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Toxicologic Pathology
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Articles

Susceptibilities of p53 Knockout and rasH2 Transgenic Mice to Urethane-Induced Lung Carcinogenesis are Inherited from their Original Strains

Masakazu Ozaki1,2, Keisuke Ozaki2, Tomoyuki Watanabe2, Satoshi Uwagawa2, Yasuyoshi Okuno2 and Tomoyuki Shirai1

1 Department of Experimental Pathology and Tumor Biology, Nagoya City University, Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan
2 Environmental Health Science Laboratories, Sumitomo Chemical Co. Ltd., Konohana-ku, Osaka, 554-8558, Japan

Correspondence: Address correspondence to: Masakazu Ozaki, Environmental Health Science Laboratories, Sumitomo Chemical Co. Ltd., 3-1-98, Kasugade-naka, Konohana-ku, Osaka, 554-8558, Japan; e-mail:ozakim{at}sc.sumitomo-chem.co.jp

In the present study, susceptibility of CB6F1 mice carrying the human prototype c-Ha-ras gene (rasH2 mice) and p53 gene knockout mice (p53 (+/–) mice) to urethane-induced lung carcinogenesis was compared under the same experimental conditions. Both strains were administered 500 ppm urethane in their drinking water for 3 weeks. At week 26, lung adenocarcinomas and adenomas were observed in 53% and 100% of rasH2 mice, respectively, and lung adenomas were observed in 67% of rasH2 littermate (non-Tg) mice. However, lung tumors were not observed in either p53 (+/–) or p53 (+/+) mice. Peliosis hepatis and hepatic hemangiomas were observed in 27% and 67% of p53 (+/–) mice, but only in 6.7% and 6.7% of the rasH2 animals, respectively. Under the same experimental conditions, BALB/c mice, the strain of origin of the rasH2 mice, developed lung adenomas at an incidence of 93%, whereas none of the C57BL/6 original strain for p53 (+/–) mice developed lung tumors. Peliosis hepatis was observed in 40% of the C57BL/6 mice, but not in BALB/c mice; hepatic and splenic hemangiomas were not observed in these animals. These results indicate that organ susceptibility of rasH2 and p53 (+/–) mice is inherited from their strains of origin, the rasH2 and BALB/c lines being much more sensitive to the induction of pulmonary carcinogenesis.

Key Words: RasH2 transgenic mice • p53 knockout mice • urethane • lung carcinogenesis • original strain mice

Toxicologic Pathology, Vol. 33, No. 2, 267-271 (2005)
DOI: 10.1080/01926230590908231
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