Akopova O V, Kolchinskaia L I, Nosar' V I, Buryĭ V A, Man'kovskaia I N, Sagach V F
Ukr Biochem J. 2014 Mar-Apr;86(2):26-40. doi: 10.15407/ubj86.02.026.
The effect of mitochondrial ATP-dependent K(+)-channel (K(+)ATP-channel) opener diazoxide (DZ) on transmembrane potassium exchange and reactive oxygen species (ROS) formation under the opening of mitochondrial permeability transition pore (MPTP) was studied in rat liver mitochondria. The activation of K(+)-cycling (K(+)-uptake and K(+)/H(+)-exchange) by DZ was established with peak effect at < or = 500 nM. It was shown that MPTP opening as well resulted in the activation of K(+)-cycling together with simultaneous activation of Ca(2+)-cycle in mitochondria. In the absence of depolarization Ca(2+)-cycle is supported by MPTP and Ca(2+)-uniporter. The stimulation of K(+)/H(+)-exchange by MPTP opening led to the activation of K(+)-cycle, but further activation of K(+)/H(+)-exchange resulted in MPTP inhibition. Under the same conditions the decrease in mitochondrial ROS production was observed. It was proposed that the decrease in ROS formation together with K(+)/H(+)-exchange activation could be the constituents of the complex effect of MPTP inhibition induced by K(+)ATP-channel opener.
在大鼠肝线粒体中，研究了线粒体ATP依赖性钾通道（K(+)ATP通道）开放剂二氮嗪（DZ）对线粒体通透性转换孔（MPTP）开放时跨膜钾交换和活性氧（ROS）生成的影响。确定了DZ对K(+)循环（K(+)摄取和K(+)/H(+)交换）的激活作用，在≤500 nM时达到峰值效应。结果表明，MPTP开放也导致K(+)循环的激活，同时线粒体中的Ca(2+)循环也被激活。在没有去极化的情况下，Ca(2+)循环由MPTP和Ca(2+)单向转运体维持。MPTP开放对K(+)/H(+)交换的刺激导致K(+)循环的激活，但K(+)/H(+)交换的进一步激活导致MPTP抑制。在相同条件下，观察到线粒体ROS生成减少。有人提出，ROS生成的减少以及K(+)/H(+)交换的激活可能是K(+)ATP通道开放剂诱导MPTP抑制的复合效应的组成部分。
