Abstract
On the impact of K(ATP) channel opening on mitochondrial reactive oxygen species production
Highlights
Mitochondrial reactive oxygen species (ROS) production was shown to be regulated by cell-specific mechanisms
One early attempt to address this question was that of Garlid’s group who conducted semi-quantitative estimation of the distribution of mKATP channel in mitochondria of different tissues. They found that in brain density of the mKATP channels in mitochondrial membrane largely prevailed over one found in heart and liver tissues, which implies a special importance of potential-dependent regulation of ROS production by ATP-sensitive K+ transport in neuronal mitochondria [7]. This was confirmed in our own studies where we found a suppression of ROS production well explained by ~20% depolarization ensuing from mKATP channel opening
Conclusions mKATP channel plays a cell-specific role in the regulation of mitochondrial ROS production
Summary
Mitochondrial reactive oxygen species (ROS) production was shown to be regulated by cell-specific mechanisms. It is that there is no means to predict an effect of mKATP channel opening on ROS production because of very contradictory results regarding this issue obtained in different tissues. Isoform distribution and the impact of mKATP channel opening on mitochondrial bioenergetics, ΔΨm, largely varies between cell types.
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