Genotoxicity of 1,4-benzoquinone and 1,4-naphthoquinone in relation to effects on glutathione and NAD(P)H levels in V79 cells.

摘要: 1,4-Benzoquinone is cytotoxic in V79 Chinese hamster cells and induces gene mutations micronuclei. The cell-damaging effects of quinones are usually attributed to thiol depletion, oxidation NAD(P)H, redox-cycling involving the formation semiquinone radicals reactive oxygen species. To elucidate role these mechanisms genotoxicity 1,4-benzoquinone, we measured various genotoxic effects, cytotoxicity, levels glutathione, NADPH, NADH, their oxidized forms all same experiment. 1,4-Naphthoquinone, which does not induce cells, was investigated for comparative reasons. had a similar effect on cofactors. Total glutathione depleted, but were slightly increased. NADPH NADH reduced at high concentrations with simultaneous increase NADP+ NAD+. Both compounds induced micronuclei, neither increased frequency sister chromatid exchange. Only 1,4-benzoquinone mutations. This observed low concentrations, where none other parameters studied affected. When depleted prior treatment quinones, induction micronuclei remained virtually unchanged. We conclude that a) depletion by two linked causally, b) mechanism different from oxidative stress c) fully protect against quinones.