The role of oxidative stress in streptozotocin-induced diabetic nephropathy in rats

Abstract

Objective: The objective of this study was to evaluate the role of oxidative stress in an experimental model of streptozotocin-induced diabetic nephropathy in rats. Materials and methods: 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 20 th 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 evalua ted. Results: 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. Conclusion: 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. Arch Endocrinol Metab. 2016;60(5):443-9

Lovastatin Alleviates Endothelial-to-Mesenchymal Transition in Glomeruli via Suppression of Oxidative Stress and TGF-β1 Signaling

“…Reactive oxygen species exerts an important effect in the development of DN (Fernandes et al, 2016). Chronic hyperglycemia-induced oxidative stress is considered the most important factor in TGF-β1 production, which can lead to renal injury and interstitial fibrosis (Forbes et al, 2008).…”

The Effect of Nano-Epigallocatechin-Gallate on Oxidative Stress and Matrix Metalloproteinases in Experimental Diabetes Mellitus

“…Pretreatment with EGCG and L-EGCG induced protection against STZ toxic effects, as demonstrated by reduction of oxidative stress parameters (Table 1, Figure 1) and by enhancement of antioxidant defense (Table 1, Figure 2), with best results for the liposomal form. STZ-induced diabetes in experimental models is followed by an enhanced production of reactive oxygen species (ROS) and consumption of cell antioxidant systems, as a consequence of necrotic and apoptotic degeneration of pancreatic β cells [66,67]. Hyperglycemia itself is another factor generating intracellular ROS [68].…”

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“…In addition, renal MAO-A activity showed a linear correlation with proteinuria (Figure 4). [1][2][3][4][5][6][7]. Free reactive oxygen species are produced continuously under physiological and pathological conditions as a result of metabolism and are balanced by the body's antioxidant defense systems.…”

“…Physiopathological mechanisms of DN is not fully understood and the reason why not all diabetic patients develop this complication is unknown. The underlying mechanisms which contribute to the evolution of DN are extremely complex, and metabolic, genetic, and several hemodynamic factors have been identified [5]. Among the metabolic factors, ROS are thought to play an important role in the development of DN [6].…”