Investigations into the formation of mutagens were carried out on cooked meat and significant mutagenic activity was detected, using the Ames test, in extracts of the cooked outer layer. This mutagenic activity appeared to be associated with amino-imidazo azaarenes (AIAs) since, after HPLC, only the subfractions co-eluting with 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline (MelQx), 2-amino-3-methylimidazo (4,5-f) quinoline (IQ) and 2-amino-3,4-dimethylimidazo (4,5-f) quinoline (MelQ) were found to be mutagenic. The formation of mutagens appeared to be reduced when additives/ingredients were incorporated into the food. The bioactivation of IQ, MelQ and MelQx to mutagens by rat hepatic preparations was preferentially catalysed by the 3-methylcholanthrene-induced cytochromes P-448, and this microsome-mediated mutagenicity was potentiated by the cytosol. Differences in the activation of IQ to mutagens between hepatic 59 preparations derived from Aroclor-pretreated Sprague-Dawley and Wistar rats were attributed to differences both in microsomal activation and cytosolic potentiation. Tryptamine inhibited the bioactivation to mutagens of IQ, MelQx and, to a lesser extent, MelQ by S9 preparations derived from Wistar rats pretreated with Aroclor 1234. This inhibitory effect was much weaker, for IQ and MelQx in S9 preparations derived from similarly pretreated Sprague-Dawley rats, whereas the bioactivation of MelQ was enhanced by tryptamine. It was concluded that there are at least two different pathways of microsomal metabolism of the AIAs, one of which is inhibited by tryptamine, the other pathway is tryptamine-insensitive.