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[Cancer Research 43, 1054-1058, March 1, 1983]
© 1983 American Association for Cancer Research

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Mutation of Chinese Hamster V79 Cells and Transformation and Mutation of Mouse Fibroblast C3H/10T1/2 Clone 8 Cells by Aflatoxin B1 and Four Other Furocoumarins Isolated from Two Nigerian Medicinal Plants

Anthony O. Uwaifo1, Paul C. Billings2 and Charles Heidelberger3

University of Southern California Cancer Research Laboratories, Los Angeles, California 90033

Mutation by aflatoxin B1 (AFB1), imperatorin, marmesin, chalepin, and 8-methoxypsoralen (MOP), with and without black light (BL; long-wavelength ultraviolet light) activation, was determined at the hypoxanthine-guanine phosphoribosyltransferase locus (8-azaguanine resistance) in Chinese hamster V79 cells and at the ouabain locus in mouse C3H/10T1/2 cells. Transformation by these furocoumarins under the same activation conditions was also investigated in C3H/10T1/2 cells. In V79 cells, AFB1 induced a 4-fold maximum mutation frequency over controls under BL activation at a concentration of 5 µg/ml; marmesin induced a 2-fold increased mutation frequency at 1.5 µg/ml; MOP induced a 19-fold increase at 10 µg/ml; chalepin induced a 3-fold increase at 5 µg/ml; and imperatorin induced a 20-fold increase at 10 µg/ml. Essentially no mutation was observed at the ouabain-resistant (Ouar) locus in C3H/10T1/2 cells with any of these compounds. In the transformation assays, type II and type III foci were observed at a 1-µg/ml addition of AFB1 with or without BL activation; while with MOP and imperatorin, these types of foci were observed only with BL activation. Marmesin, although relatively more cytotoxic than the other furocoumarins studied, with a 50% lethal dose of less than 0.5 µg/ml, was not as mutagenic or potentially carcinogenic as were AFB1, imperatorin, or MOP with BL activation. These furocoumarins are considered to be involved in the etiology of the high incidence of skin cancer in Nigeria. Our experiments reinforce that concept and suggest that exposure to these furocoumarins may constitute a real carcinogenic hazard.

1 Fellow of the International Agency for Research on Cancer, Lyon, France. Present address: Department of Biochemistry, University of Ibadan, Ibadan, Nigeria.

2 Supported by a Fellowship from Training Grant 1-T32-CA-09320 from the National Cancer Institute, NIH.

3 To whom requests for reprints should be addressed.

Received 7/ 2/82. Accepted 11/23/82.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1983 by the American Association for Cancer Research.