Hase J, Mitsui K, Shonaka E
Jpn J Exp Med. 1975 Dec;45(6):433-8.
When Clostridium perfringens theta-toxin was incubated with sheep erythrocytes the toxin activity disappeared before lysis, the fact of which suggests fixation of the toxin to erythrocyte membranes. 2. Theta-Toxin lost its activity by binding to cell membranes, and the membrane constituted inhibitor of theta-hemolysis was neither a protein, a carbohydrate nor a phosphatide, but was cholesterol. From these results this report proposes that the theta-toxin binding site of erythrocytes should be cholesterol.
当产气荚膜梭菌θ毒素与绵羊红细胞一起孵育时,毒素活性在细胞裂解前就消失了,这一事实表明毒素与红细胞膜发生了结合。2. θ毒素通过与细胞膜结合而丧失活性,构成θ溶血抑制剂的膜成分既不是蛋白质、碳水化合物,也不是磷脂,而是胆固醇。基于这些结果,本报告提出红细胞的θ毒素结合位点应为胆固醇。