1,2-Dimethylhydrazine carcinogenesis in C3HA and CBA female mice prenatally treated with diethylstilbestrol.

C3HA and CBA female mice received a single intraperitoneal (i.p.) injection of 0.1 or 0.3 mg/kg body weight (b.w.) of diethylstilbestrol (DES) at day 17 of pregnancy. The descendants, starting from the age of 2-3 months, were receiving weekly subcutaneous (s.c.) injections of 1,2-dimethylhydrazine (DMH) (8 mg/kg b.w.), total 20 injections. The survival of C3HA mice treated with DMH together with prenatal DES was considerably better than in mice treated with DMH alone, this being due to the strong inhibiting effect of DES on the induction by DMH of the hemorrhagic ovarian lesions (78.4% in DMH alone vs. 53.3 and 43.7% in groups with DES plus DMH), which frequently were the cause of animal death. Prenatal DES also inhibited the induction by DMH of clitoral gland tumors: 51.4% in the group with DMH alone vs. 26.6 and 28.1% in two groups of DES plus DMH, respectively. DES treatment, at the above doses, did not influence significantly the DMH carcinogenesis in CBA mice. Prenatal DES given to CBA mice at the dose of 1 mg/kg b.w. significantly increased the incidence of DMH-induced uterine sarcomas (42.8% vs. 73.3% in the group with DMH alone and the group receiving DMH together with prenatal DES, respectively) and accelerated their growth. The effects of prenatal DES on DMH-induced carcinogenesis correlated with the degree of hyperestrogenization produced in both strains of mice by DES.