Myricetin is a flavonol that is widely distributed in edible plants and although it has been proved to be genotoxic in bacteria and to induce significant concentration-dependent nuclear DNA degradation concurrent with lipid peroxidation, very little is known about its mechanisms of genotoxicity. In this work we tried to evaluate the role of rat cytochromes P450 in the genotoxicity of myricetin and to study the role that radicalar species may have in its mutagenicity. The results obtained show that the genotoxicity of myricetin as assessed by the induction of chromosomal aberrations is not different in V79 cells lines genetically engineered for the expression of rat cytochromes P450 1A1, 1A2, and 2B1, compared to parental cell lines. We have also been able to show that reactive oxygen species resulting from the autooxidation of myricetin at pH values above neutrality have an important role in its mutagenicity. Therefore, under some conditions, myricetin can act as a prooxidant.