EFFECTS OF CASTRATION AND TESTOSTERONE REPLACEMENT OVER SEROTONIN (PROSTATIC AND PLASMATIC): A MICE IN VIVO STUDY.
Although benign prostatic hyperplasia is one of the most prevalent human diseases, its etiology remains unknown. Recent studies described how serotonin (5-HT) inhibits benign prostatic growth through modulation of the androgen receptor in the presence of Testosterone. The aims of this work were to determine the role of Testosterone in plasmatic and prostatic serotoninergic system.
C57BL/6 mice were submitted to surgical castration and divided into 3 Groups, Group 1: supplemented with vehicle; Group 2 and 3 supplemented with different Testosterone concentrations, during 14 days. Prostatic and Plasmatic 5-HT concentrations were determined in different time points.
Normal mice prostate exhibits high levels of 5-HT. The total amount of prostatic 5-HT seems not to be regulated by the presence or absence of androgens (Fig.1). Plasmatic 5-HT concentration significantly increases after castration (Fig.2) and Testosterone supplementation strongly decreases Plasmatic 5-HT concentration (Fig.3).
We showed for the first time that the normal mice prostate produces, independently of androgens, high levels of 5-HT. This prostatic 5-HT might counteracts the stimulatory action of Testosterone in prostatic growth. The finding that androgens strongly regulate plasmatic 5-HT raises the question of a possible relationship between extra-prostatic organs and the regulation of prostatic growth.