THE INFLUENCE O F CHORIONIC GONADOTROPIN ON THE 3β-OL DEHYDROGENASE ACTIVITY OF TESTES AND ADRENALS1

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Abstract
After a temporary increase in activity, probably due to manipulation of the pituitary gland during excision, the steroid 3[beta]-ol dehydro-genase activity of the testis fell rapidly after hypophysectomy. On the basis of total activity per testis, the activity dropped rapidly during the first 5-6 days and then at a decreasing rate over the 58-day period studied. The activity per unit mass of testis reached a maximum at about 5 days after the operation and then gradually rose to concentrations well above normal by the 20th day. This high concentration was maintained throughout the 58 days studied. This is best explained by the early atrophy of the Leydig cells while the germinal epithelium degenerated later. The 3/[beta]-ol dehydrogenase appears to be primarily associated with the Leydig cells rather than with the germinal epithelium. On the injection of chorionic gonadotropin the total steroid 3[beta]-ol dehydrogenase activity of the atrophic testes rose to values more than twice normal. Since there was no simultaneous stimulation of the seminiferous epithelium, the already elevated concentration of the enzyme rose to very high levels. While the steroid 3[beta]-ol dehydrogenase activity of the adrenal glands of the hypophysectomized rats decreased wi th atrophy of the glands, the activity per unit mass did not drop significantly. On injection of chorionic gonadotropin there was no increase in the activity of this enzyme in the adrenals as there was in the testes. It seems, therefore, that the decrease in total activity after hypophysectomy was simply an indirect result of the total decrease in adrenocortical cell protein. Various systems of incubation of the atrophic testes of hypophysectomized rats with chorionic gonadotropin in vitro did not lead to any increase in 3[beta]-ol dehydrogenase activity. It is concluded that choronic gonadotropin caused an increase in steroid 3[beta]-ol dehydrogenase activity by increasing synthesis of Leydig cell protein rather than through activation of existing enzyme. This was probably an indirect result of activation of another enzymic step by the tropic hormone, an "adaptive" effect. The possibility is not ruled out that the effect on Leydig cell protein synthesis is a slower independent action of the gonadotropin.