Sakurai J, Ochi S, Tanaka H
Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Japan.
Infect Immun. 1994 Feb;62(2):717-21. doi: 10.1128/iai.62.2.717-721.1994.
The rapid phosphatidic acid (PA) formation induced by Clostridium perfringens alpha-toxin was stimulated by AlF4- in rabbit erythrocyte membranes. GTP[gamma S] [guanosine 5'-O-(3-thiotriphosphate)] stimulated the rapid 1,2-diacylglycerol formation and inositol 1,4,5-trisphosphate release induced by the toxin. On the other hand, treatment of erythrocyte lysates with phorbol 12-myristate 13-acetate (PMA) resulted in inhibition of toxin-induced PA production, and long-term PMA or 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) treatment of the lysates led to stimulation of PA formation. Furthermore, treatment of erythrocytes with the toxin caused an increase of protein kinase C activity in membrane fractions. The results suggest that toxin-induced PA formation is mediated by endogenous phospholipase C regulated through GTP-binding protein and protein kinase C in rabbit erythrocytes.
产气荚膜梭菌α毒素诱导的快速磷脂酸（PA）形成在兔红细胞膜中受到AlF4-的刺激。GTP[γS][鸟苷5'-O-(3-硫代三磷酸)]刺激了毒素诱导的快速1,2-二酰基甘油形成和肌醇1,4,5-三磷酸释放。另一方面，用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）处理红细胞裂解物会抑制毒素诱导的PA产生，而长期用PMA或1-(5-异喹啉磺酰基)-2-甲基哌嗪（H-7）处理裂解物会导致PA形成增加。此外，用毒素处理红细胞会导致膜组分中蛋白激酶C活性增加。结果表明，毒素诱导的PA形成是由通过鸟苷结合蛋白和蛋白激酶C调节的内源性磷脂酶C介导的，存在于兔红细胞中。
