Abstract
The objective of this study was to evaluate the role of oxidative stress in an experimental model of streptozotocin-induced diabetic nephropathy in rats. Wistar, adult, male rats were used in the study. Animals were divided in the following groups: Citrate (control, citrate buffer 0.01M, pH 4.2 was administrated intravenously - i.v - in the caudal vein), Uninephrectomy+Citrate (left uninephrectomy-20 days before the study), DM (streptozotocin, 65 mg/kg, i.v, on the 20th day of the study), Uninephrectomy+DM. Physiological parameters (water and food intake, body weight, blood glucose, kidney weight, and relative kidney weight); renal function (creatinine clearance), urine albumin (immunodiffusion method); oxidative metabolites (urinary peroxides, thiobarbituric acid reactive substances, and thiols in renal tissue), and kidney histology were evaluated. Polyphagia, polydipsia, hyperglycemia, and reduced body weight were observed in diabetic rats. Renal function was reduced in diabetic groups (creatinine clearance, p < 0.05). Uninephrectomy potentiated urine albumin and increased kidney weight and relative kidney weight in diabetic animals (p < 0.05). Urinary peroxides and thiobarbituric acid reactive substances were increased, and the reduction in thiol levels demonstrated endogenous substrate consumption in diabetic groups (p < 0.05). The histological analysis revealed moderate lesions of diabetic nephropathy. This study confirms lipid peroxidation and intense consumption of the antioxidant defense system in diabetic rats. The association of hyperglycemia and uninephrectomy resulted in additional renal injury, demonstrating that the model is adequate for the study of diabetic nephropathy.
Highlights
A n estimation by the World Health Organization considers that by 2030, approximately 366 million people will be diagnosed as carriers of diabetes mellitus (DM) all over the world, with an increase in mortality and morbidity rates due to complications of the disease [1]
Glomerular dysfunction is observed as microalbuminuria caused by changes in renal structure, such as thickening of the basal membrane, podocyte lesions, expansion of the mesangial matrix, which evolve to glomerular sclerosis and tubulointerstitial fibrosis associated with reduced glomerular filtration rates (GFR) [3,4]
Nx showed significant increase in kidney weight when compared with animals that were not subjected to nephrectomy (p < 0.05); and the kidney/animal weight ration showed a significant difference between the nephrectomy group and the DM one (p < 0.05)
Summary
A n estimation by the World Health Organization considers that by 2030, approximately 366 million people will be diagnosed as carriers of diabetes mellitus (DM) all over the world, with an increase in mortality and morbidity rates due to complications of the disease [1]. Microvascular changes are the main consequence of chronic hyperglycemia and lead to an imbalance in cell metabolism, with progressive lesions in several organs, such as kidneys, eyes, nerves, liver, and the vascular, immunological and gastrointestinal systems [2,3]. Diabetic nephropathy is a progressive disease that involves several mechanisms, with changes in glomerular hemodynamics, causing renal lesions, oxidative stress, inflammatory response, and fibrosis. The cumulative results of these transformations are caused by excess production of reactive oxygen species (ROS) mediated by chronic hyperglycemia. ROS generation in diabetic kidneys is caused by enzymatic and non-enzymatic systems that include glucose autooxidation, Fenton reaction catalyzed by unbound iron, and consumption of the endogenous antioxidant reserve. Production of reactive nitrogen species, such as nitric oxide radicals (NO) is important [5]
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