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首页> 外文期刊>Ukrainian Biochemical Journal >The effect of ATP-dependent K(+)-channel opener on the functional state and the opening of cyclosporine-sensitive pore in rat liver mitochondria
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The effect of ATP-dependent K(+)-channel opener on the functional state and the opening of cyclosporine-sensitive pore in rat liver mitochondria

机译：ATP依赖的K（+）通道开放剂对大鼠肝线粒体功能状态和环孢素敏感孔开放的影响

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摘要

The effect of mitochondrial ATP-dependent Ksup+/sup-channel (Ksup+/supsubАТР/sub-channel) opener diazoxide (DZ) on the oxygen consumption, functional state and the opening of cyclosporine-sensitive pore in the rat liver mitochondria has been studied. It has been established that Ksup+/supsubАТР/sub-channel activation results in the increase of the oxygen consumption rate ( V sub4/subsupS/sup) and the uncoupling due to the acceleration of Ksup+/sup-cycling, the decrease in state 3 respiration rate ( V sub3/sub) and the respiratory control ratio (RCR). Under Ksup+/supsubАТР/sub-channel activation an inhibition of oxidative phosphorylation takes place which reduces the rate of ATP synthesis and hydrolysis as well as ATP production and consequently results in the seeming increase of P/O ratio. It has been shown that the increase in ATP-dependent Ksup+/sup-uptake accompanied by the opening of mitochondrial permeability transition pore (MPTP) leads to dramatic uncoupling of the respiratory chain due to simultaneous activation of Ksup+/sup– and Casup2+/sup-cycling supported by MPTP and Casup2+/sup-uniporter as well as Ksup+/sup-channels and Ksup+/sup/Hsup+/sup-exchange. Ksup+/supsubАТР/sub-channel activation leads to the partial inhibition of MPTP, but insufficient for the restoration of mitochondrial functions. Elimination of Casup2+/sup-cycling after MPTP opening is necessary to return mitochondrial functions back to the control level which shows that MPTP could serve as the mechanism of reversible modulation of bioenergetic effects of Ksup+/supsubАТР/sub-channel activation.
机译：线粒体ATP依赖性K + 通道（K + АТР通道）二氮嗪（DZ）对耗氧量，功能的影响已经研究了大鼠肝线粒体中环孢素敏感孔的状态和开口。已经确定，K + АТР通道激活会导致耗氧率（V 4 S ）和由于K + 循环的加速，状态3呼吸速率（V 3 ）和呼吸控制比（RCR）降低而引起的解耦。在K + АТР通道激活下，发生了氧化磷酸化的抑制作用，这降低了ATP的合成和水解速度以及ATP的产生，从而导致ATP的表面活性增加。 P / O比。研究表明，ATP依赖的K + 摄取的增加伴随着线粒体通透性过渡孔（MPTP）的开放，由于K -uniporter以及K + -通道支持的> + –和Ca 2 + -循环和K + / H + 交换。 K + АТР通道激活导致MPTP的部分抑制，但不足以恢复线粒体功能。打开MPTP后消除Ca 2 + 循环对于使线粒体功能恢复到控制水平是必要的，这表明MPTP可以作为可逆调节K + < / sup> АТР-通道激活。

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