title: Prenatal exposure to low doses of bisphenol A alters the periductal stroma and glandular cell function in the rat ventral prostate.
abstract: Environmental estrogens (xenoestrogens) are chemicals that bind to estrogen receptor, mimic estrogenic actions, and may have adverse effects on both human and wildlife health. Bisphenol A (BPA), a monomer used in the manufacture of epoxy resins and polycarbonate has estrogenic activity. In male rodents prenatal exposure to BPA resulted in modifications at the genital tract level. Our objective was to examine the effects of in utero exposure to low, environmentally relevant levels, of the xenoestrogen BPA on proliferation and differentiation of epithelial and stromal cells on the prepubertal rat ventral prostate. To characterize the periductal stromal cells phenotype the expression of vimentin and smooth muscle alpha-actin was evaluated. Androgen receptor (AR) and prostatic acid phosphatase (PAP) expression were also evaluated in epithelial and stromal compartments. Prenatal exposure to BPA increases the fibroblastic:smooth muscle cells ratio and decreases the number of AR-positive cells of periductal stroma of the ventral prostate. In contrast, no differences in AR expression were observed in epithelial cells between control and BPA-treated groups. No changes in proliferation patterns were observed in epithelial and stromal compartments; however, the expression of PAP was diminished in prostate ductal secretory cells of rats in utero exposed to BPA. Our results suggest that prenatal exposure to BPA altered the differentiation pattern of periductal stromal cells of the ventral prostate. These findings are significant in light of the data on human prostate cancers where alterations in the stroma compartment may enhance the invasive and/or malignant potential of the nascent tumor.
authors.affiliation: Laboratorio de Endocrinología y Tumores Hormonodependientes, Faculty of Biochemistry and Biological Sciences, Universidad Nacional del Litoral, 3000 Santa Fe, Argentina.
authors.forename: J G
authors.initials: JG
authors.lastname: Ramos
authors.forename: J
authors.initials: J
authors.lastname: Varayoud
authors.forename: C
authors.initials: C
authors.lastname: Sonnenschein
authors.forename: A M
authors.initials: AM
authors.lastname: Soto
authors.forename: M
authors.initials: M
authors.lastname: Muñoz De Toro
authors.forename: E H
authors.initials: EH
authors.lastname: Luque
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000199:Actins / Q000032:analysis; D000818:Animals; D001559:Benzhydryl Compounds; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D004847:Epithelial Cells / Q000737:chemistry / Q000166:cytology / Q000187:drug effects; D047628:Estrogen Receptor alpha; D004968:Estrogens, Non-Steroidal / Q000008:administration & dosage* / Q000009:adverse effects; D005260:Female; D008297:Male; D010636:Phenols / Q000008:administration & dosage* / Q000009:adverse effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011467:Prostate / Q000166:cytology* / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011944:Receptors, Androgen / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D017154:Stromal Cells / Q000737:chemistry / Q000166:cytology / Q000187:drug effects; D014746:Vimentin / Q000032:analysis; D000098826:Bisphenol A Compounds
chemical_list: D000135:Acid Phosphatase; D000199:Actins; D001559:Benzhydryl Compounds; D047628:Estrogen Receptor alpha; D004968:Estrogens, Non-Steroidal; D010636:Phenols; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D014746:Vimentin; C006780:bisphenol A; D000098826:Bisphenol A Compounds