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Abstract

Volume 3, Issue 2 (June 2001) 3, 131–134;

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

S.J. Xia, C.X. Xu, X.D. Tang, W.Z. Wang, D.L. Du

1.Department of Urology, 3Department of Pathology, Shandong Provincial Hospital, Jinan, 250021, China
    2.University Department of Urology, Shanghai First People's Hospital, Shanghai, 200080, China
    

Advance online publication 1 June 2001

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 exploring the effects of these factors on prostatic growth and the pathogenesis of benign prostatic hypertrophy (BPH). Methods: The proximal and distal ends of the ductal system were incised from 20 normal prostate as well as the hypertrophic prostate tissue from 20 patients with BPH. The AR was determined by the DNA end-labeling method and dihydrotestosterone (DHT) and estrodiol (E2), by radioimmunoassay. Results: There was no significant difference in DHT and E2 density between the proximal and distal ends of the ductal systems in normal prostate. E2 appeared to be higher in BPH than in normal prostatic tissues, but the difference was statistically insignificant. In normal prostatic tissue, the AR was significantly higher in the distal than in the proximal ends of the ductal system (P<0.05), while the AR of the proximal ends was significantly higher (P<0.01) than that in the BPH tissue. No significant correlation was noted between the DHT and E2 density and the AR both in the normal prostate and BPH tissues. Conclusion: The paper 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 proximal duct, where BPH originates, and an even lower AR in the BPH tissue, suggesting the participation of apoptosis in the BPH pathogenesis

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Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.