Kinetics of Human Chorionic Gonadotropin-Induced Steroidogenic Response of the Human Testis. II. Plasma 17α-Hydroxyprogesterone, Δ4-Androstenedione, Estrone, and 17β-Estradiol: Evidence for the Action of Human Chorionic Gonadotropin on Intermediate Enzymes Implicated in Steroid Biosynthesis*

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Abstract
The time course of the rise in plasma levels of 17α-hydroxyprogesterone (OHP), Δ4-androstenedione (Δ4), es-trone (E1), and 17β-estradiol (E2) was studied in 14 normal adult volunteers after one, two (at a 24-h interval), or four (at 5-day intervals) injections of 6000 IU hCG. The patterns were quite different among the four hormones. After a single hCG injection,OHP, Δ4, and E1increased within 4 h, but E2 increased after 8-12 h. After this early rise, Δ4 decreased slightly, plateauing for 48 h, E1slightly increased, while OHP and E2 sharply rose, reaching their maximal levels at 24 h (mean, 3- and 5-fold respectively). At 48–96 h (mean, 72 h), Δ4 and E1 showed a paradoxical late rise (2- to 3-fold) significantly greater than the early one, while OHP and E2 continued to decline. When hCG injection was repeated 24 h later, Δ4 and E1 reincreased slightly within 4 h but exhibited a similar late rise delayed by about 24 h; the single maximal peak of OHP was somewhat advanced and that of E2 was amplified. When hCG was administered every 5 days, the levels of Δ4, E1, and E2 found before each hCG injection increased from days 0–10 but were not different from control values for OHP. The early responses to hCG were no longer significant after the third injection for Δ4 and E1, while they occurred each time for OHP. Variations in plasma E2 were not significant during the 4 h after any of the hCG injections. These findings suggest that 1) the hCG-induced steroidogenic block in testosterone biosynthesis occurs before the synthesis of Δ4;2) the earlier rise and lack of late increase in OHP and E2 suggest that hCG acutely stimulates the testicular aromatase while it inhibits the 17, 20-lyase activity; and 3) the drastic rise in E2 together with previous data in humans and rats suggest that this hormone might be responsible for the latter transient enzymatic defects.

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