Effect of potential-dependent potassium uptake on production of reactive oxygen species in rat brain mitochondria

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.sup.+] 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 (Δ[Ψ.sub.m]). At [K.sup.+] concentrations within the range of 0-120 mM, an increase in the initial rate of [K.sup.+]-uptake into the matrix resulted in a decrease in the steady-state rate of ROS generation due to the [K.sup.+]-induced depolarization of the mitochondrial membrane. The selective blockage of the ATP-dependent potassium channel ([K.sup.+.sub.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.sup.+] uptake. The ATP-dependent transport of [K.sup.+] was shown to be ~40% of the potential-dependent [K.sup.+] uptake in the brain mitochondria. Based on the findings of the experiments, the potential-dependent transport of [K.sup.+] was concluded to be a physiologically important regulator of ROS generation in the brain mitochondria and that the functional activity of the native [K.sup.+.sub.ATP]-channel in these organelles under physiological conditions can be an effective tool for preventing ROS overproduction in brain neurons. DOI:10.1134/S0006297914010076 Key words: potassium, brain mitochondria, reactive oxygen species, [K.sup.+.sub.ATP]-channel