Mutagenicity of cyanate, a decomposition product of MNU.
Knox reported that the short-term effects of the carcinogen methylnitrosourea (MNU) were due to the formation of its decomposition product, the cyanate ion. He showed that cell survival and DNA synthesis decreased as the concentration of MNU and the cyanate ion (NCO-) increased in the medium. Further, the product of MNU decomposition comigrated with NCO- when added to his chromatographic test system. However, Knox did not study the mutagenicity of MNU or its breakdown products. We compared the mutagenicity of MNU and potassium cyanate (KNCO) in mammalian cells. Our results demonstrate that, although it is toxic to cells, KNCO does not induce ouabain-resistant mutants in cultured Chinese hamster cells (V79).
D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D006224:Cricetinae; D003412:Cricetulus; D003485:Cyanates / Q000096:biosynthesis / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts / Q000187:drug effects; D008168:Lung; D008770:Methylnitrosourea / Q000378:metabolism*; D009152:Mutagenicity Tests; D009153:Mutagens / Q000494:pharmacology; D009607:Nitrosourea Compounds / Q000378:metabolism*
D003485:Cyanates; D009153:Mutagens; D009607:Nitrosourea Compounds; D008770:Methylnitrosourea; C024835:potassium cyanate