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

• Published in: Bulletin of experimental biology and medicine 2021-02, Vol.170 (4), p.431-435
• Main Authors: Mosentsov, A. A., Rozova, E. V., Belosludtseva, N. V., Mankovskaya, I. N., Putiy, Yu. V., Karaban, I. N., Mikheeva, I. B., Mironova, G. D.
• Format: Article
• Language: English
• Subjects: Basal ganglia; Biomedical and Life Sciences; Biomedicine; Biophysics and Biochemistry; Brain diseases; Cell Biology; Central nervous system diseases; Endothelium; Internal Medicine; Laboratory Medicine; Medulla oblongata; Mitochondria; Movement disorders; Myocardium; Neuroprotection; Oxidative stress; Parkinson's disease; Pathology; Potassium; Potassium channels; Uridine
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-021-05081-y

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 (mitoK ATP ). Here we studied the effect of modulation of mitoK ATP 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 mitoK ATP , 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 mitoK ATP is involved in the development of mitochondrial and endothelial dysfunction in experimental parkinsonism and prove the cardio- and neuroprotective effects of uridine.