Oxidative and nitrosative stress in mitochondrial of rat kidney during experimental diabetes mellitus

Abstract

Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia. Within the affected population most of the people are in the adult age. The diabetic nephropathy is characterized by patho‐physiological events, which stimulate and repress the production of nitric oxide (NO). The NO is able to react with metalloproteins that contains hemo groups. Veelken (2000) tested that renal vasodilatation mediated by NO is due to endothelial constitutive nitric oxide synthase activity and contributed to hyperfiltration and renal injury in diabetic rats. The respiratory chain is the main generating source of ROS in mitochondria of mammals at level of complexes I and III. Many evidences exist in where oxidative stress is implied in the etiology of several diabetic complications. Our interest is in the pathophysiologic role of the mitochondrial NO, and its narrow relation with oxidative and nitrosative stress during hyperglycemia. Our results showed a significant increase of NO in rat kidney mitochondrial with 1 and 6 weeks after having injected with streptozotocin, respect to the control rats. While in the week 9 no significant differences were observed. Our results also note that it has been an increase in the degree of lipoperoxidation in rats with 1, 6 and 9 weeks of hyperglycemia, respect to control. Oxidative and nitrosative stress in experimental DM affected rat kidney mitochondria. Supported by Fondos Mixtos CONACYT‐ Gob. Edo. de Michoacán (64277, 64308), COECYT and CIC‐UMSNH (2.16) grants.