Abstract
Epididymal maturation of spermatozoa including acquisition of motility and fertilizing ability depends on androgens both directly from testis and indirectly via the circulation. Androgen action via androgen receptor (AR) can cause both proliferative and anti-proliferative effects (1,2) so we have analysed changes in mouse epididymis following androgen deprivation either by orchidectomy or in prostate epithelial AR knockout (PEARKO) males with reduced androgen action also in epididymis (3). Structural changes (stereology), proliferation (PCNA) and apoptosis (TUNEL) were compared between mature intact males, orchidectomized males 3 day (3d) or 3 weeks (3w) after castration and PEARKO males (3) in the caput and cauda epididymis regions. In caput, epithelial volume decreased while stroma increased in castrates but not in PEARKO whereas lumen volume decreased only after 3 weeks of castration. Proliferating cells (per 100 tubules) were significantly increased 2.8-fold in PEARKO and 6.6-fold in 3d castrate group whereas in the 3wk castrate group proliferation was significantly decreased compared with intact controls. Apoptosis significantly increased by 3.3, 42 and 5.7-folds in PEARKO, 3d and 3wk castrate groups, respectively, compared with intact controls. In the cauda epididymis, castration significantly decreased the volume of lumen and increased stromal volume relative to intact controls. Epithelial proliferation was increased by 20-fold in 3d castrates compared with intact controls. Castration significantly increased apoptosis by 19 and 4.3-folds in 3d and 3wk castrates, respectively, compared with intact controls. We show that the androgen deprivation triggers changes in epididymis structure and cellular turnover in a region-specific and time-dependent manner. The results also reveal a role of testicular factors (presumably androgens) in suppression of epithelial proliferation in the epididymis.
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