Chlormadinone acetate (CMA) induces apoptosis on canine spontaneous benignprostatic hyperplasia (BPH)

Citation
M. Murakoshi et al., Chlormadinone acetate (CMA) induces apoptosis on canine spontaneous benignprostatic hyperplasia (BPH), ACT HIST CY, 34(4), 2001, pp. 223-228
Citations number
34
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
ACTA HISTOCHEMICA ET CYTOCHEMICA
ISSN journal
00445991 → ACNP
Volume
34
Issue
4
Year of publication
2001
Pages
223 - 228
Database
ISI
SICI code
0044-5991(2001)34:4<223:CA(IAO>2.0.ZU;2-9
Abstract
The effect of a synthetic steroidal antiandrogen, chlormadinone acetate (CM A), on spontaneous benign prostatic hyperplasia (BPH) in dogs was investiga ted. Male beagle dogs (5-8 years old) were divided into four experimental g roups. 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 interacina r fibro-muscular stroma was prominent. To evaluate the frequency of apoptos is, we counted the positive cells stained by the nick end labeling method. In group 1, the apoptotic index was 0.76 +/- 0.03%. In groups 2 to 4, apopt otic indices were 15.41 +/- 1.26%, 2.63 +/- 0.98% and 1.45 +/- 0.85%, respe ctively. Apoptotic cell death was mainly observed in the glandular epitheli al cells. Based on our data, regression of BPH after treatment with CMA may be apoptotic cell death.