Abstract. The first part of this study compares peripheral testosterone levels with intratesticular levels of the cytochromes P-450 of two key enzymes of androgen biosynthesis, i.e. mitochondrial cholesterol monooxygenase (P-450(cscc)) and microsomal steroid-17α-monooxygenase (P-450(C17α)) during puberty and early adulthood of male Wistar rats. From 4 to 10 weeks of age, the testosterone level increases 8.7-fold, the P-450(C17α) level 8.3-fold, but the P-450(cscc) level 24.5-fold as an indication of specific induction of this protein. From 13 to 50 weeks of age, the testosterone level remains constant, the P-450(cscc) level increases continuously by a factor of 1.4, but 62% of the P-450(C17α) content are lost. This discrepancy is explained by a divergent regulation of the cytochromes P-450 of the two steroid monooxygenases: a persisting induction of P-450(cscc) and a concurrent down-regulation of P-450(C17α) that may be a consequence of the high rate of Leydig cell steroid hydroxylation after puberty. Overlapping of both processes may (probably besides other developmental factors) result in a constant testosterone concentration in blood. The second part of the study compares testicular and epididymal levels of androgen-binding protein (ABP) with the peripheral testosterone level. The peripubertal increase in testicular ABP content is shown to be related only to the increase in testicular mass, whereas a specific accumulation of ABP occurs in the epididymis from 4 to 13 weeks of age. This pattern indicates an increasing secretory activity of the Sertoli cells that remains high during adulthood up to the 50th week. The parallelity of epididymal ABP accumulation and testosterone level confirms the concept of androgen-dependence of Sertoli cell secretory function.

Evidence is presented that the regulation of the cytochrome P-450(C17 alpha) of the steroid-17 alpha-monooxygenase and of the cytochrome P-450(cscc) of the cholesterol-monooxygenase by human choriogonadotropin (hCG) in vivo is mediated by differential mechanisms in the adult rat testis. An initial down-regulation of the cytochrome P-450(C17 alpha) but not of the P-450(cscc) can be demonstrated. Furthermore, induction of the cytochrome P-450(cscc) requires exposure to higher hCG doses (32% of the maximal induction rate of 43.7 pmol/(testis x d) are achieved with 4IU hCG/single dose) than induction of the P-450(C17 alpha) (59% of the maximal induction rate of 48.4 pmol/(testis x d) with 4IU hCG/single dose). Finally, induction of cytochrome P-450(cscc) starts faster after initiation of hCG treatment than induction of P-450(C17 alpha).

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