Nitroscanate (NSC) was found to be a direct acting mutagen in the Ames Salmonella tester strains TA100 and TA98 and this activity increased further in the presence of rat liver S9 mix. It was inactive in TA98NR and TA100NR, and weakly active in TA98/1,8-DNP6. A substantial fall in drug induced mutagenicity by pentachlorophenol, an inhibitor of acetyltransferase, in TA98, TA100 and YG1024 suggests the initial bioconversion of a nitro group to hydroxylamine and its further activation to the ultimate N-acetoxyarylamine. The refrigerated DMSO solution of the drug in the plate incorporation assay and freshly prepared solutions using the pre-incubation procedure indicated a fall in mutagenicity owing to the conversion of NSC to N,N'-bis-4-(p-nitrophenoxy)phenyl thiourea (NFPT). The drastic reduction in mutagenicity in the presence of 4-amino-4'-nitrodiphenyl ether (ANDE) and 4-aminodiphenyl ether (ADE) was also attributed to the conversion of NSC to the corresponding thiourea, a non-mutagen. The negligible mutagenicity of ANDE and its absence in ADE and 4-isothiocyanate diphenyl ether (ITDE) suggests that the mutagenicity of NSC is due to the nitro group, and the -NCS function is responsible for enhanced mutagenicity over nor-isothiocyanate 4-nitrodiphenyl ether (NDE).
