These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Effect of ascorbate on the DT-diaphorase-mediated redox cycling of 2-methyl-1,4-naphthoquinone.
    Author: Jarabak R, Jarabak J.
    Journal: Arch Biochem Biophys; 1995 Apr 20; 318(2):418-23. PubMed ID: 7733672.
    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 1.6.99.2), 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.
    [Abstract] [Full Text] [Related] [New Search]