CONICET | Buscador de Institutos y Recursos Humanos

UTERINE DERANGEMENTS CAUSED BY PRENATAL HYPERANDROGENISM IN A MURINE MODEL OF POLYCYSTIC OVARIAN SYNDROME.Ferreira SR (1); Goyeneche AA (2), Telleria CM (2), Motta AB (1).(1) Center of Pharmacological and Botanical Studies, University of Buenos Aires, National Scientific and Technical Research Council, Buenos Aires, Argentina; and (2) Department of Pathology, Faculty of Medicine, McGill University, Montreal, QC, Canada.Abstract: Polycystic Ovary Syndrome (PCOS) is the most common androgen-excess disorder, and affects between 5% and 10% of all women at reproductive age. PCOS typically involves the presence of ovarian cysts, oligo or anovulation and androgen excess. The etiology of PCOS remains unknown but prenatal hyperandrogenism is hypothesized as one of the main factors contributing to PCOS. PCOS is associated with several derangements involving inflammation, increased oxidative stress, insulin resistance, and cardiovascular disease.Thus, we aimed to study the impact of prenatal hyperandrogenism on the oxidative and pro-inflammatory status of the rat uterus when adult. By using a PCOS murine model, pregnant Sprague-Dawley rats were prenatally hyperandrogenized (PH) with 1 mg of testosterone. A control (C) group was generated by vehicle injection (vegetable oil). The PH female (N=120) and C (N=80) offsprings were characterized according to the estrous cycle as ovulatory (PHov) or anovulatory (PHanov) phenotypes by collecting vaginal smears from days 45 to 90 (day of sacrifice). We evaluated the proliferative, inflammatory, and oxidative status and studied the glandular morphology of the uterine tissue. Our results showed that PH increased the glandular density of the sub-epithelial and stromal uterine compartments. Lipid peroxidation was significantly increased in the PHanov group when compared with C and PHov groups(p