INTERPLAY BETWEEN OXIDATIVE STATUS AND ERYTHROCYTE FRAGILITY IN AGED SHR RATS SUBJECTED TO CHRONIC STRESS.

SEVASTEI VIANEL; BINOTTI SILVANA; FARIAS MARCOS

Merlo

Congreso; XXXV Reunión científica anual de la sociedad de Biología de Cuyo; 2017

sociedad de Biología de Cuyo

Plasma membrane fluidity modifications affect the receptors activity, enzymes and ion exchangers, altering cellular ionic homeostasis. Stress hormones and oxidative status could interact with erythrocyte membranes, impairing their elasticity and microviscosity. This can affect erythrocytedeformability and its passage through the capillaries, increasing their fragility. Oxidative status and stress reactivity rise with age. In this work we evaluate oxidative status and erythrocyte fragility in response to chronic stress in old spontaneously hypertensive rats (SHR). Control (n=6) and stressed (n=6, movement restriction, 1 h/day, 3 times/week /45 days) male SHR rats of 12 months of age were used. Erythrocyte osmotic fragility, hemogram, corticosterone, glycemia, malondialdehyde, total antioxidant capacity and bilirubin plasma levels were determined. Superoxide dismutase (SOD) and catalase (CAT) activity and total nitrites (NOx) levels were measured in the erythrocyte cytosolic fraction. In the membrane fraction, malondialdehyde, carbonyls levels and ATPase activity were determined. Increased corticosterone, glycemia, conjugated and total bilirubin and reduced plasma antioxidant capacity in stressed rats were observed. Lower CAT activity and NOx levels and increase in SOD activity in cytosolic fraction were found. In membrane fraction, stress increased carbonyls and MDA and decreased ATPase activity. These changes could affect erythrocyte deformability and be responsible for the greater erythrocyte fragility found in stressed rats. Chronic stress in hypertensive individuals would cause changes in erythrocyte functionality, ionic imbalance and increased osmotic fragility, which may contribute to the development of microvascular complications.