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Title: Benzo(a)pyrene dione-benzo(a)pyrene diol oxidation-reduction couples; involvement in DNA damage, cellular toxicity, and carcinogenesis

Journal Article · · J. Toxicol. Environ. Health; (United States)

Three isomeric quinone metabolites of the environmental carcinogen benzo(a)pyrene undergo reversible, univalent oxidation-reduction cycles involving the corresponding benzo(a)pyrene diols and intermediate semiquinone radicals. Under anaerobic conditions, benzo(a)pyrene 1,6-dione, benzo(a)pyrene 3,6-dione, and benzo(a)pyrene 6,12-dione are readily reduced by mild biological agents such as NADH and glutathione. The benzo(a)pyrene diols, in turn, are very rapidly autooxidized to diones when exposed to air. Substantial amounts of hydrogen peroxide are produced during these autooxidations. The benzo(a)pyrene diol/benzo(a)pyrene dione interconversions proceed by one-electron steps; the corresponding semiquinone radicals were detected as intermediates when the reactions were carried out at high pH. Benzo(a)pyrene diones are electron-acceptor substrates for NADHdehydrogenase. Catalytic amounts of these metabolites, together with this respiratory enzyme, function as cyclic oxidation-reduction couples to link NADH and molecular oxygen in the continuous production of hydrogen peroxide. Benzo(a)pyrene diones induce strand scissions when incubated with T7 DNA. The damage is modified by conditions that indicate that reduced oxygen species propagate the reactions responsible for strand scission. Benzo(a)pyrene diones are cytotoxic at low concentrations to cultured hamster cells. The cytotoxic effect can be substantially reduced by depletion of oxygen from the growth medium and the atmosphere in which the cells are incubated. The results support the hypothesis that the biological activity of benzo(a)pyrene diones is due to the regenerative oxidation-reduction cycles involving quinone and hydroquinone forms; activated oxygen species and semiquinone radicals formed during these cycles are most likely responsible for the observed cytotoxic action. The role of activated oxygen species in carcinogenesis is discussed.

Research Organization:
Johns Hopkins Univ., Baltimore, MD
OSTI ID:
5801658
Journal Information:
J. Toxicol. Environ. Health; (United States), Vol. 16:5
Country of Publication:
United States
Language:
English