Biochemical and pharmacological studies on Clostridium perfringens alpha toxin

我们最近证实，α毒素引起的大鼠离体主动脉收缩与磷脂酰肌醇代谢和钙摄取有关，并且该毒素可收缩大鼠的离体回肠。本研究旨在明确收缩效应对平滑肌组织的模式作用。提示大鼠离体主动脉对毒素的收缩反应与刺激组织内皮细胞释放花生四烯酸产生血栓素A_2有关。另一方面，该毒素可诱导大鼠回肠磷脂酰肌醇代谢和钙摄取。但对组织中花生四烯酸的释放和丙二醛的产生无刺激作用。因此，该毒素的最初作用似乎是刺激磷脂酰肌醇代谢和钙摄取。

We have recently demonstrated that alpha toxin-induced contraction of rat isolated aorta was associated with phosphatidyl inositol metabolism and Ca uptake and that the toxin contracted the rat isolated ileum. The present study was undertaken to define the mode action of the contractile effect on smooth muscle tissues. It was suggested that the contractile response of rat isolated aorta to the toxin is associated with stimulation of thromboxane A_2 production from arachidonic acid released by the toxin in the endothelial cells of the tissue. On the other hand, the toxin induced phosphatidyl inositol metabolism and Ca uptake in the rat isolated ileum. However, it caused no stimulation of arachidonic acid release and malondialdehyde production in the tissue. Therefore, it appears that the initial action of the toxin is stimulation of phosphatidyl inositol metabolism and Ca uptake.