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Estradiol Inhibition of Luteinizing Hormone-Stimulated Progesterone Synthesis in Isolated Bovine Luteal Cells^*

MARVIN T. WILLIAMS and JOHN M. MARSHf

Department of Biochemistry, The Endocrine Laboratory, University of Miami School of Medicine Miami, Florida 33152

Abstract

The effects of several steroid hormones on progesterone synthesis and cAMP accumulation in isolated bovine corpora luteal cells were investigated in an attempt to determine if any of the steroids would affect the basal level of these processes or their response to gohadotropin. Isolated bovine corpora luteal cells responded to LH with a significant (P < 0.05) increase in progesterone synthesis and cAMP accumulation when incubated at 37 C for up to 1 h. Exogenous cAMP and analogs of cAMP also significantly stimulated steroidogenesis in these incubated cells. Stimulation of progesterone synthesis by 1 µg/ml LH was significantly suppressed (P < 0.05) in the presence of 5–10 µg/ml estradiol. This inhibition appeared to be largely specific for 17β-estradiol, in that other steroids such as estrone, estriol, 17-estradiol, cortisol, and dihydrotestosterone were not inhibitory. Testosterone was found to be inhibitory, but it is uncertain if this effect was due to the androgen itself or to its conversion to estradiol. Estradiol did not affect the increase in endogenous cAMP caused by LH in these cells, but did inhibit the effect of exogenous dibutyryl cAMP on progesterone synthesis. The magnitude of this inhibition of the effect of dibutyryl cAMP was not, however, equal to the estradiol inhibition of the stimulation of progesterone synthesis by LH.

These data indicate that estradiol, a possible physiological luteolytic agent, has a direct inhibitory action on the corpus luteum and produces its suppression by blocking the stimulatory effect of LH at a step after cAMP.

Footnotes

^* This work was supported in part by grants from NIH (HD-03248 and HD-08747) and the Ford Foundation (0338).

To whom reprint requests should be addressed.

Received November 2, 1977.