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Received July 9, 2013; Revision received September 16, 2013
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.
KEY WORDS: potassium, brain mitochondria, reactive oxygen species, K+ATP-channel