title: Mechanisms of induction of chromosomal aberrations by hydroquinone in V79 cells.
abstract: Hydroquinone occurs naturally in bacteria and plants and it is also manufactured for commercial use. Human exposure to this compound can occur by environmental, occupational, dietary and cigarette smoke exposure and from exposure to benzene, which can be metabolized to this compound. However, the main source of exposure to this compound is dietary, since hydroquinone is a naturally occurring compound in many foods. Hydroquinone can be metabolized to benzoquinones, which are potent haematotoxic, genotoxic and carcinogenic compounds that can also induce the formation of radical species, predisposing cells to oxidative damage. In order to clarify the involvement of radical species in the genotoxicity of hydroquinone, the induction of chromosomal aberrations in V79 cells was studied along with the assessment of the production of hydroxyl radicals at different pH values (6.0, 7.4 and 8.0), as well as the effect of antioxidant enzymes [catalase and superoxide dismutase (SOD)] on the clastogenic effect of hydroquinone. The results obtained indicate that the clastogenic activity of hydroquinone is dependent on the pH, suggesting that deprotonation is a fundamental step leading to DNA lesions under the experimental conditions used. The addition of S9 mix, SOD or SOD and catalase significantly decreased the clastogenic activity, suggesting the involvement of superoxide anion and hydrogen peroxide in the genotoxicity of hydroquinone. However, other species generated in the auto-oxidation process of hydroquinone, such as the semiquinone radical or the quinone, also seem to play a role in its genotoxicity, since the addition of antioxidant enzymes (catalase and SOD) or S9 mix do not lead to a complete abolition of the observed genotoxic activity. These results suggest the existence of at least two mechanisms associated with the genotoxic activity of this compound.
authors: Department of Genetics, Faculty of Medical Sciences, New University of Lisbon, Rua da Junqueira 96, 1349-008 Lisboa, Portugal.
authors: Maria
authors: M
authors: do Céu Silva
authors: Jorge
authors: J
authors: Gaspar
authors: Isabel
authors: I
authors: Duarte Silva
authors: Daniela
authors: D
authors: Leão
authors: José
authors: J
authors: Rueff
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D016227:Benzoquinones / Q000378:metabolism*; D002374:Catalase / Q000494:pharmacology; D002869:Chromosome Aberrations / Q000187:drug effects*; D004249:DNA Damage; D006861:Hydrogen Peroxide / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D006873:Hydroquinones / Q000633:toxicity*; D017665:Hydroxyl Radical / Q000378:metabolism*; D008297:Male; D009152:Mutagenicity Tests; D009153:Mutagens / Q000633:toxicity*; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism
chemical_list: D000975:Antioxidants; D016227:Benzoquinones; D006873:Hydroquinones; D009153:Mutagens; D013481:Superoxides; C025232:semiquinone radicals; D017665:Hydroxyl Radical; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; C031927:hydroquinone