Abstract

Diabetes mellitus, a metabolic disorder characterized by chronic hyperglycemia, exerts broad systemic effects that 
extend beyond glucose dysregulation. Central to these effects is an imbalance between reactive oxygen species 
(ROS) production and the body’s antioxidant defense systems, leading to persistent oxidative stress. In diabetic 
conditions, increased ROS generation arises from glucose auto-oxidation, mitochondrial dysfunction, activation of 
alternative metabolic pathways, and formation of advanced glycation end products (AGEs), while antioxidant 
networks such as superoxide dismutase, catalase, glutathione peroxidase, and non-enzymatic antioxidants are 
simultaneously compromised. This redox imbalance contributes to cellular and molecular damage, impairs immune 
surveillance by disrupting innate and adaptive immune responses, and undermines tissue integrity through 
endothelial dysfunction, chronic inflammation, and genomic instability. Moreover, oxidative stress accelerates 
diabetic complications such as neuropathy, nephropathy, retinopathy, and macrovascular disease. Understanding 
these mechanisms has profound implications for prevention, early detection, and therapeutic interventions. 
Emerging strategies aimed at restoring antioxidant capacity and modulating immune function may mitigate the 
progression of diabetic complications.