triolein and Prostatic-Hyperplasia

We describe a procedure for monitoring changes in canine prostatic size. Metal beads were sutured to the surface of the prostate and the interbead distances were derived from two X-rays taken at right angles. Prostatic hyperplasia was induced by castration and injection of 5 alpha-androstane-3 alpha, 17 beta-diol and 17 beta-estradiol. Prostatic regression was caused by castration without further treatment. Although growth of the prostate was nonuniform, changes in prostatic volume were shown to be related to the third power of the distance between appropriate beads. This monitoring technique can be repeated every 2nd day if necessary, and thus has an advantage over procedures that require repeated laparotomies. Significant increases in prostatic volume could be detected within 5 days after steroid injection.

Topics: Androstenediol; Animals; Biometry; Disease Models, Animal; Dogs; Drug Administration Schedule; Estradiol; Laparotomy; Male; Organ Size; Prostate; Prostatic Hyperplasia; Triolein

To gain insight into the mechanism by which steroidal hormones influence the development of canine prostatic hyperplasia, nuclear and cytosolic androgen- and estrogen-receptor content, as measured under exchange conditions by the binding of [(3)H]R1881 (methyltrienolone) and [(3)H]estradiol, respectively, were quantitated in the prostates of purebred beagles of known age. In young dogs with spontaneously arising and experimentally induced (androstanediol plus estradiol treatment) prostatic hyperplasia, nuclear, but not cytosolic, prostatic androgen-receptor content was significantly greater than that determined in the normal prostates of age-matched dogs (3,452+/-222 and 4,035+/-274 fmol/mg DNA vs. 2,096+/-364 fmol/mg DNA, respectively). No differences were observed between the androgen-receptor content of the normal prostates of young dogs and the hyperplastic prostates of old dogs. The cytosolic and nuclear estrogen-receptor content of spontaneously arising prostatic hyperplasia in both young and old animals was similar to that found in normal prostates. The administration of estradiol plus androstanediol to castrate dogs significantly increased the prostatic nuclear androgen-receptor content over that found in dogs treated only with androstanediol. This estradiol-associated increase in nuclear androgen-receptor content was accompanied by the development of benign prostatic hyperplasia. Estradiol treatment of castrate dogs resulted in an increase in prostatic nuclear estrogen-receptor content, in the appearance of a putative prostatic cytosolic progesterone receptor, and in an alteration of the epithelium of the prostate to one characterized by squamous metaplasia. Treatment of castrate dogs with both estradiol and androstanediol resulted in a reduction in prostatic nuclear estrogen-receptor content, disappearance of the progesterone receptor, and loss of squamous metaplasia. An increase in nuclear androgen-receptor content, thus, appears to be an important event in the development of both spontaneously arising and experimentally induced canine prostatic hyperplasia. The mechanism of androgen-estrogen synergism in the experimental induction of canine benign prostatic hyperplasia may be explained by estradiol-mediated increases in nuclear androgen-receptor content. Because androstanediol blocked certain estradiol-mediated events within the prostate, a negative feedback mechanism may exist in which the response of the canine prostate to estrogens is modul

Topics: Androstane-3,17-diol; Animals; Castration; Cell Nucleus; Cytosol; Dog Diseases; Dogs; Estradiol; Male; Prostate; Prostatic Hyperplasia; Receptors, Androgen; Receptors, Estrogen; Receptors, Steroid; Triolein