Search

Introduction: Oxidative stress has a well-known role in diabetic nephropathy, and mitochondria are the major source of reactive oxygen species production. This study aimed to assess the effect of tempol, a superoxide dismutase mimetic agent, on mitochondrial antioxidant enzymes and cell viability in diabetic nephropathy., Materials and Methods: Adult male Wistar rats were divided into 4 groups of 7 animals. Diabetes mellitus was induced by injection of streptozotocin in 2 groups, the rat in one of which were also treated with tempol for 4 weeks. Another group without diabetes mellitus received tempol, and the last group was the control. At the end of the treatment period, the kidney mitochondria were isolated and their antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, and catalase were assessed. Malondialdehyde, total antioxidant capacity, and kidney cells viability were studied, as well., Results: The diabetic group was significantly different compared with the control group in malondialdehyde, catalase, and glutathione peroxidase activities. Superoxide dismutase and total antioxidative capacity did not show any significant differences among the four groups. Moreover, the diabetic group treated with tempol had significantly different glutathione peroxidase level and kidney cells viability, compared to the other diabetic group (P < .05) Conclusions. Diabetic nephropathy induces changes in mitochondrial antioxidative biomarkers and cells viability, some of which can be modified by tempol administration in rats.

Background: One of common mechanisms in pathophysiology of chronic kidney diseases is epithelial-mesenchymal transition (EMT). On the other hand oxidative stress has been known to participate in kidney damage of diabetic nephropathy (DN)., Objectives: We studied if tempol, a well-known antioxidant agent, can ameliorate EMT in DN induced in male rats., Materials and Methods: Twenty-seven male rats were equally divided in to 4 groups. Group I (control or C), group II (diabetic or D), group III (T) rats which was given tempol (100 mg/kg/day) by gavages for 28 days and group IV (D&T) was diabetic rats that also received same dose of tempol. After treatment, their kidneys were studied by immunohistochemicalstaining., Results: Pathological changes in the kidney were detected concurrently with increasing kidney weight and urinary albumin excretion. In addition, EMT indices, i.e. decline of E-cadherin and increase of α SMA staining were significantly emerged in the renal tubular cells of diabetic group and were partially modified in diabetic group which were simultaneously treated by tempol., Conclusions: Tempol can modify, but not significantly, EMT induced by DN.

Introduction: Diabetic nephropathy (DN) is the most common cause of the chronic kidney disease in the world. Oxidative stress on the other hand has a major and well known role in its pathophysiology., Objectives: The aim of the study is to figure out if tempol, a synthetic antioxidant agent, modifies DN and to determine its relevance to changes of serum oxidative biomarkers., Materials and Methods: Twenty-seven male rats were equally divided in to 4 groups (7 rats for each group). Group I (control or C), group II (diabetic or D), groups III (Tempol) which were given tempol (100 mg/kg/day) by gavages for 28 days and group IV (D&T) which includes diabetic rats that also received same dose of tempol. After treatment, blood samples were isolated. Enzymatic scavengers including catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, lipid peroxidation (LPO), total antioxidant capacity (TAC) and total thiol molecules (TTM) were measured. Blood urea nitrogen (BUN), creatinine (Cr) an albumin/Cr ratio were evaluated as well. Statistical differences were assessed with one-way analysis of variance (ANOVA) by SPSS followed by Tukey t test., Results: Oxidative stress biomarkers modified and Alb/Cr ratio increased in diabetic group (II), however, they were altered to normal in group IV (D&T) compared with diabetic group (D)., Conclusion: Tempol can modify oxidative stress biomarkers and presumably nephropathy in diabetic rats.

Endoplasmic reticulum produces folds and exports proteins. There are studies showing the role of endoplasmic reticulum in pathogenesis of diabetic complications including diabetic nephropathy. This article reviews the pathophysiology associated with the role of endoplasmic reticulum in diabetic nephropathy and the therapeutic aspects of this finding.

Diabetic nephropathy is a major cause of end-stage renal disease throughout the world. Elevated oxidative stress in diabetic patients results from overproduction of reactive oxygen species and decreased efficiency of antioxidant defenses. Moreover, diabetes-associated metabolic disorders impair activities of enzymes of the mitochondrial respiratory chain complex. Therefore, oxidative stress is closely related to mitochondrial dysfunction. This paper reviews studies of mitochondrial dysfunction in diabetic nephropathy.

Diabetic nephropathy is the leading cause of chronic kidney disease and end-stage renal disease. Oxidative stress has been recognized as a major contributor to its pathogenesis. Defensive mechanisms have also widely been studied. One of them, the NF-E2-Related Factor 2, is reviewed in this article.