Mutagenesis, Vol. 15, No. 1, 91-97,
January 2000
© 2000 UK Environmental Mutagen Society/Oxford University Press
Aflatoxin B1-induced mitotic recombination in L5178Y mouse lymphoma cells
Department of Oto-Rhinolaryngology and 1 Department of Toxicology, University of Würzburg, Versbacher Straße 9, 97078 Würzburg, Germany and 2 National Institutes of Health, Research Triangle Park, NC 27709, USA
Aflatoxin B1 is a human hepatocarcinogen. It is also a known point mutagen in bacteria and mammalian cells. This mutagenic activity may be at least partly responsible for its carcinogenic activity. However, recent studies show that aflatoxin B1 induces mitotic recombination in the yeast Saccharomyces cerevisiae. Because numerous reports have implicated mitotic recombination in mechanisms leading to carcinogenesis and because no one has shown that aflatoxin B1 induces recombination in mammalian cells, we decided to examine the ability of aflatoxin B1 to induce recombination in a mammalian cell line. We used a combination of methods, analysis for loss of heterozygosity and whole chromosome in situ hybridization, to identify mechanisms of chromosome mutation, including mitotic recombination in the mammalian L5178Y mouse lymphoma cell system. Our experiments revealed that mitotic recombination caused ~60% or more of the aflatoxin B1-induced mutagenic lesions in this cell system. Thus, mitotic recombination plays an important role in aflatoxin B1-induced mutagenesis in mammalian cells and possibly in chemically induced mutagenesis and carcinogenesis. This work suggests that multiple genetic lesions may be involved in aflatoxin B1-induced pathology.
3 To whom correspondence should be addressed. Tel: +1 919 541 2150; Fax: +1 919 541 2242; Email: caspary{at}niehs.nih.gov
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