Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, 01601, Ukraine.
Biochemistry (Mosc). 2014 Jan;79(1):44-53. doi: 10.1134/S0006297914010076.
The effect of potential-dependent potassium uptake on reactive oxygen species (ROS) generation in mitochondria of rat brain was studied. It was found that the effect of K+ uptake on ROS production in the brain mitochondria under steady-state conditions (state 4) was determined by potassium-dependent changes in the membrane potential of the mitochondria (ΔΨm). At K+ concentrations within the range of 0-120 mM, an increase in the initial rate of K(+)-uptake into the matrix resulted in a decrease in the steady-state rate of ROS generation due to the K(+)-induced depolarization of the mitochondrial membrane. The selective blockage of the ATP-dependent potassium channel (K(ATP)(+)-channel) by glibenclamide and 5-hydroxydecanoate resulted in an increase in ROS production due to the membrane repolarization caused by partial inhibition of the potential-dependent K+ uptake. The ATP-dependent transport of K+ was shown to be ~40% of the potential-dependent K+ uptake in the brain mitochondria. Based on the findings of the experiments, the potential-dependent transport of K+ was concluded to be a physiologically important regulator of ROS generation in the brain mitochondria and that the functional activity of the native K(ATP)(+)-channel in these organelles under physiological conditions can be an effective tool for preventing ROS overproduction in brain neurons.
研究了依赖电势的钾摄取对大鼠脑线粒体中活性氧（ROS）生成的影响。研究发现，在稳态条件下（状态 4），钾摄取对脑线粒体中 ROS 产生的影响取决于线粒体膜电势（ΔΨm）的钾依赖性变化。在 0-120mM 的钾浓度范围内，由于钾诱导的线粒体膜去极化，基质中钾摄取的初始速率增加会导致 ROS 生成的稳态速率降低。用格列本脲和 5-羟癸酸选择性阻断 ATP 依赖性钾通道（K(ATP)(+)-通道）会导致 ROS 产生增加，这是由于部分抑制依赖电势的钾摄取引起的膜复极化所致。结果表明，脑线粒体中 ATP 依赖性 K+转运约占依赖电势的 K+摄取的 40%。基于实验结果，得出结论：依赖电势的 K+转运是脑线粒体中 ROS 生成的生理上重要的调节剂，在生理条件下，这些细胞器中天然 K(ATP)(+)-通道的功能活性可以成为预防脑神经元中 ROS 过度产生的有效工具。
