Protective role of pinacidil against adrenaline-induced myocardium injury in guinea pig liver mitochondria |
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Authors: | Halyna Tkachenko Nataliya Kurhalyuk |
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Institution: | (1) Department of Hygiene and Toxicology, Danylo Halytskiy Lviv National Medical University, 79010 Lviv, Ukraine;(2) Department of Animal Physiology, Institute of Biology and Environment Protection, Pomeranian University, 76-200 Słupsk, Poland |
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Abstract: | We investigated the role of the ATP-sensitive potassium channel opener pinacidil and blocker glibenclamide on guinea pig liver
mitochondrial function, and a possible significance of pinacidil in the pharmacological treatment during myocardium dystrophy.
First, a series of experiments was performed to determine the effect of pinacidil and glibenclamide on mitochondrial oxygen
consumption. We found that pinacidil increased the rate of mitochondrial respiration for FAD-generated substrate (succinate
oxidation), but was most effective for α-ketoglutarate oxidation with enhancement of respiratory control ratio. Oxidation of FAD-generated substrate inhibited efficiency
of phosphorylation for α-ketoglutarate oxidation in pinacidil-treated animals. Glibenclamide decreased the rate of respiration with the lowest value
of efficiency of phosphorylation, especially for α-ketoglutarate oxidation. A second series of experiments was performed to determine the effects of pinacidil and glibenclamide
on oxidative phosphorylation during adrenaline-induced myocardium dystrophy. The increase in respiratory control ratio and
efficiency of phosphorylation for α-ketoglutarate oxidation was greater than for succinate oxidation in mitochondria of pinacidil-pretreated animals during myocardium
dystrophy. Inhibitory analysis with malonate suggested that endogenous succinate increased oxidation of NADH-generated substrates
in mitochondria. Pinacidil is mainly involved in the adrenaline-induced alterations of mitochondrial function due to elevation
of phosphorylation efficiency for α-ketoglutarate oxidation and a decreased level of lipid peroxidation. |
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Keywords: | KATP channels pinacidil glibenclamide adrenaline-induced myocardium dystrophy mitochondria oxidative phosphorylation lipid peroxidation |
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