Induction and mutagenesis of prophage lambda in Escherichia coli K12 by metabolites of aflatoxin B1.
Like most carcinogens, aflatoxin B1 must be activated by mammalian microsomal enzymes to give rise to coupounds active on bacteria. These compounds act as inducers of E. coli K12 (lambda) at a high efficiency, whereas unmodified aflatoxin B1 has no effect. Moreover, metabolites of aflatoxin B1 have a mutagenic action on phage lambda, as shown by the appearance of clear plaque mutants. We propose the hypothesis that the same derivative is responsible for carcinogenesis of liver cells by aflatoxin B1. Therefore, our system provides a simple way of measuring in vitro, in the same assay, the mutagenic and inducing activities of compounds to which the cells are permeable, thereby detecting potentially carcinogenic agents.
D000348:Aflatoxins / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D002273:Carcinogens / Q000302:isolation & purification / Q000494:pharmacology; D002463:Cell Membrane Permeability; D003090:Coliphages / Q000187:drug effects*; D004926:Escherichia coli; D008110:Liver Extracts; D008242:Lysogeny; D008297:Male; D008930:Mitochondria, Liver; D009153:Mutagens / Q000494:pharmacology; D009154:Mutation; D051381:Rats
D000348:Aflatoxins; D002273:Carcinogens; D008110:Liver Extracts; D009153:Mutagens