Diabetes mellitus is a chronic metabolic disorder marked by persistent hyperglycemia due to impaired insulin production, insulin resistance, or both. Type 1 diabetes results from autoimmune destruction of pancreatic β-cells, while Type 2 diabetes, the most prevalent form, is associated with insulin resistance and relative insulin deficiency. The global burden of diabetes is rising sharply, particularly in developing nations, driven by sedentary lifestyles and unhealthy dietary patterns. Chronic hyperglycemia in diabetes leads to a spectrum of complications, including retinopathy, nephropathy, neuropathy, and cardiovascular diseases. A central mechanism linking diabetes to its complications is oxidative stress—a state where excessive reactive oxygen species (ROS) overwhelm the body’s antioxidant defenses. While ROS are integral to normal cellular signaling, their overproduction damages lipids, proteins, and DNA, contributing to insulin resistance, β-cell dysfunction, and inflammation. Mitochondrial dysfunction and activation of enzymes like NADPH oxidases further exacerbate ROS generation. Antioxidant systems, both enzymatic and non-enzymatic, attempt to maintain redox balance, but are often insufficient in diabetes. Understanding the complex interplay between oxidative stress and diabetes pathophysiology is critical for developing novel therapeutic strategies. Targeting oxidative stress through antioxidants or modulation of mitochondrial function holds promise in improving insulin sensitivity and reducing diabetic complications.