17β-HYDROXYSTEROID DEHYDROGENASE ACTIVITY IN HUMAN TESTES

1967 ◽  
Vol 56 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Edgar J. Schoen

ABSTRACT In vitro 17β-hydroxysteroid dehydrogenase activity in testicular tissue from 7 men subjected to orchiectomy for prostatic carcinoma was measured by the conversion rate of androstenedione to testosterone. Prior to orchiectomy, 3 of the patients were untreated: 3 had received stilboestrol. 5 mg daily for one month; 1 had received stilboestrol, 2 mg daily for one month. There was evidence that stilboestrol in a dosage of 5 mg daily for one month prior to orchiectomy led to suppression of testosterone formation from androstenedione. 17β-Hydroxysteroid dehydrogenase activity could be demonstrated in small quantities of testicular homogenate, and thus offers an additional technique for assessing testicular androgenic function in man.

1977 ◽  
Vol 72 (1) ◽  
pp. 17-26 ◽  
Author(s):  
A. H. PAYNE ◽  
R. P. KELCH ◽  
E. P. MURONO ◽  
J. T. KERLAN

SUMMARY Hypothalamic content of gonadotrophin-releasing hormone (GnRH), serum LH and FSH, capacity of the testis to synthesize testosterone in vitro, and testicular 5-ene-3β-hydroxysteroid dehydrogenase-isomerase and 17β-hydroxysteroid dehydrogenase were measured in groups of rats at approximately 5 day intervals from birth to day 64 and at days 74 and 89. The capacity of the testes to synthesize testosterone in vitro was measured in the presence of a saturating dose of rat LH. Gonadotrophin-releasing hormone increased steadily from 0·17 ng per hypothalamus at birth to a maximum of 7 ng at day 52 and then remained constant. LH concentrations were highly variable and often exceeded adult values between days 10 and 32. After day 32 a steady rise was observed which reached adult values between days 37 and 42. FSH concentrations markedly increased from 255 ng/ml observed at birth and day 10 to a peak value of 1000 ng/ml at day 32. Subsequently there was a steady decline in FSH values until day 74 when the concentration returned to values found at birth. 5-ene-3β-Hydroxysteroid dehydrogenase-isomerase activity exhibited a rapid increase between days 12 and 19 followed by an even greater rate of increase between days 19 and 32 when adult levels were attained. 17β-Hydroxysteroid dehydrogenase activity was very low between birth and day 22. Enzyme activity began to increase at day 22 with a rapid increase in activity observed between days 37 and 58. The increase in capacity to synthesize testosterone closely followed the increase in 17β-hydroxysteroid dehydrogenase activity. The study demonstrates that during sexual maturation in the male rat, changes in serum LH and FSH do not reflect changes in hypothalamic GnRH. The appearance of Leydig cells as monitored by 5-ene-3β-hydroxysteroid dehydrogenase-isomerase activity precedes by approximately 20 days the increase in testicular capacity to synthesize testosterone in vitro. The latter coincides with the increase in 17β-hydroxysteroid dehydrogenase activity. These results suggest that 17β-hydroxysteroid dehydrogenase is a limiting factor in the ability of the testis to respond to LH stimulation.


1967 ◽  
Vol 38 (1) ◽  
pp. 61-NP ◽  
Author(s):  
C. G. PIERREPOINT ◽  
JEAN McI. GALLEY ◽  
K. GRIFFITHS ◽  
J. K. GRANT

SUMMARY The metabolism of [7α-3H]pregnenolone and [4-14C]dehydroepiandrosterone (DHA) by a Sertoli cell tumour of the testis from a dog with signs of feminization has been studied in vitro and compared with the metabolism of the normal canine testis. The tumour formed oestrone and oestradiol-17β from DHA thus providing direct evidence for the synthesis of oestrogen by this type of neoplasm. Relative or complete inactivity of several enzyme systems involved in the synthesis of testosterone was found in the tumour tissue, and the conversion of either precursor to testosterone was considerably less than in the normal testis. Suggestive evidence is presented for the occurrence of steroid-specific 17α-hydroxylase and 3β-hydroxysteroid dehydrogenase-isomerase systems in canine testicular tissue. The formation of sulphates of pregnenolone and DHA was shown both in normal and in neoplastic tissues and, in addition, the tumour either formed the sulphate of 17α-hydroxypregnenolone or caused the 17α-hydroxylation of pregnenolone sulphate.


