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+ 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.