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产气荚膜梭菌α毒素对离体大鼠输精管的作用。

Effect of Clostridium perfringens alpha toxin on the isolated rat vas deferens.

作者信息

Sakurai J, Nomura S, Fujii Y, Oshita Y

出版信息

Toxicon. 1985;23(3):449-55. doi: 10.1016/0041-0101(85)90028-5.

DOI:10.1016/0041-0101(85)90028-5
PMID:2862722
Abstract

Alpha toxin produced by Clostridium perfringens potentiated norepinephrine-evoked contraction in the isolated rat vas deferens, but itself caused no contraction within 60 min. The potentiating activity was dependent on the dose of the toxin and was quantitatively related to the phospholipase C activity of the toxin preparation.

摘要

产气荚膜梭菌产生的α毒素可增强去甲肾上腺素诱发的离体大鼠输精管收缩,但在60分钟内其本身不会引起收缩。增强活性取决于毒素的剂量,并且在数量上与毒素制剂的磷脂酶C活性相关。

相似文献

1
Effect of Clostridium perfringens alpha toxin on the isolated rat vas deferens.产气荚膜梭菌α毒素对离体大鼠输精管的作用。
Toxicon. 1985;23(3):449-55. doi: 10.1016/0041-0101(85)90028-5.
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Contraction induced by Clostridium perfringens alpha toxin in the isolated rat ileum.产气荚膜梭菌α毒素在离体大鼠回肠中诱导的收缩。
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Contraction of the rat isolated aorta caused by Clostridium perfringens alpha toxin (phospholipase C): evidence for the involvement of arachidonic acid metabolism.产气荚膜梭菌α毒素(磷脂酶C)引起的大鼠离体主动脉收缩:花生四烯酸代谢参与的证据。
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引用本文的文献

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Perfringolysin O: The Underrated Clostridium perfringens Toxin?产气荚膜杆菌溶素O:被低估的产气荚膜梭菌毒素?
Toxins (Basel). 2015 May 14;7(5):1702-21. doi: 10.3390/toxins7051702.
2
Evidence for coupling of Clostridium perfringens alpha-toxin-induced hemolysis to stimulated phosphatidic acid formation in rabbit erythrocytes.产气荚膜梭菌α毒素诱导兔红细胞溶血与刺激磷脂酸形成偶联的证据。
Infect Immun. 1993 Sep;61(9):3711-8. doi: 10.1128/iai.61.9.3711-3718.1993.
3
Excitatory effect of Clostridium perfringens alpha toxin on the rat isolated aorta.产气荚膜梭菌α毒素对大鼠离体主动脉的兴奋作用。
Br J Pharmacol. 1986 Jul;88(3):531-9. doi: 10.1111/j.1476-5381.1986.tb10233.x.
4
Contraction of the rat isolated aorta caused by Clostridium perfringens alpha toxin (phospholipase C): evidence for the involvement of arachidonic acid metabolism.产气荚膜梭菌α毒素(磷脂酶C)引起的大鼠离体主动脉收缩:花生四烯酸代谢参与的证据。
Br J Pharmacol. 1989 May;97(1):119-24. doi: 10.1111/j.1476-5381.1989.tb11931.x.