Apoptosis and hormonal milieu in ductal system of normal prostate and benign prostatic hyperplasia

Citation
Sj. Xia et al., Apoptosis and hormonal milieu in ductal system of normal prostate and benign prostatic hyperplasia, ASIAN J AND, 3(2), 2001, pp. 131-134
Citations number
15
Categorie Soggetti
Reproductive Medicine
Journal title
ASIAN JOURNAL OF ANDROLOGY
ISSN journal
1008682X → ACNP
Volume
3
Issue
2
Year of publication
2001
Pages
131 - 134
Database
ISI
SICI code
1008-682X(200106)3:2<131:AAHMID>2.0.ZU;2-C
Abstract
Aim: To study the apoptotic rate (AR) and the androgen and estrogen milieu in the proximal and distal ductal systems of prostate, in order to help exp loring the effects of these factors on prostatic growth and the pathogenesi s of benign prostatic hypertrophy (BPH). Methods: The proximal and distal e nds of the ductal system were incised from 20 normal prostate as well as th e hypertrophic prostate tissue from 20 patients with BPH. The AR was determ ined by the DNA end-labeling method and dihydrotestosterone (DHT) and estro diol (E-2), by radioimmunoassay. Results: There was no significant differen ce in DHT and E-2 density between the proximal and distal ends of the ducta l systems in normal prostate. E-2 appeared to be higher in BPH than in norm al prostatic tissues, but the difference was statistically insignificant. I n normal prostatic tissue, the AR was significantly higher in the distal th an in the proximal ends of the ductal system (P < 0.05), while the AR of th e proximal ends was significantly higher (P < 0.01) than that in the BPH ti ssue. No significant correlation was noted between the DHT and E-2 density and the AR both in the normal prostate and BPH tissues. Conclusion: The pap er is the first time describing a difference in AR in different regions of the ductal system of normal prostate, while the hormonal milieu is similar, indicating a functional inhomogeneity of these regions. A low AR in the pr oximal duct, where BPH originates, and an even lower AR in the BPH tissue, sug gesting the participation of apoptosis in the BPH pathogenesis.