EFFECT OF OESTRADIOL-17β ON TESTICULAR OUTPUT OF ASCORBIC ACID AND 17-Oxosteroids INDUCED BY HUMAN CHORIONIC GONADOTROPHIN

Abstract

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-17\g=b\.Eight adult male mongrel dogs weighing 9-6-15-1 kg were used. Four animals were given 20 µg oestradiol-ß (dissolved in 0-2 ml sesame oil)/animal into their necks 16 and 1 h before the beginning of the experiment. The remaining four animals received solvent (sesame oil) alone as a control. Each dog was then anaesthetized with sodium pentobarbitone (25 mg/kg, injected i.v.) and the left spermatic vein cannulated (Yamashita, 1966). Four hours after the last injection of oestrogen or solvent alone, 20 i.u. HCG (CG-10, Sigma Co.)/kg body wt were injected into the left saphenous vein over 15 s. Samples (about 10 ml) of spermatic venous blood were taken for 3-to 6-min periods 30 and 10 min before, and 15, 30, 60, 90, 120 and 180 min after the injection of HCG. One millilitre of plasma from each sample was analysed for ascorbic acid by the method of Roe & Kuether (1943) and 3 ml for total 17-oxosteroids by a slight modification (Yamashita, 1966) of the method of Gardner (1953). The discharge rate of ascorbic acid by one testis (ng/kg/min) was calculated by multiplying the concentration of ascorbic acid in spermatic venous plasma (ng/ml) by the spermatic venous plasma flow (ml/kg/min), and the secretion rate of 17-oxosteroids was also determined.In oestrogen-untreated animals, i.v. injection of HCG produced a considerable discharge of ascorbic acid from the testis, reaching a maximum rate within 15 min of the injection and returning to near pre-injection levels after 120 min (Fig. 1 a): simultaneously it brought about an increased secretion of 17-oxosteroids over a 3-h period of observation (Fig. 1 b). In oestrogentreated animals, the administration of HCG effected a slight increase in testicular ascorbic acid discharge. The responses 15, 30 and 60 min after the injection were significantly (P<0-01) less than those of oestrogen-untreated animals (Fig. 1 a). Although 17-oxosteroid secretion increased considerably over a 3-h period of observation a delay in the initiation of testicular secretion was observed, since there were significant differences in the secretion of 17-oxosteroids 15, 30 and 60 min after the injection of HCG with and without oestradiol-170 (P<0-01)