Inhibition of Aminoimidazoquinoxalinc‐type and Aminoimidazol‐4‐one‐type Mutagen Formation in Liquid Reflux Models by l‐Tryptophan and Other Selected Indoles

The essential amino acid l‐tryptophan (l‐Trp) was found to be an effective inhibitor of the development of mutagenicity (Ames test) in liquid‐reflux models known to produce identified IQ‐type mutagens, such as 2‐amino‐3,8‐dimethylimidazo[4,5‐f]quinoxaline (MeIQ(x)) and 2‐amino‐3,7,8‐trimethylimidazo[4,5‐f]qninoxaline (7,8‐DiMeIQ(x)), and in reflux models recently developed in our laboratory that have been found to produce novel IQ‐“like” mutagens (aminoimidazol‐4‐ones), which we have identified as 2‐amino‐1‐methyl‐5‐propylideneimidazol‐4‐one (TCP‐1), and 2‐amino‐5‐ethylidene‐1‐methylimidazol‐4‐one (TCP‐2 or ACP). Selected indoles other than l‐Trp were also found to be effective inhibitors of mutagen formation in these same reflux models. A mechanism of inhibition of mutagen formation based on the preferential reaction of mutagen precursor aldehydes with the indole‐ring nitrogen of these inhibitors, rather than with creatinine, is indicated, and a new “concerted condensation model” for the formation of IQ‐type mutagens proposed.