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Mutagenesis vol. 13 no. 6 pp. 625-630, 1998
© 1998 UK Environmental Mutagen Society/Oxford University Press

research-article

Specific mutational spectrum of dimethylnitrosamine in the lacI transgene of Big Blue® C57BL/6 mice

Xue Wang1, Takayoshi Suzuki1, Toshiaki Itoh1, Masamitsu Honma1, Akiyoshi Nishikawa2, Fumio Furukawa2, Michihito Takahashi2, Makoto Hayashi1,4, Takeshi Kato3 and Toshio Sofuni1

1Division of Genetics and Mutagenesis, National Institute of Health Sciences 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158 2Division of Pathology, National Institute of Health Sciences 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158 3Radiation Biology Center, Kyoto University Yoshidakonoe-cho, Sakyo-ku, Kyoto-shi, Kyoto 606, Japan

Dimethylnitrosamine (DMN) produces tumors in mice predominantly in the liver, but also in the kidney and lung. It forms O6-methylguanine adducts in DNA, which induce G:C->A:T transitions. We have analyzed the spectra of spontaneous and DMN-induced mutations in the lad transgene of the Big Blue® mouse (C57BL/6). In both cases, mutations in the liver, kidney and lung were predominantly base substitutions, among which G:C->A:T transitions were the most frequent. In contrast, a high incidence of short deletions (2–23 bp) was only found in the liver of treated mice. The deletions often occurred at direct repeat sequences. Single-base deletion incidence was also higher in the liver than in the kidney and lung. These results imply that accumulation of DNA lesions or their repair in liver is different from other organs. Spontaneous and induced base substitutions and deletions appeared to be randomly distributed in the lacI gene and an apparent hotspot was not observed, except for a 4 bp deletion of a (TGGC)3 sequence at positions 621–632. The present data demonstrate, for the first time, that DMN induces short deletions especially in the liver, although the mechanism involved needs further investigation.

4To whom correspondence should be addressed. Tel: +81 3 3700 9872; Fax: +81 3 3700 2348; Email: hayashi{at}nihs.go.jp


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