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[局部麻醉剂对光系统II供体部位电子传递的抑制机制]

[Mechanism of inhibition by local anesthetics of electron transport at the donor site of the photosystem II].

作者信息

Semin B K, Chudinovskikh M N, Ivanov I I

出版信息

Biokhimiia. 1987 Aug;52(8):1279-85.

PMID:3311175
Abstract

The mechanism of inhibition by local anaesthetics of the procaine group of electron transport at the donor site of photosystem II (PS II) from pea chloroplasts was investigated. It was found that besides the inactivation of the O2 release system the anaesthetics used at one order of magnitude lesser concentration exert an uncoupling effect. With a rise in pH the inhibiting activity increases; however, this process is not coupled with the protonophore effect but is due to the generation of a neutral form of the amine. The increment of the inhibiting activity of the anaesthetics in the course of deprotonation seems to be regulated by changes in the coefficient of distribution between the membrane and the aqueous phase. The rate of inactivation of the H2O-dissociating complex increases considerably upon illumination. Electron transport through PS II in anaesthetic-treated chloroplasts in restored by diphenylcarbaside, but not by hydroxylamine. It is concluded that the anaesthetics induce the inhibition by interacting with the electron carrier. The role of the Ca2+--calmodulin-like protein in the functioning of the electron transport chain of PS II is discussed.

摘要

研究了普鲁卡因类局部麻醉药对豌豆叶绿体光系统II(PS II)供体部位电子传递的抑制机制。结果发现,除了使氧气释放系统失活外,浓度低一个数量级的麻醉药还会产生解偶联效应。随着pH值升高,抑制活性增强;然而,这一过程与质子载体效应无关,而是由于胺的中性形式的产生。麻醉药在去质子化过程中抑制活性的增加似乎受膜与水相之间分配系数变化的调节。光照时,水离解复合物的失活速率显著增加。经麻醉处理的叶绿体中通过PS II的电子传递可被二苯基卡巴腙恢复,但不能被羟胺恢复。得出的结论是,麻醉药通过与电子载体相互作用诱导抑制作用。讨论了Ca2+ - 钙调蛋白样蛋白在PS II电子传递链功能中的作用。

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Biokhimiia. 1987 Aug;52(8):1279-85.
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