Metabolism and mutagenicity of acrylonitrile: an in vivo study.
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.
D000181:Acrylonitrile / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D001711:Biotransformation; D008297:Male; D006899:Mixed Function Oxygenases / Q000378:metabolism; D009152:Mutagenicity Tests; D009153:Mutagens / Q000652:urine*; D009570:Nitriles / Q000633:toxicity*; D051381:Rats; D012486:Salmonella typhimurium / Q000187:drug effects
D009153:Mutagens; D009570:Nitriles; D006899:Mixed Function Oxygenases; D000181:Acrylonitrile