Park J W, Jahng T A, Rho H W, Park B H, Kim N H, Kim H R
Department of Biochemistry, Chonbuk National University Medical School, Chonju, South Korea.
Biochim Biophys Acta. 1994 Aug 24;1194(1):166-70. doi: 10.1016/0005-2736(94)90216-x.
Calcium in millimolar concentrations protected mouse erythrocytes from hemolysis caused by Vibrio vulnificus cytolysin without affecting the release of intracellular K+ from the cells. This effect was maximal at 25 mM CaCl2. The protection was not absolute and could be partially overcome by increased concentrations of cytolysin. Calcium failed to block both the binding and oligomer formation of cytolysins on the erythrocyte membrane. After pore formation, the continued presence of calcium is required for the prevention of hemolysis. There was hardly any inflow of calcium into the erythrocytes through pores as measured by 45Ca2+ uptake. The presence of calcium after the abolition of Ca2+ gradient by ionomycin cannot inhibit the hemolysis caused by cytolysin. These results suggest that calcium exerts its major inhibitory effect on V. vulnificus cytolysin-induced hemolysis as an osmotic protectant, and that cytolysin may become an useful tool for permeabilizing cells selectively for small ions such as potassium or sodium while preventing the Ca2+ flow.
毫摩尔浓度的钙可保护小鼠红细胞免受创伤弧菌溶血素引起的溶血作用，且不影响细胞内钾离子的释放。此效应在25 mM氯化钙时达到最大。这种保护并非绝对的，溶血素浓度增加可部分克服这种保护作用。钙不能阻止溶血素在红细胞膜上的结合和寡聚体形成。形成孔道后，预防溶血需要持续存在钙。通过45Ca2+摄取测量，几乎没有钙通过孔道流入红细胞。离子霉素消除Ca2+梯度后钙的存在不能抑制溶血素引起的溶血。这些结果表明，钙作为一种渗透保护剂，对创伤弧菌溶血素诱导的溶血发挥主要抑制作用，并且溶血素可能成为一种有用的工具，用于选择性地使细胞对钾或钠等小离子通透，同时防止Ca2+流动。
