Effect of cyproterone acetate in comparison to flutamide and megestrol acetate on the ventral prostate, seminal vesicle, and adrenal glands of adult male rats

The Prostate ◽  
1987 ◽  
Vol 11 (4) ◽  
pp. 361-375 ◽  
Author(s):  
M. Fathy El Etreby ◽  
Ursula-F. Habenicht ◽  
Thomas Louton ◽  
Yukishige Nishino ◽  
Helmut G. Schröder
1979 ◽  
Vol 180 (2) ◽  
pp. 313-318 ◽  
Author(s):  
Coral A. Lamartiniere ◽  
Cindy S. Dieringer ◽  
Etsuko Kita ◽  
George W. Lucier

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.


1965 ◽  
Vol 49 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Fred A. Kind ◽  
M. Maqueo ◽  
Ralph I. Dorfman

ABSTRACT Various neutral steroids were studied in intact male rats for their ability to influence testicular function, particularly spermatogenesis. The compounds were injected once daily for 21 days, starting at 21 days of age. One day after the last injection, testicular histology and testis, ventral prostate, and seminal vesicle weights were determined. In some experiments, after the standard 21 day treatment period, testicular histology and function were evaluated after 30 and 60 day post-treatment recovery periods. 2α-Hydroxymethyl-17β-hydroxy-5α-androstan-3-one, 2-hydroxy-5α-androst-2-en-17β-ol, 2,17α-dimethyl-5α-androst-2-en-17β-ol and 2-formyl5α-androst-2-en-17β-ol caused decreases in testicular, ventral prostate and seminal vesicle weight and produced arrest of spermatogenesis. These effects were reversible and testis weight and histology, as well as fertility, were restored in the post-treatment period. 19-Norprogesterone, which did not produce convincing testicular atrophy, did cause significant decreases in ventral prostate and seminal vesicle weight. Chlormadinone showed a similar picture, although direct antagonistic testicular effects were also seen. The lowered ventral prostate and seminal vesicle weights produced by these compounds may be an expression of their antiandrogenic activity.


1987 ◽  
Vol 116 (2) ◽  
pp. 193-199 ◽  
Author(s):  
Santosh K. Varma ◽  
Eric Bloch

Abstract. The oestrogen mestranol (0, 0.01, 0.1 mg/kg body weight per day) and the progestins medroxyprogesterone-acetate and norethisterone (0, 2, 20 mg/kg body weight per day each) in sesame oil were intubated intragastrically daily during gestational days 14.5 through 19.5 to pregnant rats. Males were studied as 20.5-day-old foetuses and 4-month-old adults for serum testosterone and LH concentrations, in vitro testosterone synthesis, anogenital distance (foetuses only) and testes, seminal vesicle and ventral prostate weights. Administration of 0.1 mg mestranol decreased by 35 to 70% basal and LH-stimulated testosterone synthesis by both foetal and adult testes in vitro (P < 0.01). Foetal body weights (P < 0.05), but not anogenital distances, were significantly decreased. Testosterone content in adult sera was reduced significantly (P < 0.05) to less than 50% of control. Testes, ventral prostate, seminal vesicle and epididymal weights were unaffected by treatment. Medroxyprogesterone acetate or norethisterone administration did not alter testes endocrine function in foetal or adult offspring. In a small number of rats, pregnant for 10.5, 14.5 or 18.5 days, [3H]ethinyloestradiol was intubated and foetal and placental tissue examined for appearance and content of radioactivity. Radioactivity was detected in 10.5, 14.5 and 18.5 days old placentas, and 14.5 and 18.5 days old foetal liver, gonads and external genitalia. With [3H]medroxyprogesterone acetate, radioactivity was localized in 14.5 day placenta and foetal tissues. Thin-layer chromatographic analysis showed most of the activity to migrate as authentic ethinyloestradiol or medroxyprogesterone acetate. The results demonstrate inhibition of testicular testosterone synthesis by mestranol, presumably by being transferred across the placenta and acting in the foetus. The diminished activity of adult testes indicates a permanent effect of in utero mestranol exposure on testes function.


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