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.