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Superoxide-induced reduction of coenzyme Q and its interaction with vitamin E synergistically protects human kertinocytes against oxidative stress.
Shvedova AA; Tyurina YY; Tyurin VA; Kisin E; Kikuchi Y; Quinn PJ; Kagan VE
Toxicologist 2001 Mar; 60(1):42
Enhanced production of superoxide is commonly associated with the induction of oxidative stress. It has been suggested that, in the presence of ubiquinone, superoxide can act as an antioxidant via reduction of ubiquinone to semiubiquinone/ubiquinol. The latter couple can scavenge radicals directly or act as an antioxidant through its interactions with vitamin E phenoxyl radical, which leads to vitamin E recycling. To investigate the hypothesis, we used normal human epidermal keratinocytes (NHEK) supplemented with vitamin E, ubiquinone or combination thereof NHEK were exposed to oxidative stress induced by lipid-soluble azo-initiator of peroxyl radicals, AMVN, in the presence and in the absence of superoxide-generating system (xanthine oxidase/xanthine). We established conditions under which either vitamin E alone or ubiquinone alone has only caused a slight protection against AMVN-induced oxidation of NHEK phospholipids as assayed by metabolically-integrated oxidation-sensitive fluorescent parinaric acid (PnA). The protection of NHEK supplemented with vitamin E was not enhanced by ubiquinone; however in the presence of xanthine oxidase/xanthine, synergistic protection against AMVN-induced phospholipid peroxidation was observed as compared to the effects of either vitamin E alone or ubiquinone alone. Xanthine/ oxidase induced production of superoxide was able to reduce ubiquinone hence contribute to effective vitamin E recycling. We conclude that the mechanism of superoxide driven reduction of ubiquinone to semiubiquinone/ubiquinol can facilitate recycling of vitamin E, by which it enhances antioxidant protection of keratinocytes.
Vitamins; Synergism; Oxidation; Antioxidants; Antioxidation; Phospholipids
Issue of Publication
The Toxicologist. Society of Toxicology 40th Annual Meeting, March 25-29, 2001, San Francisco, California
Page last reviewed: September 2, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division