Repercussions of castration and vasectomy on the ductal system of the rat ventral prostate

Abstract

Diseases, such as cancer and benign prostatic hyperplasia, are related to disruption of the mechanism regulating the balance between cell proliferation and apoptosis in prostatic cells. Since castration and vasectomy might alter that balance, this study evaluates the cell proliferation, apoptosis and height of the secretory epithelium of the ventral-prostate ductal system post-castration and vasectomy. Immunohistochemical (PCNA and Ki67), cytochemical (Fuelgen reaction) and morphometric investigation have been carried out. Cell proliferation indices decreased significantly in both regions of the ventral-prostate ductal system after castration compared to the sham-operated group. The apoptotic index increased significantly after 48 h, declining 7 days post-castration. The cell proliferation indices did not differ after 48 h significantly; however, they increased 7 days post-vasectomy in both regions. The apoptotic index did not differ significantly in either time post-vasectomy. Castration caused an imbalance in favor of apoptosis, whereas vasectomy caused an imbalance in favor of cell proliferation.

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

“…Other studies also show that the increase of apoptosis in response to androgen deprivation occurs predominantly in the ventral lobe (Banerjee et al, 1995(Banerjee et al, , 2000. Nevertheless, the increase of the apoptotic index detected in the present study was less than that observed by other authors (Garcia-Florez et al, 2005;Pereira et al, 2006). This difference might be explained by several circumstances: (a) the different stage of development of the animals (peripubertal versus adult); (b) the different model of androgen deprivation (androgenic blockade versus surgical castration).…”

“…However, Kim et al (2002) found diminution in cell proliferation evidenced by immunostaining for Ki-67 in castrated rats with implants of prostate cancer cell lines. The differences were remarkable when comparing our PCNA results with those from other studies, because in surgically castrated and/or estrogen-treated adult rats, the index of PCNA-positive cells decreased significantly according to other authors (Garcia-Florez et al, 2005;Pereira et al, 2006). These discrepancies could be either due to the stage of the development of the animals (prepubertal versus adult), the model of androgen deprivation (pharmacological versus surgical castration), or the methodology employed for counting cells.…”

“…These discrepancies could be either due to the stage of the development of the animals (prepubertal versus adult), the model of androgen deprivation (pharmacological versus surgical castration), or the methodology employed for counting cells. Although in the present study, no comparison of PCNA results with Ki 67 estimates of proliferating cells were carried out, other authors indicate that the index of Ki 67-positive cells in the ventral region presented a pattern similar to that of the PCNA-index (Pereira et al, 2006).…”

“…As we have focused our study on the epithelium, the epithelial regressive changes observed (i.e., a decrease in the amount of epithelial cells) could be either due to a low rate of cell proliferation, an increase of the apoptosis, or both. The androgenic blockade causes a decrease in the global size of the peripubertal ventral prostate, according to that described by other authors, which concern the regressive changes shown in the prostate after androgenic deprivation in both adult and prepubertal rats (Vilamaior et al, 2006;Pereira et al, 2006;Augusto et al, 2008). Controversy exists regarding the influence of PL on the prostate of pharmacologically castrated rats (either immature or mature).…”

“…Mouse monoclonal and rabbit polyclonal antibodies were used as primary antibodies. To detect PCNA and AR immunoreactivities, (Pereira et al, 2006;Cordeiro et al, 2008), sections were incubated with a monoclonal anti-PCNA antibody (Biomeda, Foster City, CA) diluted at 1:200, and with a polyclonal anti-AR antibody (Calbiochem, Cambridge, MA), diluted at 1:60. Pretreatment of sections by heat in citrate buffer pH 6.0, using a pressure cooker (Martin et al, 2001), was performed to enhance AR immunostaining.…”