The mutagenicity of flavonols seems to depend on the number and position of hydroxyl groups in the B ring. Galangin is a flavonol that does not have any hydroxyl group in the B ring and has been suggested to be a substrate of cytochromes P450 which, through the hydroxylation of the B ring, could metabolise it to more genotoxic products. The present study was undertaken to test this hypothesis. Using high performance liquid chromatography we show that glangin is sequentially transformed to kaempferol and then to quercetin by a mechanism dependent on cytochrome P450 reactions. The metabolites of galangin are responsible for its mutagenicity in Salmonella typhimurium reversion assay and for the induction of chromosomal aberrations in V79 cells.