Author(s): Jarabak R, Jarabak J, Jarabak R, Jarabak J
Abstract Share this page
Abstract Following the two-electron reduction of 2-methyl-1,4-naphthoquinone by rat liver DT-diaphorase (also called NAD(P)H: (quinone acceptor) oxidoreductase, EC 18.104.22.168), the hydroquinone product is slowly autoxidized to the quinone in buffered solutions at pH 7.0. The autoxidation, which generates the superoxide radical (O2-.) and other reactive oxygen species, is the rate-limiting step in the oxidation-reduction (redox) cycling of the quinone. The addition of ascorbate to these reaction mixtures increases the rate of redox cycling. Two mechanisms are proposed to explain this increase: (1) ascorbate reduces the quinone in a one-electron reduction and (2) if Fe(3+)-EDTA is present, ascorbate reduces the metal chelate in a one-electron reduction. Both mechanisms produce O2-. which initiates the free radical chain reaction that results in autoxidation of the hydroquinone. Although ascorbate may be a physiologically important antioxidant under some conditions, the studies reported here show that ascorbate is a prooxidant in the redox cycling of 2-methyl-1,4-naphthoquinone and, as such, could increase the potential toxicity of this quinone.
This article was published in Arch Biochem Biophys
and referenced in Journal of Cancer Science & Therapy