This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Billings, P. C. Articles by Heidelberger, C. Search for Related Content PubMed PubMed Citation Articles by Billings, P. C. Articles by Heidelberger, C.

Influence of Benzoflavone on Aflatoxin B₁-induced Cytotoxicity, Mutation, and Transformation of C3H/10T Cells^1,2,

University of Southern California, Comprehensive Cancer Center Research Laboratory, Los Angeles, California 90033

Aflatoxin B₁ (AFLB₁), a metabolite of the fungus Aspergillus flavus, is hepatotoxic and hepatocarcinogenic in several animal species and is thought to play an etiological role in human liver cancer. C3H/10T clone 8 mouse embryo fibroblasts are killed, mutated, and morphologically transformed byAFLB₁. 7,8-Benzoflavone, a known inhibitor of aryl hydrocarbon hydroxylase, inhibits this enzymatic activity in C3H/10T cells. Furthermore, benzoflavone inhibits the binding of AFLB₁ to the DNA of C3H/10T cells. Benzoflavone also inhibits AFLB₁-induced cytotoxicity and mutation of C3H/10T cells, as well as inhibiting the activation of AFLB₁ into mutagenic metabolites capable of reverting the Ames Salmonella tester strain TA98. Interestingly, benzoflavone had no effect on the oncogenic transformation of these cells by AFLB₁. Therefore, benzoflavone inhibits the DNA binding, cytotoxic, and mutagenic effects of AFLB₁ but does not reduce the morphological transformation of C3H/10T cells by this mycotoxin.

¹ This paper is dedicated to Dr. Charles Heidelberger.

² This work was supported by a grant from the R. J. Reynolds Corporation and by an Occupational and Environmental Health Grant from the Dupont Corporation.

³ Supported by a fellowship from Training Grant 1-T32-CA-09320 from the National Cancer Institute, NIH. To whom requests for reprints should be addressed, at University of Southern California, Comprehensive Cancer Center Research Laboratory, 1303 N. Mission Rd., Los Angeles, Calif. 90033.

⁴ Supported by a Fellowship from the International Agency for Research on Cancer, Lyon, France. Current address: Department of Biochemistry, University of Ibadan, Ibadan, Nigeria.

Received 11/ 1/82. Accepted 3/10/83.