Investigation of pathophysiologic mechanisms of acute cardiogenic shock by necrotizing toxins from gas gangrene bacilli.

培养的大鼠胎心心肌细胞的收缩已被细胞膜上的α-毒素形成孔道所阻止。提示线粒体肌病可能是由于胞浆内Ca~(2+)和Gt~(2+)过多所致的线粒体肌病所致的心肌细胞ATP生成减少和脱水所致。338位和342位的色氨酸、340位的疏水氨基酸和339位的负电荷氨基酸在α-毒素的细胞结合和细胞毒活性中起着重要的作用。

Contraction of cultured cardiomyocytes from rat fetus heart ventricles have been stopped by pore formation of alpha-toxin on cell membranes. It was suggested that decrease of ATP productions and desiccation of ATP in cardiomyocytes have been caused by mitochondrial myopathy from Ca^<2+> excess in cytoplasm. It has been clear that tryptophan of 338th and 342th, hydrophobic amino acids of 340th and negative charged amino acids of 339th play an important roles in cell binding and cytotoxic activities of alpha-toxin.