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A strong teratogen-6-aminonicotinamide (6-AN)-was tested for its ability to induce cytotoxicity and mutagenicity in Chinese hamster ovary (CHO) cells. Tests were performed in the presence and absence of a metabolic activation system (S-9 mix). Cytotoxicity was evaluated in CHO cells by the total protein content. The two single-gene mutation systems in CHO cells have been investigated. Both involve evaluating the response of the hypoxanthine-guanine phosphoribosyl transferase (HGPRT) locus and specific inhibitors of the cellular (Na2+K+)-ATPase using 6-thioguanine and ouabain as selective agents, respectively. From our results, 6-AN showed a higher cytotoxic effect at concentrations over 1 x 10(-1) mg/ml. Cytotoxicity was significantly different with and without S-9 mix. 6-AN was cytotoxic per se, however, when 6-AN was biotransformed, in the presence of S-9 mix no biological activity (cytotoxic) was detected. Non-significant mutagenic activity was detected with 6-AN in the presence and in the absence of the metabolic activation system.

A strong teratogen—6‐aminonicotinamide (6‐AN)—was tested for its ability to induce cytotoxicity and mutagenicity in Chinese hamster ovary (CHO) cells. Tests were performed in the presence and absence of a metabolic activation system (S‐9 mix). Cytotoxicity was evaluated in CHO cells by the total protein content. The two single‐gene mutation systems in CHO cells have been investigated. Both involve evaluating the response of the hypoxanthine‐guanine phosphoribosyl transferase (HGPRT) locus and specific inhibitors of the cellular (Na+ + K+)‐ATPase using 6‐thioguanine and ouabain as selective agents, respectively. From our results, 6‐AN showed a higher cytotoxic effect at concentrations over 1 × 10−1 mg/ml. Cytotoxicity was significantly different with and without S‐9 mix. 6‐AN was cytotoxic per se, however, when 6‐AN was biotransformed, in the presence of S‐9 mix no biological activity (cytotoxic) was detected. Non‐significant mutagenic activity was detected with 6‐AN in the presence and in the absence of the metabolic activation system. © 1996 Wiley‐Liss, Inc.