Abstract
The effects of testosterone and 17β-estradiol (E2) on the prostate of castrated rats were investigated by histopathological and immunohistochemical procedures. Male Sprague-Dawley rats were divided into four experimental groups. Group 1 consisted of intact controls. The other animals were castrated. In group 2, rats were sacrificed 2 days after castration. The castrated animals were treated for 6 weeks with 1) testosterone 1 mg/head (Group 3) and 2) testosterone 1 mg/head plus E2 10 μg/head (Group 4). A significant increase in prostatic weight occurred after 6 weeks treatment with testosterone alone (Group 3) and in combination with E2 (Group 4). The greatest increase in prostatic weight were noted in Group 4. Histopathologically, glandular hyperplasia of the prostate was clearly observed, and the number of bromo-deoxyuridine (BrdU)-positive cells showed a significant increase over that induced by testosterone alone. Immunohistochemical localization of glutathione-peroxidase (GSH-PO) which effectively reduces the lipid peroxides, was predominantly observed in the glandular epithelial cells of the prostate. The intensity of GSH-PO staining in the glandular epithelial cells was remarkably decreased after castration (Group 2), and that it was clearly recovered by testosterone (Group 3)-or testosterone plus E2 (Group 4)- treatment to the castrated rats. In addition, androgen receptor (AR) was mainly localized in nuclei, but not in cytoplasm. Furthermore, immunodetectable AR rapidly declined after androgen withdrawal (Group 2) and returned to intact levels of staining intensity after androgen replacement (Groups 3 and 4). Thus, GSH-PO in the glandular epithelial cells suggest the very close relationship to the status of testosterone action to the cells. Therefore, it was strongly suggested that GSH-PO in the glandular epithelial cells of the rat prostate was testosterone-dependent.
