title: Exposure to ethinylestradiol during prenatal development and postnatal supplementation with testosterone causes morphophysiological alterations in the prostate of male and female adult gerbils.
abstract: Steroids perform significant functions in prostatic development and growth, so that interferences of this equilibrium may predispose the gland to the development of diseases during the life. Embryonic and neonatal exposure to xenoestrogens, many of them with endocrine-disrupting potential, has been related to the induction of disturbances in reproductive system organs. Thus, this study aimed to analyse morphological and immunocytochemical aspects of prostate in both male and female adult gerbils either exposed to ethinylestradiol during the prenatal phase (pregnant females received 10 μg/kg, by gavage) (EE group) or exposed to testosterone (1 mg/kg) during the postnatal period (EE/T group). Serological analysis revealed a rise in estradiol levels in adult males and females of the EE group. A higher incidence of prostatic intraepithelial neoplasia (PIN) was observed in the male and female prostate of the treated groups, besides an increase in collagen and reticular fibres. Immunocytochemistry showed an increase in prostatic epithelial cells immunoreactive to AR and a presence of a smooth muscle layer, evidenced by α actin, in injured regions this way absent in prostatic epithelial buds. These pieces of evidence suggest that the alterations verified in the prostate in adulthood of both sexes may be due to the high oestrogen levels. Either males or females of the EE/T group showed normalized estradiol levels, although prostatic lesions could be observed. While the prostatic gland of male gerbils was more affected than the female prostate, this study showed that the exposure to EE during this critical period of development disrupts the prostate of both sexes in terms of prostatic lesions.
authors.affiliation: Graduate Program in Cell and Structural Biology, Institute of Biology, Campinas State University, UNICAMP, Campinas, SP, Brazil.
authors.forename: Ana Paula Silva
authors.initials: AP
authors.lastname: Perez
authors.forename: Manoel Francisco
authors.initials: MF
authors.lastname: Biancardi
authors.forename: Rejane Maira
authors.initials: RM
authors.lastname: Góes
authors.forename: Fernanda Alcântara
authors.initials: FA
authors.lastname: dos Santos
authors.forename: Sebastião Roberto
authors.initials: SR
authors.lastname: Taboga
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002467:Cell Nucleus / Q000187:drug effects / Q000473:pathology; D004359:Drug Therapy, Combination; D004958:Estradiol / Q000097:blood; D004997:Ethinyl Estradiol / Q000097:blood / Q000633:toxicity*; D005260:Female; D005849:Gerbillinae; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011467:Prostate / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D019048:Prostatic Intraepithelial Neoplasia / Q000209:etiology / Q000473:pathology; D011471:Prostatic Neoplasms / Q000209:etiology / Q000473:pathology; D012737:Sex Factors; D013739:Testosterone / Q000633:toxicity*
chemical_list: D013739:Testosterone; D004997:Ethinyl Estradiol; D004958:Estradiol