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British Journal of Cancer logoLink to British Journal of Cancer
. 1973 Dec;28(6):544–551. doi: 10.1038/bjc.1973.184

Induction of Mutations in DNA-repair Deficient Bacteria by a Liver Microsomal Metabolite of Aflatoxin B1

R C Garner, C M Wright
PMCID: PMC2008936  PMID: 4593223

Abstract

Certain strains of Salmonella typhimurium and Escherichia coli, particularly those which are very sensitive to u.v. light, are killed when incubated with rat liver mixed function oxidases and aflatoxin B1. UvrA or recA strains of E. coli are more susceptible than the wild-type strain, while the double mutant uvrA recA is the most sensitive strain yet tested. The aflatoxin B1 metabolite is also able to induce reverse mutations in 2 histidine auxotrophic strains of S. typhimurium, one strain of which is reverted specifically by frame shift mutagens and the other by agents inducing base pair substitutions.

Pretreatment of rats with either 3-methylcholanthrene or benzo(a)pyrene, both inducers of liver microsomal mixed function oxidases, did not alter the amount of lethal aflatoxin B1 metabolite formed, whereas an increase was observed after phenobarbitone pretreatment. Addition of the nucleophiles methionine, cysteine, glutathione, sodium thiosulphate or sodium sulphide, or the epoxide hydrase inhibitor, cyclohexene oxide to the toxicity assay medium did not alter bacterial killing by the aflatoxin B1 metabolite. 2,3-Dimercaptopropanol had some protective action.

Toxic metabolites were also formed when 5-methoxysterigmatocystin, O-methylsterigmatocystin, parasiticol or versicolorin A, but not vericolorin B, were incubated with mixed function oxidases. The relationship between the metabolite of aflatoxin B1 lethal to bacteria and that which initiates liver cancer is discussed.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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