CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Changes in serum corticosterone levels and adrenal cortex nitric oxide synthase activity in streptozotocin-diabetic rats: involvement of oxidative stress
Autor/es:
REPETTO EM; CIPELLI JM; SANCHEZ R; ASTORT F; MARTINEZ CALEJMAN C; DI GRUCCIO JM; PIROLI GG; ARIAS P; CYMERYNG CB
Lugar:
Roma (Italia)
Reunión:
Congreso; 44th Annual Meeting of the EASD; 2008
Institución organizadora:
European Association for the Study of Diabetes (EASD)
Resumen:
Background/Aim: Increased oxidative stress has been associated with the pathogenesis of a variety of chronic diabetic complications. Multiple biochemical mechanisms have been proposed to increase oxidative stress in diabetes. The aim of the present study was to evaluate different parameters of oxidative stress and its role in the induction of nitric oxide synthase (NOS) activity in the adrenal cortex of streptozotocin (STZ) treated rats. Materials and Methods: Animals: male Wistar rats were treated with STZ (40 mg/kg ip in three consecutive days). A group of animals were subjected to antioxidant treatment (melatonin 7.5 mg/kg or á-tocopherol 100 mg/kg, vo). Thiobarbituric acid-reactive substances (TBARS; an index of lipid peroxidation), HO-1 expression, superoxide dismutase (SOD), catalase and NOS activities, and reduced glutathione (GSH) levels were determined adrenal cortex homogenates. Results: Hyperglycaemia was accompanied by a significant increase in tissue TBARS levels after 4 weeks of treatment. NOS activity was increased from the second to the 8th week of treatment. GSH and antioxidant enzyme activities (HO-1, SOD and catalase) were increase by 4-8 weeks. Antioxidant treatment reduced TBARS levels and prevented the increase in HO-1 and NOS activity. Conclusions: Our results suggest that increased oxidative stress in the adrenal cortex of STZ-treated rats is associated with the increase in NOS activity. Upregulation of HO-1, SOD and catalase activities are probably involved in cytoprotective mechanisms triggered by the production of reactive oxygen or nitrogen species or by other parameters of cell damage associated with this disease.