Effect of streptozotocin on glutathione and lipid peroxide levels in various tissues of rats

In this study, the effect of streptozotocin (STZ) on lipid peroxidation and glutathione (GSH) content was investigated in the liver, pancreas and kidney of rats. Lipid peroxide levels were significantly increased in homogenates and mitochondrial fractions of the liver, kidney acid pancreas after STZ administration. GSH levels in hepatic acid pancreatic tissues were decreased but unchanged in the kidney of diabetic rats. GSH content in hepatic mitochondrial fraction was also decreased compared to control group. On the other hand, the destruction of pancreatic beta-cells was also observed histopathologically. Our results indicate that oxidative stress may play an important role in STZ induced diabetes and mitochondrial fraction may be the target in this toxicity

Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

Given their essential function in aerobic metabolism, mitochondria are intuitively of interest in regard to the pathophysiology of diabetes. Qualitative, quantitative, and functional perturbations in mitochondria have been identified and affect the cause and complications of diabetes. Moreover, as a consequence of fuel oxidation, mitochondria generate considerable reactive oxygen species (ROS). Evidence is accumulating that these radicals per se are important in the pathophysiology of diabetes and its complications. In this review, we first present basic concepts underlying mitochondrial physiology. We then address mitochondrial function and ROS as related to diabetes. We consider different forms of diabetes and address both insulin secretion and insulin sensitivity. We also address the role of mitochondrial uncoupling and coenzyme Q. Finally, we address the potential for targeting mitochondria in the therapy of diabetes. Antioxid. Redox Signal. 12, 537–577