Summary The mutagenicity of dimethyl, diethyl, di- n -propyl, di- n -butyl, methyl- n -butyl, morpholine, piperidine, methylphenyl, ethyl- t -butyl and diphenyl nitrosamines was investigated using a mammalian metabolic activation system. Reverse mutation from streptomycin dependence to non-dependence in strain Sd-B(TC) of Escheyichia coli was used as the marker for mutagenicity. With this assay system the mutagenicity of metabolic breakdown products was determined by incubating the compounds with a rat liver preparation in the presence of bacterial cells. Reverse mutation was induced by all carcinogenic compounds tested, except methylphenylnitrosamine, whereas two non-carcinogenic compounds, ethyl- t -butyl nitrosamine and diphenyl nitrosamine did not give a significant increase in the rever sion frequency. The frequency of mutants induced by the compounds was decreased markedly by preincubation of the compounds with the liver preparation and the cofactor system prior to the addition of bacterial cells.
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