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首页> 外文期刊>Ukrainian Biochemical Journal >The effect of permeability transition pore opening on reactive oxygen species production in rat brain mitochondria
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The effect of permeability transition pore opening on reactive oxygen species production in rat brain mitochondria

机译：渗透性过渡孔的开放对大鼠脑线粒体活性氧产生的影响

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The influence of mitochondrial permeability transition pore (MPTP) opening on reactive oxygen species (ROS) production in the rat brain mitochondria was studied. It was shown that ROS production is regulated differently by the rate of oxygen consumption and membrane potential, dependent on steady-state or non-equilibrium conditions. Under steady-state conditions, at constant rate of Casup2+/sup-cycling and oxygen consumption, ROS production is potential-dependent and decreases with the inhibition of respiration and mitochondrial depolarization. The constant rate of ROS release is in accord with proportional dependence of the rate of ROS formation on that of oxygen consumption. On the contrary, transition to non-equilibrium state, due to the release of cytochrome c from mitochondria and progressive respiration inhibition, results in the loss of proportionality in the rate of ROS production on the rate of respiration and an exponential rise of ROS production with time, independent of membrane potential. Independent of steady-state or non-equilibrium conditions, the rate of ROS formation is controlled by the rate of potential-dependent uptake of Casup2+/sup which is the rate-limiting step in ROS production. It was shown that MPTP opening differently regulates ROS production, dependent on Casup2+/sup concentration. At low calcium MPTP opening results in the decrease in ROS production because of partial mitochondrial depolarization, in spite of sustained increase in oxygen consumption rate by a cyclosporine A-sensitive component due to simultaneous work of Casup2+/sup-uniporter and MPTP as Casup2+/sup-influx and efflux pathways. The effect of MPTP opening at low Casup2+/sup concentrations is similar to that of Casup2+/sup-ionophore, A-23187. At high calcium MPTP opening results in the increase of ROS release due to the rapid transition to non-equilibrium state because of cytochrome c loss and progressive gating of electron flow in respiratory chain. Thus, under physiological conditions MPTP opening at low intracellular calcium could attenuate oxidative damage and the impairment of neuronal functions by diminishing ROS formation in mitochondria.
机译：研究了线粒体通透性过渡孔（MPTP）开口对大鼠脑线粒体中活性氧（ROS）产生的影响。结果表明，取决于稳态或非平衡条件，ROS的产生受到耗氧率和膜电位的调节不同。在稳态条件下，在恒定的Ca 2 + 循环速率和耗氧量下，ROS的产生依赖于电势，并随着呼吸和线粒体去极化的抑制而降低。恒定的ROS释放速率与ROS生成速率与耗氧量成比例关系。相反，由于线粒体释放出细胞色素c并抑制了呼吸，因此过渡到非平衡状态导致ROS生成速率与呼吸速率成比例的损失，并且ROS生成呈指数增长。时间，与膜电位无关。与稳态或非平衡条件无关，ROS的形成速率受Ca 2 + 的电势依赖性吸收速率控制，Ca 2 + 是ROS生产中的限速步骤。结果表明，MPTP的开放取决于Ca 2 + 的浓度而不同地调节ROS的产生。在低钙的情况下，尽管由于Ca 2 + -的同时作用，环孢素A敏感组分的耗氧率持续增加，但由于部分线粒体去极化，MPTP开放导致ROS的产生减少。单向转运蛋白和MPTP作为Ca 2 + 流入和流出途径。在低Ca 2 + 浓度下打开MPTP的效果类似于Ca 2 + -离子载体A-23187的效果。在高钙的情况下，由于细胞色素c的丧失和呼吸链中电子流的逐步门控，MPTP的开放会导致ROS释放的增加，这是由于其迅速过渡到非平衡状态所致。因此，在生理条件下，低细胞内钙的MPTP开放可通过减少线粒体中ROS的形成来减弱氧化损伤和神经元功能的损害。

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