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Do mitochondriotropic antioxidants prevent chlorinative stress-induced mitochondrial and cellular injury?

By M. Whiteman, J. P. E. Spencer, H. H. Szeto and J. S. Armstrong

Abstract

Reactive chlorine species such as hypochlorous acid ( HOCl) are cytotoxic oxidants generated by activated neutrophils at the sites of chronic inflammation. Since mitochondria are key mediators of apoptosis and necrosis, we hypothesized that mitochondriotropic antioxidants could limit HOCl-mediated intracellular oxidative injury to human fetal liver cells, preserve mitochondrial function, and prevent cell death. In this current study, we show that recently developed mitochondria-targeted antioxidants ( MitoQ and SS31) significantly protected against HOCl-induced mitochondrial damage and cell death at concentrations >= 25 nM. Our study highlights the potential application of mitochondria-specific targeted antioxidants for the prevention of cellular dysfunction and cell death under conditions of chlorinative stress, as occurs during chronic inflammation

Publisher: Mary Ann Leibert Inc
Year: 2008
OAI identifier: oai:centaur.reading.ac.uk:12857
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