The Shift from C-19 to C-21 Steroid Synthesis in Spawning Male Common Carp, Cyprinus carplo, is Regulated by the Inhibition of Androgen Production by Progestogens Produced by Spermatozoa1

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Abstract
There is a rapid shift in the steroidogenic pathway from androgen to progestogen production in spawning male common carp, Cyrpinus carpio. Experiments were conducted to determine the mechanism regulating this shift using in vitro cutures of testicular fragments and isolated sperm of sperm of spermiating male carp. The level of 11-ketotestosterone (11-KT) continually increased for 48 h with or without gonadotropin (GtH) stimulation, suggesting that 11-KT is the principal androgen produced by carp testes. Ovine prolactin (oPRL) enhanced GtH-stimulated 11-KT production, but by itself had no effect. Gonadotropin, carp pituitary extract, and pregnenolone all enhanced the production of 11-KT, testosterone (T), and 17.alpha.-hydroxyprogesterone (17-P) in a dose-dependent manner. No 17.alpha.,20.beta.-dihydroxy-4-pregnen-3-one (17,20.beta.-P) was detected in response to any of these agents; 17.alpha.,20.alpha.-dihydroxy-4-pregnen-3-one (17,20.alpha.-P) was not measured. Both 17,20.beta.-P and 17,20.alpha.-P inhibited 11-KT production in a dose-dependent manner in the presence of either GtH, 17-P, or T. Isolated sperm and testicular fragment preparations both produced 17,20.beta.-P and approximately tenfold more 17,20.alpha.-P when incubated with 17-P. Only testicular fragments, however, produced 11-KT. We conclude that androgen synthesis occurs only within somatic cells of common carp tests. GtH, and perhaps PRL, stimulates the production of steroid precursors that, under normal physiological conditions, are metabolized to androgens. We hypothesize that during the pre-spawning GtH surge, the rate-limiting enzyme in androgen biosynthesis, C-17,20-lyase, becomes saturated with its substrate 17-P, which is then able to diffuse out of the somatic cells to the spermatozoa, where it is metabolized to 17,20.beta.-P and 17,20.alpha.-P. These progestogens feed back on the somatic cells and inhibit the activities of androgen biosynthetic ezymes, including C-17,20-lyase. This process initiates a short-loop, positive feedback mechanism whereby the inhibition of C-17,20-lyase leads to the increased production of progestogens by the spermatozoa, which further inhibit C-17,20-lyase, and so on. These events result in a very rapid drop in androgen levels and a simultaneous rise in the progestogens that control the process of spermiation.

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