“Metformin is able to restore ovarian cyclicity in hyperandrogenized mice: role of oxidative balance”

SANDER V; PIEHL L; FACORRO G; RUBIN DE CELLIS E; MOTTA AB

Miami

Congreso; The Interamerican Society of Hypertension and the Consortium for Southeastern Hipertensión Control Joint Scientific Sessions; 2007

The Interamerican Society of Hypertension and the Consortium for Southeastern Hipertensión Control

Polycystic ovary syndrome (PCOS), which is characterized by hyperandrogenism, is associated with multiple cardiovascular risk factors, such as hypertension, obesity, insulin resistance and menstrual irregularity. In previous studies we have demonstrated that the hyperandrogenization with dehydroepiandrosterone (DHEA) modified the ovarian steroidogenesis and the estral cycle in prepuberal Balb/c mice. Treatment with metfmormin (Met), an insulin-sensitizing drug, was able to restore these parameters. In view that reactive oxygen species (ROS) are involved in corpus luteum regression; the aim of the present study was to evaluate the effects of DHEA and Met on the oxidative balance during luteolysis.  Prepuberal Balb/c mice were injected i.p with equine chorionic gonadotropin  (eCG:10UI/mouse,day 0) to induce ovulation and formation of corpora lutea that remain functional for 11 days. Mice were treated 24 y 48 hours before euthanasia (day 11): DHEA(sc, 60mg/kg), Met(oral 50mg/kg), DHEA+Met y  control vehicle (Veh), n=10 animals/treatment-assay. In ovarian tissue superoxide dismutase (SOD) and catalase(CAT) activities were studied, the DMPO/°OH  adduct was evaluated by electronic spin resonance (ESR), lipoperoxidation index (LPO) and glutathione formation (GSH) were measured. Serum progesterone (P4) and ovarian prostaglandin F-2alfa(PGF-2a) were quantified by radioimmunoassay (RIA). SOD was increased in DHEA and DHEA+Met(p