title: Pre-natal exposure of mice to bisphenol A elicits an endometriosis-like phenotype in female offspring.
abstract: Endometriosis is a chronic gynecological disease characterized by the growth of endometrial tissue outside the uterine cavity. Exposure to endocrine disruptors during critical period of development causes long-lasting effects, being the genital system one of the targets. This study describes the effects on female genital system caused by developmental exposure to the endocrine-disrupting chemical bisphenol A (BPA) during pre- and peri-natal development in mice. To this end, timed pregnant Balb-C mice were treated from day 1 of gestation to 7 days after delivery with BPA (100, or 1000 microg/kg/day). After delivery, pups were held for 3 months; then, pelvic organs were analyzed in their entirety and livers of both pups and moms were studied for the presence of BPA. We found in the adipose tissue surrounding the genital tracts of a consistent number of treated animals, endometriosis-like structure with the presence of both glands and stroma and expressing both estrogen receptor and HOXA-10. Moreover, cystic ovaries, adenomatous hyperplasia with cystic endometrial hyperplasia and atypical hyperplasia were significantly more frequent in treated animals respect to the controls. Finally, BPA was found in the livers of exposed moms and female offspring. In conclusion, we describe for the first time an endometriosis-like phenotype in mice, elicited by pre-natal exposition to BPA. This observation may induce to thoroughly reconsider the pathogenesis and treatment of endometriosis, considering the high incidence of endometriosis and the problems caused by associated infertility.
authors.affiliation: Fondazione Italiana Endometriosi, Rome, Italy.
authors.forename: Pietro G
authors.initials: PG
authors.lastname: Signorile
authors.forename: Enrico P
authors.initials: EP
authors.lastname: Spugnini
authors.forename: Luigi
authors.initials: L
authors.lastname: Mita
authors.forename: Pasquale
authors.initials: P
authors.lastname: Mellone
authors.forename: Alfredo
authors.initials: A
authors.lastname: D'Avino
authors.forename: Mariangela
authors.initials: M
authors.lastname: Bianco
authors.forename: Nadia
authors.initials: N
authors.lastname: Diano
authors.forename: Lucia
authors.initials: L
authors.lastname: Caputo
authors.forename: Francesca
authors.initials: F
authors.lastname: Rea
authors.forename: Rosa
authors.initials: R
authors.lastname: Viceconte
authors.forename: Marianna
authors.initials: M
authors.lastname: Portaccio
authors.forename: Emanuela
authors.initials: E
authors.lastname: Viggiano
authors.forename: Gennaro
authors.initials: G
authors.lastname: Citro
authors.forename: Riccardo
authors.initials: R
authors.lastname: Pierantoni
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Sica
authors.forename: Bruno
authors.initials: B
authors.lastname: Vincenzi
authors.forename: Damiano G
authors.initials: DG
authors.lastname: Mita
authors.forename: Feliciano
authors.initials: F
authors.lastname: Baldi
authors.forename: Alfonso
authors.initials: A
authors.lastname: Baldi
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds; D004715:Endometriosis / Q000139:chemically induced* / Q000209:etiology* / Q000378:metabolism; D005260:Female; D005836:Genitalia, Female / Q000187:drug effects / Q000196:embryology; D007150:Immunohistochemistry; D051379:Mice; D008807:Mice, Inbred BALB C; D010636:Phenols / Q000008:administration & dosage / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D014599:Uterus / Q000187:drug effects / Q000196:embryology; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds