HYPERANDROGENISM: APOPTOSIS & OXIDATION ON FOLLICULOGENESIS

LEANDRO MARTIN VELEZ; ALICIA BEATRIZ MOTTA

Chascomus

Congreso; XVI Jornadas Anuales de la SAB; 2014

SAB

Polycystic ovary syndrome (PCOS) is a heterogeneous disease responsible for infertility in women. Both ovarian apoptotic-antiapoptotic pathway and oxidant/antioxidant balance is related to infertility. Here, we propose to study whether hyperandrogenism alters ovarian follicular development by assessing apoptosis-related pathway: BCL2 (anti-apoptotic) and BAX (pro-apoptotic), lipid peroxidation (LPO) and the anti-oxidant glutathione (GSH) content. We used a PCOS model developed in rats by subcutaneous administration of dehydroepiandrosterone (DHEA). Immature Sprague Dawley rats were injected with vehicle (Control group), equine chorionic gonadotropin (eCG group) to induce folliculogenesis, or eCG plus DHEA to induce folliculogenesis and hyperandrogenism (group eCG+HA). We found that gene and protein expression of BCL2 increased whereas those corresponding to BAX decreased in groups eCG and eCG+HA versus Control. In addition, the BAX/BCL2 ratio decreased in eCG group versus eCG+HA and Control. The GSH content decreased and LPO increased in eCG+HA group versus eCG and Control. We conclude that both the ovarian apoptosis and the oxidant/antioxidant balance are altered in the PCOS rat model, and that alterations could affect normal ovarian folliculogenesis.