Abstract

To analyse the mechanism for the earlier reported decline in estrogen synthesis by the periovulatory rat follicle, prepubertal rats injected with 8 IU PMS on day 28 were killed following the endogenous gonadotrophin surge (15.00–18.00) on day 30. Isolated preovulatory follicles were incubated for 2 h in a chemically defined medium. Steroids were measured by specific RIA methods. Follicles exposed in vivo to the gonadotrophin surge and extirpated 19.00–22.00 h on day 30 secreted significantly lower amounts of androstenedione, testosterone and estradiol-17β but significantly higher amounts of progesterone than did follicles extirpated from rats in which the gonadotrophin surge had been prevented by a Nembutal injection. Secretion of estradiol-17β by follicles isolated following the endogenous gonadotrophin surge remained low when LH, FSH or dibutyryl cyclic 3′,5′-AMP was added to the medium. However, the addition of testosterone (0.1–1 μg/ml) or androstenedione (1 μg/ml) to the incubation medium restored estradiol biosynthesis to values similar to those seen prior to gonadotrophin exposure. There was no effect of 5α-dihydrotestosterone or 17α-hydroxyprogesterone on the estradiol-17β synthesis. The results indicate that cleavage of the 17:20 sidechain rather than the aromatase enzyme limits estradiol synthesis in the periovulatory follicle following the gonadotrophin surge. It is suggested that the combined action of LH and FSH of the gonadotrophin surge might explain the lack of inhibitory effect on the aromatase enzyme recently reported by Katz and Armstrong (1976) 6–8 h after the injection of LH.

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