Effect of calcium ions on staphylococcal alpha-toxin-induced hemolysis of rabbit erythrocytes.
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.
D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity*; D002122:Calcium Chloride / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects; D006460:Hemolysin Proteins; D006461:Hemolysis / Q000187:drug effects*; D007700:Kinetics; D011817:Rabbits; D012413:Rubidium / Q000097:blood; D013210:Staphylococcus / Q000472:pathogenicity
D001427:Bacterial Toxins; D006460:Hemolysin Proteins; C021091:staphylococcal alpha-toxin; D002122:Calcium Chloride; D012413:Rubidium