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

Whiteman, M., Spencer, J. P. E., Szeto, H. H. and Armstrong, J. S. (2008) Do mitochondriotropic antioxidants prevent chlorinative stress-induced mitochondrial and cellular injury? Antioxidants & Redox Signaling, 10 (3). pp. 641-650. ISSN 1523-0864

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To link to this item DOI: 10.1089/ars.2007.1879

Abstract/Summary

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.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences
Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
ID Code:12857
Uncontrolled Keywords:Antioxidants/*pharmacology, Humans, Hypochlorous Acid/*toxicity, Membrane Potentials/drug effects, Mitochondria/*drug effects, Superoxides/metabolism, permeable peptide antioxidants, hypochlorous acid, targeted, antioxidants, oxidative damage, glutathione depletion, reperfusion, injury, endothelial-cells, apoptosis, transition, death
Publisher:Mary Ann Leibert Inc

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