Effect of Potential-Dependent Potassium Uptake on Production of Reactive Oxygen Species in Rat Brain Mitochondria

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O. V. Akopova^*, L. I. Kolchinskaya, V. I. Nosar, V. A. Bouryi, I. N. Mankovska, and V. F. Sagach

Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, ul. Bogomol’tsa 4, 01601 Kiev-24, Ukraine; E-mail: a-dubensky@mail.ru

^* To whom correspondence should be addressed.

Received July 9, 2013; Revision received September 16, 2013

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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 (ΔΨ_m). 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.

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KEY WORDS: potassium, brain mitochondria, reactive oxygen species, K⁺_ATP-channel

DOI: 10.1134/S0006297914010076

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