Impaired prepubertal uterine responsivity after neonatal exposure to steroid hormone esters.

Injection of neonatal rats on day 3 after birth with a single dose of 5 microgram or 100 microgram estradiol benzoate (EB) or 30 microgram or 1,250 microgram testosterone propionate (TP) drastically impairs the development of uterine growth response to exogenous estradiol on day 21 of life. Reduction of uterine responsivity was augmented by EB treatment compared to TP treatment. This may be explained by an apparent reduction in available cytoplasmic estrogen binding sites in the uterus with a concomitant decrease in nuclear retention of the receptor-estrogen complex which was in addition to the effect upon estrogen-stimulated metabolic activity (glucose oxidation) resultant from either TP or EB exposure. The degree of reduced uterine responsivity at 21 days of age directly corresponds to the degree of reduction in the ovarian weights observed in the neonatally treated rats. Neonatal ovariectomy on day 3 of life also produced a uterine response syndrome characteristic of neonatal estrogenization. Thus, it is suggested that endogenous estrogen secretion during infancy may be important in end organ conditioning in the development of a functionally competent uterus.