Role of SOD and GPx in Mitigating Oxidative Stress in Streptozotocin-Induced Diabetic Rats

Abstract

Diabetes mellitus is a chronic disease characterized by an increase in blood glucose levels, which leads to oxidative stress as a consequence. Streptozotocin works by damaging pancreatic beta cells, resulting in hyperglycemia. This chronic hyperglycemia can increase the production of free radicals. Moreover, streptozotocin can cause significant oxidative stress by damaging cellular DNA, lipids, and proteins. The excessive free radicals can deplete antioxidant reserves like SOD and GPx, as they are utilized to neutralize the free radicals. The aim of this study is to understand the role of SOD and GPx in reducing oxidative stress in streptozotocin-induced diabetic rats. Spectrophotometric analysis was utilized to quantify SOD and GPx levels in rat tissues, providing insights into the extent of oxidative damage. The results revealed that while the levels of SOD showed no significant difference after streptozotocin induction, but there was a noticeable decrease in SOD levels. In contrast, GPx levels decreased significantly following induction. In conclusion, this study underscores the relevance of monitoring SOD and GPx levels as biomarkers for assessing oxidative stress in diabetic conditions and guiding therapeutic interventions.