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. 2021 Feb;170(4):431-435.
doi: 10.1007/s10517-021-05081-y. Epub 2021 Mar 16.

Does the Operation of Mitochondrial ATP-Dependent Potassium Channels Affect the Structural Component of Mitochondrial and Endothelial Dysfunctions in Experimental Parkinsonism?

A A Mosentsov  1 , E V Rozova  2 , N V Belosludtseva  1 , I N Mankovskaya  2 , Yu V Putiy  2 , I N Karaban  3 , I B Mikheeva  1 , G D Mironova  4
Affiliations

Does the Operation of Mitochondrial ATP-Dependent Potassium Channels Affect the Structural Component of Mitochondrial and Endothelial Dysfunctions in Experimental Parkinsonism?

A A Mosentsov et al. Bull Exp Biol Med. 2021 Feb.

Abstract

We have previously demonstrated that the development of oxidative stress in some pathologies can be prevented by activation of the mitochondrial ATP-dependent potassium channel (mitoKATP). Here we studied the effect of modulation of mitoKATP on the development of mitochondrial and endothelial dysfunction in the medulla oblongata and myocardium of rats with experimental parkinsonism. It is known that uridine-5'-diphosphate, activator of mitoKATP, does not penetrate the plasma membrane, but it can be synthesized in cells from exogenous uridine that is delivered into cells by special transport systems. Our results suggest that mitoKATP is involved in the development of mitochondrial and endothelial dysfunction in experimental parkinsonism and prove the cardio- and neuroprotective effects of uridine.

Keywords: mitochondria; mitochondrial ATP-dependent potassium channel; parkinsonism; rotenone; uridine.

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