Salmonella mutagenicity of musk ambrette depends on both microsomal and bacterial enzyme activity.
Former studies revealed musk ambrette as a mutagen in Salmonella typhimurium TA 100 in the presence (+S9) but not in the absence (-S9) of an exogenous metabolizing system. To clarify the role of bacterial nitroreductases (NR) in the toxification of musk ambrette to mutagenic metabolites the compound was examined with the Salmonella/mammalian microsome assay using the NR deficient strain S.typhimurium TA 100 NR in the presence and absence of S9. Musk ambrette showed mutagenicity in Salmonella typhimurium TA 100 (+S9) but no mutagenicity in the NR deficient strain TA 100 NR (+S9). Additionally, no mutagenicity was detected in both TA 100 (-S9) and TA 100 NR (-S9). These results indicate the need for both mammalian microsomal enzymes and bacterial nitroreductases to cause the mutagenicity of musk ambrette.
Mersch-Sundermann
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Institute of Medical Microbiology and Hygiene, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany.
Emig
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M
D004136:Dinitrobenzenes / Q000378:metabolism / Q000633:toxicity*; D008862:Microsomes, Liver / Q000378:metabolism*; D009153:Mutagens / Q000633:toxicity*; D009601:Nitroreductases / Q000502:physiology*; D012486:Salmonella typhimurium / Q000201:enzymology*
D004136:Dinitrobenzenes; D009153:Mutagens; C020422:musk ambrette (artificial); D009601:Nitroreductases