Enzymological Studies of Rat Luteinized Ovaries in Relation to Acute Reduction of Aromatizable Androgen Formation and Stimulated Production of Progestins*

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Abstract
Female rats received an injection of 10 IU PMS gonadotropin (PMSG) sc at 21 days of age. One group of the animals was then injected with 30 IU hCG sc at 23 days of age (PMSG-hCG treatment), and the other was not given hCG (PMSG treatment). All the animals were sacrificed at 24 days of age. The ovarian weight was increased by the PMSG treatment and further increased by additional hCG, whereas the uterine weight was increased by PMSG but decreased by hCG. The supernatant fluid obtained by centrifugation at 10,000 × g of homogenates of the ovaries was incubated with 14C-labeled steroids in the presence of the required cofactor to measure steroid-metabolizing enzyme activities. After PMSG-hCG treatment, activities of 17α-hydroxylase and C-17-C-20 lyase per mg protein or per pair of ovaries decreased markedly compared with those of the PMSG-treated group, whereas the aromatase and 20α-hydroxysteroid dehydrogenase activities were enhanced significantly. The activity of Δ5-3β-hydroxysteroid dehydrogenase coupled with Δ4-Δ5-isomerase per pair of ovaries also was stimulated by the PMSG-hCG treatment. After PMSG treatment, the activity of Δ4-5alpha;-reductase per mg protein decreased significantly in comparison with that of the control which received no gonadotropin, but the activities of Δ5-3β-hydroxysteroid dehydrogenase coupled with the isomerase, 17α-hydroxylase, C-17-C-20 lyase, and aromatase per pair of ovaries increased compared with the control. Serum progesterone increased after PMSG treatment and was further enhanced by additional hCG. Serum 17α-hydroxyprogesterone, testosterone, and 17β-estradiol increased in the PMSG-treated group but decreased after the additional administration of hCG. The relationship between the steroidogenic enzyme activities in the ovaries and the serum concentration of steroids was examined from the preovulatory phase induced by PMSG to the luteal phase induced by the additional hCG.