86Rb释放来测量)。短暂去除钙足以消除其保护作用,这表明其作用涉及膜状态的可逆改变。α毒素诱导的溶血过程的三个步骤为:(i)与特定受体结合,(ii)形成跨膜孔,以及(iii)细胞裂解。我们得出结论,钙在第二步起作用,通过阻碍形成跨膜六聚体孔所需的α毒素的横向移动。