title: Oral exposure to low-dose bisphenol A aggravates testosterone-induced benign hyperplasia prostate in rats.
abstract: The declining level of androgen during aging, associated with an inclining level of estrogen, has been hypothesized to be important in the development of benign prostatic hyperplasia (BPH). Within physiologic range, increasing estrogen levels can stimulate prostate to develop and permanently increase prostate size. As an estrogenic endocrine disruptor, bisphenol A (BPA) might be stimulatory to prostate development. We further hypothesized that low dose BPA could induce hyperplasia prostate to proliferate and aggravate the symptom of BPH in male SD rats. BPH was induced by testosterone and then treated with BPA (10, 30, or 90 μg/kg, i.g., daily), 17β-estradiol (E(2); 50.0 μg/kg, s.c., daily), or vehicle for 4 weeks. We found that weight and volume in rats treated with low dose BPA (10 μg/kg) was higher than that of model control, and BPA significantly increased the relative weight of prostate (p < 0.01). For prostate lobes, BPA 10 μg/kg/day significantly increased relative weight of ventral prostate (VP), weight and relative weight of dorsolateral prostate (DLP) (p < 0.05). And histopathology results showed that height of epithelial cell (HEC) of VP and DLP in BPA group were significantly higher than that of model control (p < 0.01). BPA could also decrease testosterone level and increase prostate-specific antigen level. E(2) treatment also showed an obvious effect on relative weight of VP and DLP, HEC, and hormone levels. We concluded that environment exposure to low dose of BPA may induce prostate to proliferate and aggravate testosterone-induced benign hyperplasia prostate in rats.
authors.affiliation: Fudan University, Shanghai, China. wwjh_731@yahoo.com.cn
authors.forename: Jian-Hui
authors.initials: JH
authors.lastname: Wu
authors.forename: Xiu-Rong
authors.initials: XR
authors.lastname: Jiang
authors.forename: Gui-Ming
authors.initials: GM
authors.lastname: Liu
authors.forename: Xiang-Yun
authors.initials: XY
authors.lastname: Liu
authors.forename: Gui-Lin
authors.initials: GL
authors.lastname: He
authors.forename: Zu-Yue
authors.initials: ZY
authors.lastname: Sun
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001559:Benzhydryl Compounds; D013196:Dihydrotestosterone / Q000097:blood; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000008:administration & dosage / Q000633:toxicity*; D004847:Epithelial Cells / Q000187:drug effects / Q000473:pathology; D004958:Estradiol / Q000097:blood; D004968:Estrogens, Non-Steroidal / Q000008:administration & dosage / Q000633:toxicity*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010636:Phenols / Q000008:administration & dosage / Q000633:toxicity*; D011388:Prolactin / Q000097:blood; D011467:Prostate / Q000187:drug effects* / Q000473:pathology; D017430:Prostate-Specific Antigen / Q000097:blood; D011470:Prostatic Hyperplasia / Q000097:blood / Q000139:chemically induced* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D013739:Testosterone / Q000097:blood / Q000633:toxicity; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D013196:Dihydrotestosterone; D052244:Endocrine Disruptors; D004958:Estradiol; D004968:Estrogens, Non-Steroidal; D010636:Phenols; D011388:Prolactin; D017430:Prostate-Specific Antigen; D013739:Testosterone; C006780:bisphenol A; D000098826:Bisphenol A Compounds