Korean J Urol.
1999 Jul;40(7):925-932.
Effects of Androgen on Telomerase Activity in the Adult Rat Penis
- Affiliations
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- 1Department of Urology & Institute of Andrology, Yonsei University College of Medicine, Seoul, Korea.
Abstract
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PURPOSE: Telomerase functions to maintain telomere length and its activity are generally present in most cancer cells, germ line cells but typically are not present in normal somatic cells. Among few exceptions, telomerase activity is detected in hematopoietic stem cells and in physiologically renewable cell populations. The adult rat penis exhibits the ability to regenerate during androgen replacement after castration, we hypothesized that a pool of cells with regenerating potential is present in the adult rat penis, and therefore assayed for the telomerase activity in the castrated and androgen replaced adult rat penis.
MATERIALS AND METHODS
Adult male Sprague Dawley rats were divided into 4 groups; control, castration, and androgen(testosterone, DHT) replacement after castration. Percentage of apoptotic cells assessed by morphological analysis(apoptotic index, TUNEL), and proliferating cells incorporating Ki-67(proliferating index) were analyzed. Telomerase activity was detected by using a PCR-based telomerase assay(Telomeric repeat amplification protocol).
RESULTS
Following castration, serum testosterone significantly decreased from day 1. Normal penis was found to be telomerase positive. Since serum testosterone decreased after castration, a significant decrease for the activity of telomerase was noted with a decrease in the proliferating index and an increase in apoptotic index in the penis. Replacement of androgen after castration increased the telomerase activity with an increase in the proliferating index and a decrease in apoptotic index in the penis.
CONCLUSIONS
These results provide evidence for the ability of androgen to regulate telomerase activity in the adult rat penis, and the adult rat penis retains throughout life the potential to regenerate in response to androgen replacement following castration-induced apoptotic cell death.