Whiteman, M., Spencer, J. P. E.
ORCID: https://orcid.org/0000-0003-2931-7274, 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
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.
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| Item Type | Article |
| URI | https://reading-clone.eprints-hosting.org/id/eprint/12857 |
| Identification Number/DOI | 10.1089/ars.2007.1879 |
| Refereed | Yes |
| Divisions | 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) |
| 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 |
| Download/View statistics | View download statistics for this item |
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