Tong S, Smith J, Manson D, Gorrod J W, Ioannides C
Anticancer Res. 1986 Sep-Oct;6(5):1107-12.
The mutagenicity of 2-naphthylamine and its major metabolites in the Ames test was determined in the absence and presence of activation systems derived from rats and hamsters. In the absence of an activation system only N-hydroxy-2-naphthylamine and 2-nitrosonaphthalene were mutagenic. In the presence of activation systems derived from control and 3-methylcholanthrene-treated hamsters and Arochlor 1254-treated rats only 2-naphthylamine exhibited a mutagenic response while its hydroxy-derivatives and 2-acetamidonaphthalene were devoid of mutagenicity. Pretreatment of rats with 3-methylcholanthrene or Arochlor 1254 enhanced the mutagenicity of 2-naphthylamine while treatments with phenobarbitone, safrole and clofibrate had no significant effect. In the hamster treatment with only 3-methylcholanthrene increased the mutagenicity of 2-naphthylamine. It is concluded that the metabolic activation of 2-naphthylamine proceeds via N-hydroxylation which is preferentially catalysed by the 3-methylcholanthrene inducible forms of cytochrome P-450, whereas ring-hydroxylation appears to be a deactivation pathway.
