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首页> 外文期刊>American Journal of Physiology >Opening mitoKATP increases superoxide generation from complex I of the electron transport chain.
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Opening mitoKATP increases superoxide generation from complex I of the electron transport chain.

机译：开放的mitoKATP增加了电子传输链的复合物I产生的超氧化物。

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摘要

Opening the mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)) increases levels of reactive oxygen species (ROS) in cardiomyocytes. This increase in ROS is necessary for cardioprotection against ischemia-reperfusion injury; however, the mechanism of mitoK(ATP)-dependent stimulation of ROS production is unknown. We examined ROS production in suspensions of isolated rat heart and liver mitochondria, using fluorescent probes that are sensitive to hydrogen peroxide. When mitochondria were treated with the K(ATP) channel openers diazoxide or cromakalim, their ROS production increased by 40-50%, and this effect was blocked by 5-hydroxydecanoate. ROS production exhibited a biphasic dependence on valinomycin concentration, with peak production occurring at valinomycin concentrations that catalyze about the same K(+) influx as K(ATP) channel openers. ROS production decreased with higher concentrations of valinomycin and with all concentrations of a classical protonophoretic uncoupler. Our studies show that the increase in ROS is due specifically to K(+) influx into the matrix and is mediated by the attendant matrix alkalinization. Myxothiazol stimulated mitoK(ATP)-dependent ROS production, whereas rotenone had no effect. This indicates that the superoxide originates in complex I (NADH:ubiquinone oxidoreductase) of the electron transport chain.
机译：打开线粒体ATP敏感的K（+）通道（mitoK（ATP））可增加心肌细胞中活性氧（ROS）的水平。 ROS的这种增加对于保护心肌免受缺血再灌注损伤是必要的。然而，依赖mitoK（ATP）刺激ROS产生的机制尚不清楚。我们使用对过氧化氢敏感的荧光探针检查了离体大鼠心脏和肝脏线粒体悬浮液中的ROS产生。当线粒体用K（ATP）通道开放剂二氮嗪或cromakalim处理时，它们的ROS产生增加了40-50％，而这种作用被5-羟基癸酸酯所阻止。 ROS的生产表现出对valinomycin浓度的双相依赖性，并且在valinomycin浓度产生峰值生产，其催化的K（+）流入量与K（ATP）通道开放剂大致相同。随着更高浓度的缬氨霉素和所有浓度的经典质子体解偶联剂，ROS的产生均降低。我们的研究表明，ROS的增加是由于K（+）流入基质而引起的，并伴随着基质的碱化。 Myxothiazol刺激了mitoK（ATP）依赖的ROS产生，而鱼藤酮则没有作用。这表明超氧化物起源于电子传输链的复合物I（NADH：泛醌氧化还原酶）。

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