Dehydroepiandrosterone (DHA) induced precocious ovulation: Correlative changes in blood steroids, gonadotropins and cytosol estradiol receptors of anterior pituitary gland and hypothalamus

Abstract

The administration of dehydroepiandrosterone (DHA) to immature female rats results in a precocious ovulation followed by ovulatory failure. Earlier studies suggested that the peripheral conversion of DHA to estrogens may be involved in the induction of precocious ovulation. This study demonstrates a significant elevation in serum levels of DHA, androstenedione, testosterone, 5α-dihydrotestosterone (DHT), and estradiol within 2 h of DHA administration. That these changes were due to conversion of administered DHA and not due to secretion of endogenous steroids was suggested by no initial changes in the C-21 precursors such as 17 hydroxyprogesterone and progesterone. Furthermore, serum estradiol levels dropped dramatically after DHA withdrawal. The series of events leading to precocious ovulation, namely the rise in blood estradiol, the depletion of cytoplasmic estradiol receptors of the anterior pituitary gland and the hypothalamus, followed by the preovulatory surge of gonadotropins leading to ovulation, are similar to those found in pregnant mare serum gonadotropin (PMSG) induced precocious ovulation, the onset of natural puberty, and during ovulation in the adult cycling rat.