Abstract

The mutagenic activity present in urine of animals treated with acrylonitrile (ACN) is tentatively related to the excretion of three urinary metabolites: thiocyanate (SCN-), hydroxyethylmercapturic acid (OH-MA), and cyanoethylmercapturic acid (CN-MA). It is shown that the route of administration and animal species affect SCN- excretion but not the excretion of hydroxyethyl- and cyanoethylmercapturic acids or the mutagenicity of urine from ACN-treated animals. Various pretreatments (phenobarbital, CoCl2, diethylmaleate, trichloroacetonitrile) decrease the mutagenicity of urine from ACN-treated animals and decrease the excretion of SCN- and OH-MA. None of the quantified urinary metabolites is responsible for urinary mutagenicity.

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