Abstract
Benign prostate hyperplasia is a dysfunctional disease with an elevated prevalence. Despite the accepted impact of aging and testosterone (TES) in its pathophysiology, its aetiology remains unknown. Recent studies described that serotonin (5-HT) inhibits benign prostate growth through the modulation of the androgen receptor, in the presence of TES. Accordingly, this work aimed to determine the impact of castration and TES replacement in plasmatic and prostatic 5-HT regulation. C57BL/6 mice were submitted to surgical castration and divided into three groups, continually exposed to either vehicle or different TES doses for 14 days. Plasmatic 5-HT concentration was measured before and after castration, and after TES reintroduction. Finally, total prostatic weight and intra-prostatic 5-HT were determined in the different groups. Our results demonstrate that mice prostate exhibits high 5-HT tissue levels and that intra-prostatic total 5-HT was independent of castration or TES reintroduction, in all studied groups. Also, 5-HT plasmatic concentration significantly increased after castration and then normalized after TES administration. Our findings revealed that mice prostate has a high 5-HT content and that total prostatic 5-HT levels do not depend on androgens’ action. On the other hand, castration induced a significant increase in plasmatic 5-HT concentration, raising the hypothesis that androgens might be regulating the production of extra-prostatic 5-HT.
Highlights
Benign prostate hyperplasia is a dysfunctional disease with an elevated prevalence
Several reports have demonstrated that neuroendocrine cells (NEC) and 5-HT are significantly decreased in Benign prostate hyperplasia (BPH) when compared to normal p rostate[11,12,13]
Considering the recognized effect that 5-HT seems to have on prostatic growth, in the present study, we aimed to evaluate the impact of androgen modulation over the main neuroendocrine prostatic factor, namely 5-HT
Summary
Benign prostate hyperplasia is a dysfunctional disease with an elevated prevalence. Despite the accepted impact of aging and testosterone (TES) in its pathophysiology, its aetiology remains unknown. If hypogonadic or even normogonadic men are treated with supra-physiologic TES concentrations, their prostate glands do not increase in size[7] These findings were, in part, responsible for the development of the saturation hypothesis for prostate growth that claims androgens are crucial for prostatic growth (benign or malignant); the concentration of TES necessary for saturation of all prostatic androgen receptors (AR) is near the castration range, concluding that androgens are not the cause of BPH nor prostate cancer[7]. We demonstrated that mice depleted from peripheral 5-HT had a higher prostatic mass, and an up-regulation of the A R14 This data suggests that depletion of 5-HT in the prostate transition zone could be the etiologic factor responsible for the development and progression of BPH through neuroendocrine dysregulation. In this study, we evaluated the effect of TES over plasmatic and prostatic 5-HT concentration using a murine model of hypogonadism
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