Journal Article

Mutational specificity of aflatoxin B1. Comparison of <i>in vivo</i> host-mediated assay with <i>in vitro</i> S9 metabolic activation

María-José Prieto-Alamo, Juan Jurado, Nieves Abril, Cecilia Díaz-Pohl, George Bolesfoldi and Pueyo Carmen

in Carcinogenesis

Volume 17, issue 9, pages 1997-2002
Published in print September 1996 | ISSN: 0143-3334
Published online September 1996 | e-ISSN: 1460-2180 | DOI:
Mutational specificity of aflatoxin B1. Comparison of in
                        vivo host-mediated assay with in vitro S9
                    metabolic activation

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An intrasanguineous host-mediated assay was used to determine the pattern of mutagenesis induced by the carcinogen aflatoxin Bl in the lacl gene of Escherichia coli recovered from rat liver. To investigate the influence of different types of metabolic activation, the mutation spectrum induced by AFB1 activated in vitro by a commercially prepared S9 microsomal fraction from Aroclor 1254-treated rats was also obtained. A total of 281 forward mutations affecting the N-terminal region of the lacl gene were characterized by DNA sequencing analysis. AFB1 induced similar type of mutations with similar site specificity when activated by the standard S9 fraction or by employing a rat host-mediated assay. These results indicate the ability of the in vitro S9 fraction to mimic the in vivo metabolism, suggesting that the same active metabolite, presumably AFB1 8, 9-epoxide, is responsible for generating a similar pattern of DNA damage, as reflected in the similarity of mutational spectra. For both activation systems, most mutations (>90%) were base substitutions that occurred primarily at G: C pairs. Somewhat over one-half of G: C targeted substitutions were GC>TA transversions, other mutations being evenly divided between G: C>AT transitions and GC>CG trans-versions. The mutational specificity exhibited by activated AFB1 can be explained by incorporation of different bases opposite a single type of non-instructive lesion during error-prone DNA synthesis. To what extent the mutations are due to the main adduct (AFB1-N7-Gua), its imidazole-ring-opened derivative or an apurinic site remains unknown.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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