1979 ◽  
Vol 83 (3) ◽  
pp. 369-378 ◽  
Author(s):  
F. K. HABIB ◽  
G. RAFATI ◽  
M. R. G. ROBINSON ◽  
S. R. STITCH

The in-vitro metabolism of testosterone in benign and malignant prostatic tissue was examined and distinct quantitative differences between the two types of specimens were observed. The major metabolite of testosterone in the hyperplastic prostate was 5α-dihydrotestosterone and a high 3α(β)-hydroxysteroid dehydrogenase activity was also detected. In the malignant tissue, 5α-reductase activity was considerably reduced and there was little or no androstanediol formed; the 17β-dehydrogenase activity was, however, higher than in the benign tissue. The decrease in 5α-reductase was always followed by a compensatory change in the 3α(β)-hydroxysteroid dehydrogenase of the malignant prostate. The present study revealed that the ratio of the mean activities of 5α-reductase to 3α(β)-hydroxysteroid dehydrogenase in the two types of specimen always remained a constant. Although the antioestrogen, tamoxifen, induced an inhibitory effect on the activities of 5α-reductase and 17β-hydroxysteroid dehydrogenase in the gland, the present investigation also suggested that tamoxifen stimulated the activity of 3α(3β)-hydroxysteroid dehydrogenase. In blood, the action of tamoxifen appeared to be confined to the displacement of androgens from the binding sites on the sex hormone binding globulin.


1966 ◽  
Vol 35 (2) ◽  
pp. 185-192 ◽  
Author(s):  
A. FAVINO ◽  
A. H. BAILLIE ◽  
K. GRIFFITHS

SUMMARY Androgen synthesis after administration of cadmium chloride to rats has been studied histologically, histochemically and biochemically. Incubation in vitro of testicular tissue removed 10 days after cadmium administration revealed markedly decreased testosterone synthesis. After 100 and 150 days, testosterone synthesis in vitro had increased progressively and significantly, but there was a marked decrease in the testosterone: androstenedione ratio. Surviving Leydig cells, giving typical histochemical reactions for 3β-, 16β- and 17β-hydroxysteroid dehydrogenase, were observed under the tunica albuginea immediately after cadmium poisoning. Fifty days after the cadmium treatment, mesenchymal cells, giving a histochemical 3α- and 16α-hydroxysteroid dehydrogenase reaction, but no other hydroxysteroid dehydrogenase reaction of normal Leydig cells, grew into the testes from the tunica albuginea. Weight, citric acid and fructose contents of seminal vesicles of cadmium-treated rats fell nearly to castration levels, but showed some degree of recovery thereafter. Studies in vitro on adrenal tissue from cadmium-poisoned rats suggested that the rate of testosterone biosynthesis from pregnenolone was increased.


1982 ◽  
Vol 99 (4) ◽  
pp. 588-593 ◽  
Author(s):  
E. Kokko ◽  
O. Jänne ◽  
A. Kauppila ◽  
L. Rönnberg ◽  
R. Vihko

Abstract. The administration of danazol, 200 mg three times daily, from the 3rd to the 23rd day of the cycle to normally menstruating women exhibited the following actions on the human endometrium: significantly reduced cytosol oestrogen and progestin receptor concentrations, and declined 17β-hydroxysteroid dehydrogenase activity. Very similar results were obtained during medroxyprogesterone acetate (100 mg daily) treatment for the same period of time. Danazol administration did not decrease circulating gonadotrophin levels but clearly suppressed luteal serum oestradiol and progesterone concentrations. Danazol was found to bind in vitro to endometrial progestin receptor with an affinity approximately 3% of that of progesterone. These findings are compatible with the notion that a local progestin-like rather than a systemic action of danazol is the way by which its therapeutic effect is exerted. This may be potentiated by the suppression of circulating oestradiol levels.


Sign in / Sign up

Export Citation Format

Share Document