Chlormadinone Acetate (CMA) Induces Apoptosis on Canine Spontaneous Benign Prostatic Hyperplasia (BPH).

Abstract

The effect of a synthetic steroidal antiandrogen, 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 0.3 mg/kg/day, p.o., respectively, for 6 months. In group 1, glandular hyperplasia of the prostate was clearly detected. In groups 2 to 4, CMA produced marked atrophy of the glandular epithelium. The interacinar fibro-muscular stroma was prominent. To evaluate the frequency of apoptosis, we counted the positive cells stained by the nick end labeling method. In group 1, the apoptotic index was 0.76H0.03%. In groups 2 to 4, apoptotic indices were 15.41H1.26%, 2.63H0.98% and 1.45H0.85%, respectively. Apoptotic cell death was mainly observed in the glandular epithelial cells. Based on our data, regression of BPH after treatment with CMA may be apoptotic cell death.

Immunohistochemical Studies of the Effect of Chlormadinone Acetate (CMA) on Prostatic Hyperplasia.

“…In this review, we focus on the localization of androgen receptor (AR), 5 alpha-reductase type I and type II in order to clarify the atrophic effect of CMA administration on canine BPH [14][15][16][17][18][19].…”