Department of Pathophysiology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki, Japan
(Received 17 February 1975)
The mechanism underlying the depletion of ascorbic acid content of steroid-producing tissues in response to trophic hormones is poorly understood. Previous work (Koba, Kawao & Yamashita, 1971) has shown that, in the dog, the discharge of ascorbic acid as well as 17-oxosteroids into spermatic venous blood by testicular tissue stimulated with human chorionic gonadotrophin (HCG) can be suppressed by the prior administration of methylenedianiline, an amphenone analogue capable of inhibiting testicular steroidogenesis (Yamashita, 1967). Since oestrogens have been shown to be effective inhibitors of the glucose-6-phosphate dehydrogenase necessary for corticosteroid synthesis in the rat adrenal (McKerns, Coulomb, Kaleita & De Renzo, 1958), we have studied male dogs pretreated with oestradiol-17β.
Eight adult male mongrel dogs weighing 9·6–15·1 kg were used. Four animals were given 20 μg oestradiol-17β (dissolved in 0·2 ml sesame oil)/
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