Diabetic neuropathy is a frequent and debilitating consequence of diabetes mellitus, characterised by chronic hyperglycaemia-induced nerve damage. The pathophysiology of diabetic neuropathy is significantly influenced by oxidative stress, as demonstrated by recent investigations. Oxidative stress, which is brought on by an imbalance among the production of reactive oxygen species (ROS) and the antioxidant protective mechanisms, damages cells and tissues. When diabetic neuropathy is present, elevated glucose levels promote an excessive release of ROS, which leads to inflammation, apoptosis, and mitochondrial dysfunction. Furthermore, oxidative stress sets up inflammatory pathways that exacerbate neuronal damage by activating microglia and releasing cytokines that promote inflammation. These mechanisms work together to cause the sensory and motor abnormalities seen in diabetes patients as well as neurodegenerative disorders including Alzheimer’s, Parkinson’s, and diabetic neuropathy. Potential treatment targets can be identified by comprehending the molecular pathways via which oxidative stress affects neuronal damage. To slow the course of diabetic neuropathy, antioxidant therapy that lower ROS levels and strengthen endogenous antioxidant defences are being investigated. Larger-scale preclinical as well as clinical studies of biological indicators of oxidative stress and to provide more dependable and therapeutically relevant outcomes in this sector, therapies are needed.