Procymidone is a fungicide with anti-androgenic properties widely used to protect fruits from fungal infection, which induces an excessive reactive oxygen species production in male reproductive organs. In this study, to clarify whether procymidone affect the cellular antioxidant system of prostate at onset of puberty, gene expression patterns of the representative antioxidant enzymes such as cytoplasmic glutathione peroxidase (GPx1), phospholipid hydroperoxide GPx (PHGPx), selenoprotein P (SePP), cytoplasmic copper/zinc superoxide dismutase (SOD1), and manganese SOD (SOD2) were investigated in the rat ventral prostates exposed to procymidone using real-time RT-PCR analyses. Seven-week-old Sprague-Dawley rats castrated at 6 weeks old were treated with procymidone (25, 50, or 100 mg/kg per day) orally for 7 consecutive days after testosterone propionate (0.4 mg/kg per day) administration by subcutaneous injection. As compared to normal control animals, GPx1 mRNA expression in prostates significantly increased by the administration with TP and/or procymidone. However, PHGPx and SOD1 mRNA levels significanatly decreased by over 25 mg/kg of procymidone treatment and SePP and SOD2 mRNA levels was significanatly reduced by over 50 mg/kg of procymidone treatment. These findings indicate that procymidone may affect the antioxidant system of prostatic cells in up-regulation mode of GPx1, but in down-regulation modes of PHGPx, SePP, SOD1, and SOD2, suggesting that procymidone may affect differently the cellular antioxidant system of prostate according to the exposure doses.

Direct communication between neighboring cells through connexin (Cx)-based gap junction is a crucial biolo– gical manner to regulate functions of a tissue consisting of multi-cell types. The present research evaluated expressional changes of Cx isoforms in the caput epididymis of adult rat exposed to estradiol benzoate (EB) or flutamide (Flu) at the early postnatal age. A single subcutaneous administration of EB at a low-dose [0.015 g /kg body weight (BW)] or a high-dose (1.5 g/kg BW) or Flu at a low-dose (500 g/kg BW) or a high-dose (5 mg/kg BW) was performed to an animal at 1 week of age. Quantitative real-time PCR analysis was employed to determine expressional changes of Cx isoforms. The transcript levels of Cxs30.3 and 37 were decreased by a low-dose EB treatment, while decreases of Cxs31, 31.1, 32, 40, and 45 transcript levels were observed with a low-dose EB treatment. The treatment of a high-dose EB resulted in expressional reduction of Cxs30.3, 31, 31.1, 37, 40, 43, and 45. The Flu treatment at a low dose caused increases of Cxs26, 37, and 40 transcript levels but decreases of Cxs31.1, 43, and 45 transcript levels. Increases of Cxs30.3, 31, 37, and 40 mRNA amounts were induced by a high-dose Flu treatment. However, exposure to a high-dose Flu produced expressional decreases of Cxs31.1, 32, and 43 in the adult caput epididymis. These observations suggest that exposure to EB or Flu at the neonatal period could lead to aberrant expression of Cx isoforms in the adult caput epididymis.