ESTRÉS OXIDATIVO EN MUJERES POSTMENOPÁUSICAS CON HIPERCOLESTEROLEMIA

FURLÁN MS; ZIRULNIK F; GATICA LV; FORNERIS ML; GIMÉNEZ MS

Potrero de los Funes- San Luis (Argentina)

Congreso; XXIV Reunión Anual de la Sociedad de Biología de Cuyo; 2006

Sociedad de Biología de Cuyo

Estrogens exert a direct atheroprotective action on blood vessels, and indirect action on lipid metabolism. In menopause, the estradiol deficit predisposes to hypercholesterolemia, which originates endothelial dysfunction by increasing oxidative stress and reducing of vascular NO bioavailability enhancing the atherosclerotic process. The aim of this study was to determine whether the hypercholesterolemia in menopause induces oxidative stress, alters endothelial function and modifies paroxonasa enzyme activity (PON1) which has antioxidant capacity. 37 postmenopausal women with hypercholesterolemia (HPW) and 39 normocholesterolemic postmenopausal women (NPW) were studied. In hypercholesterolemic women: total cholesterol, LDL-c and TBARS levels were increased (P < 0.0001), and the nitrite levels decreased (P < 0.0001) in relation to NPW group. PON1 activity, HDL-c,  stradiol and androstenedione levels were similar in both groups. Total cholesterol and LDL-c were positively correlate with TBARS (P < 0.0001), and negatively with nitrite (P < 0.0001; P = 0.001, respectively). TBARS and nitrite were inversely correlated (P = 0.006). These results suggest that the increase of oxidative stress is associated to hypercholesterolemia and the decrease of NO to the oxidative stress imposed on the endothelium.