Estresse oxidativo pulmonar em ratos diabéticos submetidos a hiperóxia

Abstract

Oxidative stress is much studied both in the etiology and pathophysiology of chronic diseases, and in the mechanisms involved in triggering them. The hyperglycemia of diabetes is associated with oxidative stress through the production of oxidizing agents, so the purpose of this study was to evaluate the pulmonary oxidative stress in diabetic rats submitted to hyperoxia for 90 minutes. Forty male Wistar rats, (8 weeks of age) were divided into four groups, each containing 10 animals, according to their level of oxygen exposure: the control group (21% oxygen) and the 50%, 75% and 100% oxygen (hyperoxia) groups. In each of the four groups, 5 animals were randomly subjected to induction of diabetes by means of an intraperitoneal injection of streptozotocin (STZ) at a dose of 55 mg/kg. Animals that developed a blood glucose level > 250 mg/dl were considered diabetic. 72 hours after induction of diabetes, there was a significant difference in blood glucose in the experimental groups relative to the control. Malondealdehyde (MDA) - a marker of oxidative stress, is one of the substances that react with thiobarbituric acid (TBA). The quantification of MDA concentration is considered a parameter to evaluate a rate of cellular lipoperoxidation. In the experimental groups there was a significant difference in the concentration of malondialdehyde (MDA) in lung tissue and blood plasma (p<0.05), with the exception of the experimental group exposed to 50% oxygen. In the control groups, significant differences in the MDA concentration present in plasma and lung tissue were also observed (p<0.05), with the exception of animals in the control group exposed to 75% oxygen. The MDA concentration in lung tissue with respect to the diabetic and non-diabetic groups showed a significant difference in the 21% group; however, there was no difference in the 75 and 100% groups. Our results suggest that in diabetic animals high oxygen concentrations (75 or 100%) do not appear to exert deleterious effects on lipid peroxidation in lung tissue.