Role of mitochondrial calcium in hypochlorite induced oxidative damage of cells

Hypochlorite (HOCl) is one of the most important mediators inflammatory processes. Recent evidence demonstrates that changes in intracellular calcium pool play a significant role damaging effects hypochlorite and other oxidants. Mitochondria are shown to be targets hypochlorite. But little known about mitochondrial HOCl-induced dysfunction. Using isolated rat liver mitochondria, we showed oxidative damage mitochondria (GSH oxidation mixed protein-glutathione formation without membrane lipid peroxidation) alterations functional parameters (decrease respiratory activity efficiency phosphorylation, NADH FADH coenzyme levels, potential) under action (50–300 μM). Simultaneously, release swelling were demonstrated. In presence EGTA, HOCl less pronounced, reflecting direct involvement Ca2+ mechanisms oxidant-induced injury. Furthermore, exposure HeLa cells resulted considerable increase cytoplasmic concentrations decrease ones. Applying specific inhibitors transfer systems, demonstrated key redistribution ions act as from endoplasmic reticulum into cytoplasm.