Role of mitochondrial calcium in hypochlorite induced oxidative damage of cells.

Autor: Cheshchevik VT; Department of Biotechnology, Polessky State University, ulitsa Dnieprovskoy Flotilii, 23, 225710, Pinsk, Belarus. Electronic address: cheshchevik.v@polessu.by., Krylova NG; Department of Biophysics, Belarusian State University, Prospekt Nezavisimosti 4, 220030, Minsk, Belarus., Сheshchevik NG; Department of Biotechnology, Polessky State University, ulitsa Dnieprovskoy Flotilii, 23, 225710, Pinsk, Belarus., Lapshina EA; Department of Biochemistry, Yanka Kupala State University of Grodno, Bulvar Leninskogo Komsomola 50, 230030, Grodno, Belarus., Semenkova GN; Department of Biophysics, Belarusian State University, Prospekt Nezavisimosti 4, 220030, Minsk, Belarus., Zavodnik IB; Department of Biochemistry, Yanka Kupala State University of Grodno, Bulvar Leninskogo Komsomola 50, 230030, Grodno, Belarus.
Jazyk: angličtina
Zdroj: Biochimie [Biochimie] 2021 May; Vol. 184, pp. 104-115. Date of Electronic Publication: 2021 Feb 17.
DOI: 10.1016/j.biochi.2021.02.009
Abstrakt: Hypochlorite (HOCl) is one of the most important mediators of inflammatory processes. Recent evidence demonstrates that changes in intracellular calcium pool play a significant role in the damaging effects of hypochlorite and other oxidants. Mitochondria are shown to be one of the intracellular targets of hypochlorite. But little is known about the mitochondrial calcium pool changes in HOCl-induced mitochondrial dysfunction. Using isolated rat liver mitochondria, we showed the oxidative damage of mitochondria (GSH oxidation and mixed protein-glutathione formation without membrane lipid peroxidation) and alterations in the mitochondrial functional parameters (decrease of respiratory activity and efficiency of oxidative phosphorylation, NADH and FADH coenzyme levels, and membrane potential) under hypochlorite action (50-300 μM). Simultaneously, the mitochondrial calcium release and swelling were demonstrated. In the presence of EGTA, the damaging effects of HOCl were less pronounced, reflecting direct involvement of mitochondrial Ca 2+ in mechanisms of oxidant-induced injury. Furthermore, exposure of HeLa cells to hypochlorite resulted in a considerable increase in cytoplasmic calcium concentrations and a decrease in mitochondrial ones. Applying specific inhibitors of calcium transfer systems, we demonstrated that mitochondria play a key role in the redistribution of cytoplasmic Ca 2+ ions under hypochlorite action and act as mediators of calcium release from the endoplasmic reticulum into the cytoplasm.
(Copyright © 2021 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.)
Databáze: MEDLINE
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