Frameshift mutagenesis by chloroquine in Escherichia coli and Salmonella typhimurium.
Chloroquine can be detected as a direct-acting mutagen in plate-incorporation assays using the excision-deficient Salmonella typhimurium strain TA97, but very much more effectively using the repair-proficient Escherichia coli strain DG1669 which carries the lacZ19124 marker. When tested at concentrations of 200-1000 micrograms/plate with strain DG1669, the mutagenicity of chloroquine is enhanced by the addition of Aroclor-induced rat-liver S9. Further experiments indicated that chloroquine-induced reversion frequencies were essentially identical in wild-type, recA, umuC and uvrC derivatives of DG1669, as well as in strains carrying the mutation enhancing plasmid pKM101, over a wide range of doses (0-1200 micrograms/plate). These results suggest that neither excision repair nor SOS-type repair are important in chloroquine-induced frameshift mutagenesis.
D000818:Animals; D002738:Chloroquine / Q000493:pharmacokinetics / Q000633:toxicity*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D008110:Liver Extracts / Q000378:metabolism; D009152:Mutagenicity Tests; D009153:Mutagens / Q000493:pharmacokinetics; D009154:Mutation; D051381:Rats; D012486:Salmonella typhimurium / Q000187:drug effects / Q000235:genetics*
D008110:Liver Extracts; D009153:Mutagens; D002738:Chloroquine