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.) inje ction of 0.1 or 0.3 mg/kg body weight (b.w.) of diethylstilbestrol (DE S) 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 surv ival of C3HA mice treated with DMH together with prenatal DES was cons iderably 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 he morrhagic ovarian lesions (78.4% in DMH alone vs. 53.3 and 43.7% in gr oups with DES plus DMH), which frequently were the cause of animal dea th. 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 g roups of DES plus DMH, respectively. DES treat ment, at the above dose s, 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. significan tly increased the incidence of DMH-induced uterine sarcomas (42.8% vs. 73.3% in the group with DMH alone and the group receiving DMH togethe r with prenatal DES, respectively) and accelerated their growth. The e ffects of prenatal DES on DMH-induced carcinogenesis correlated with t he degree of hyperestrogenization produced in both strains of mice by DES. (C) 1997 Wiley-Liss, Inc.