Immunolocalization of Androgen Receptor (AR) and Steroid 5 Alpha-Reductase Type II (5 Alpha-Reductase Type II) in Canine Prostate. Effect of Antiandrogen, Chlornradinone Acetate (CMA).

Abstract

The effect of a synthetic steroidal anti−androgen, chlormadinone acetate(CMA), on spontaneous benign prostatic hyperplasia(BPH)in dogs was investigated. Male beagle dogs(5−8 years old) were divided into four experimental groups. Group 1 consisted of untreated controls. Groups 2 to 4 received CMA 0.03, 0.1, and 0.3mg/kg/day, p.o., respectively, for 6 months. In group 1, glandular hyperplasia of the prostate was clearly detected. The glandular epithelial cells showed uniformly intense nuclear staining for androgen receptor(AR). AR was also localized in the nuclei of the fibro−muscular stromal cells. Immunolocalization of 5 alpha−reductase type II was clearly detected in the interacinar stromal cells, but not in the glandular epithelial cells. In groups 2 to 4, CMA produced marked atrophy of the glandular epithelium. The interacinar fibro−muscular stroma was prominent. The intensity of the nuclear staining for AR in both epithelial and stromal cells was negative or very weak. Furthermore, the immunoreaction for 5 alpha−reductase type II in the interacinar stromal cells was negative or very weak. The decreased AR−immunostaining may be explained by the decrease in the number of AR and it may play a key role in the down−regulation of 5 alpha−reductase type II gene expression by CMA. The atrophy after treatment with CMA may be due to shrinkage of both glandular and stromal compartments in the prostate tissue.