Androgen receptor content of nafoxidine treated experimentally induced canine prostatic hyperplasia
Trachtenberg, J.
Clinical and Investigative Medicine. Medecine Clinique et Experimentale 8(1): 29-34
1985
ISSN/ISBN: 0147-958X PMID: 2580656 Document Number: 243881
An estrogen stimulated increase in prostatic androgen receptor content has been postulated as the mechanism by which canine prostatic hyperplasia can be induced in the castrate dog treated with androstanediol and estradiol but not by androstanediol alone. In order to determine if the potent anti-estrogen Nafoxidine would inhibit this estrogen-associated development of prostatic hyperplasia, 2 week castrate young mongrel male dogs were injected for 1 month with either a) carrier solution (group 1), b) Nafoxidine (group 2), c) androstanediol and estradiol (group 3), or d) androstanediol and estradiol and Nafoxidine (group 4). At the termination of the experimental period the prostates of the animals in groups 1 and 2 were small (3.1 +/- 0.3 g (X +/- SEM) and 8.6 +/- 1.4 g respectively) and were atrophic histologically. The prostates in groups 3 and 4 were significantly heavier (24.7 +/- 3.0 g and 23.6 +/- 3.6 g respectively) than those in groups 1 and 2 and displayed glandular hyperplasia histologically. The dihydrotestosterone content of the prostatic tissue in groups 1 and 2 were similar (4.65 +/- 2.01 ng/mg DNA (X +/- SEM) and 3.13 +/- 0.65 ng/mg DNA respectively) and were significantly less than that of groups 3 and 4 (19.98 +/- 4.70 ng/mg DNA and 19.62 +/- 2.42 ng/mg DNA). The prostates of groups 3 and 4 thus displayed gravimetric, histologic and biochemical evidence of prostatic hyperplasia.