title: Detrimental effects of hyperandrogenism on uterine functions.
abstract: The aim of the present work was to study some of the adverse effects produced by hyperandrogenism on the uterine function. Daily injection of dehydroepiandrosterone (DHEA: 6 mg/ 100 g body weight, sc) for 20 consecutive days induced polycystic ovaries in BALB/c mice. In this model, we found that DHEA produced alterations on uterine histology closely related to the development of tumour structures. In addition, hyperandrogenism induced a pro-inflammatory and a pro-oxidant condition represented by increased levels of prostaglandin F2 alpha production and uterine nitric oxide synthase (NOS) activity and by a decrease in both superoxide dismutase (SOD) and catalase (CAT) activities together with a decrease in the levels of the antioxidant metabolite glutathione (GSH). DHEA also induced an increase in CD4+ together with a decrease in the CD8+ T lymphocytes that infiltrate the uterine tissue. We conclude that this intricate network of regulators could be responsible for the low rate of implantation observed in women with polycystic ovary syndrome.
authors.affiliation: Laboratorio de Fisio-patología Ovárica, (CEFYBO), Universidad de Buenos Aires (UBA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
authors.forename: Evelin
authors.initials: E
authors.lastname: Elia
authors.forename: Susana
authors.initials: S
authors.lastname: Vighi
authors.forename: Eduardo
authors.initials: E
authors.lastname: Lombardi
authors.forename: Alicia Beatriz
authors.initials: AB
authors.lastname: Motta
mesh_terms: D000276:Adjuvants, Immunologic / Q000633:toxicity*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D002374:Catalase / Q000037:antagonists & inhibitors / Q000378:metabolism; D051545:Cyclooxygenase 1 / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000187:drug effects; D003687:Dehydroepiandrosterone / Q000633:toxicity*; D015237:Dinoprost / Q000096:biosynthesis; D005260:Female; D005978:Glutathione / Q000037:antagonists & inhibitors / Q000378:metabolism; D017588:Hyperandrogenism / Q000473:pathology / Q000503:physiopathology*; D008565:Membrane Proteins / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D019001:Nitric Oxide Synthase / Q000187:drug effects / Q000378:metabolism; D010053:Ovary / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D011085:Polycystic Ovary Syndrome / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D011458:Prostaglandins E / Q000096:biosynthesis; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000378:metabolism; D014599:Uterus / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000276:Adjuvants, Immunologic; D008565:Membrane Proteins; D011458:Prostaglandins E; D003687:Dehydroepiandrosterone; D015237:Dinoprost; D002374:Catalase; D019001:Nitric Oxide Synthase; C077623:Ptgs2 protein, mouse; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496512:Ptgs1 protein, mouse; D013482:Superoxide Dismutase; D005978:Glutathione