The potential of X pa / and X pa / / p53 / mice for short-term carcinogenicity assays was evaluated with di(2-ethylhexyl)phthalate (DEHP). Groups of 15 male and female Xpa / mice, received diets containing 0, 1,500, 3,000, or 6,000 ppm DEHP, and wild-type (WT) and X pa / / p53 / mice 0 or 6,000 ppm DEHP for 39 weeks. X pa / , X pa / / p53 / , and WT males, fed 2,500 ppm p-cresidine, served as a positive control. In all models, the survival was not altered by DEHP. Increased incidences of nonneoplasti c lesions were recorded in testes and kidneys with no apparent difference between the models. The only liver tumors in all models were adenomas in males with no statistically signi cantly increased incidence. For p-cresidine, the survival was decreased ( p < 0.05) only in transgenic models. Statistically signi cantly increased incidences of nonneoplasti c lesions were recorded in the liver, urinary bladder, and nasal cavity in all models, and in kidneys in transgenic models. The only tumors with statistically signi cantly increased incidence were liver adenomas in transgenic models (XPA: 1 vs 7; 'XPA/p53': 0 vs 12; WT: 0 vs 5, p 0.053) and urinary bladder carcinomas in XPA/p53 model (0 vs 7). The negative carcinogeni c response to DEHP and the positive response to p-cresidine support the expected sensitivity to genotoxic carcinogens in these transgenic models.

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