Relation of the Testis to Adrenal Enzyme Activity and Adrenal Corticosterone Production in the Rat

Abstract

Castration of male rats after puberty results in decreased production of corticosterone by adrenal slices. Replacement with small doses of a depot preparation of testosterone phenylace-tate increases adrenal corticosterone production. Large daily doses of testosterone propionate do not change corticosterone production by adrenal glands from castrated rats and decrease production in intact rats. Castration increases adrenal cholesterol but lowers adrenal glycogen and phosphorylase, phosphodiesterase and 5-nucleotidase activities. Testosterone replacement restores the activities of these enzymes. Adrenal glucose-6-phosphate dehydrogenase and malic de-hydrogenase activities are increased by castration. No changes are obtained in glucose-6-phosphatase, hexokinase, phosphoglucoisomerase, ATP-ase, isocitric dehydrogenase and lactic dehydrogenase. Corticosterone production in vitro, by adrenal homogenates from castrated rats is decreased compared to that by homogenates from intact or testosterone-treated castrated animals when NADP and glucose-6-phosphate are added. Equalization, but with significantly lower levels of corticosterone production, is obtained with the addition of NADPH alone. The decrement in adrenal corticosterone production in castrated rats remains after either unilateral adrenalectomy or administration of massive doses of ACTH. Corticosterone production is stimulated in adrenal slices or homogenates obtained from hypophysectomized, castrated rats given testosterone. These data suggest that the effects of testosterone are related to dose. Small amounts stimulate and large amounts inhibit ardrenal capacity to produce corticosterone. The effects of castration and testosterone replacement on corticosterone production may partially depend on changes in adrenal capacity to generate NADPH. However, other unexplained factors appear to be involved also. The adrenal responses to castration and testosterone are independent of changes in endogenous ACTH secretion.