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.

Genistein is a product of naturally occurring isoflavones at relatively high levels in soybeans. The harmful effects of ethanol are attributed to the induction of biological processes which lead to an increase in the generation of reactive oxygen species in fetuses. In this study, we investigated the effects of genistein ( and /ml) on gene expressions of the representative cellular antioxidative enzymes in ethanol (1 /ml)-treated mouse fetuses during the critical period (embryonic days 8.5~10.5) of organogenesis using a semi-quantitative RT-PCR analysis. The mRNA levels of cytosolic glutathione peroxidase (GPx), phospholipid hydroperoxide GPx, cytosolic CU,Zn-superoxide dismutase (SOD), and mitochondrial SOD were significantly decreased in ethanol-treated fetuses. However, the mRNA levels of ethanol plus genistein-treated fetuses were significantly higher than those of ethanol alone fetuses. These results indicate that genistein can up-regulate the expressions of GPx and SOD mRNAs reduced by the ethanol treatment in fetuses.

Drinking of excessive ethanol during pregnancy induces a fetal alcohol syndrome. Genistein is one of naturally occurring isoflavones at relatively high levels in soybeans. In this study, we investigated the effects of genistein ( and /ml) on the ethanol (1 /ml)-induced teratogenesis of developing mouse embryos during the critical period (embryonic days 8.5~10.5) of organogenesis using a whole embryo culture system and then morphological scoring analysis. Ethanol-treated embryos exhibited a variety of developmental abnormalities. However, the total morphological scores for ethanol plus genistein groups were significantly higher than those of ethanol alone group (p<0.05). In particular, there were significant increases in the ethanol plus /ml of genistein group on the scores for heart, optic system, branchial bar, mandibular process, and caudal neural tube and further in the ethanol plus /ml of genistein group on the scores for heart, hind-, mid-, and forebrains, optic system, branchial bars, maxillary and mandibular processes, caudal neural tube, forelimb, hindlimb, and somites as compared with those of ethanol alone group (p<0.05). These results indicate that genistein has a preventive effect against ethanol-induced teratogenesis.