Oxidative stress is induced by an imbalance in reactive oxygen species (ROS) production and the body’s antioxidant defenses. While ROS serve essential roles in cellular signaling and immunology, their excessive buildup damages DNA, lipids, and proteins, contributing to serious diseases like cancer, neurological disorders, and cardiovascular disease. Oxidative DNA damage, such as strand breakage and 8-hydroxyguanine production, causes genomic instability and increases cancer risk. Lipid peroxidation produces damaging byproducts such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE), which impair membrane integrity and worsen neurological and cardiovascular disorders. Similarly, protein oxidation reduces enzymatic activity, resulting in neurodegeneration in disorders like Alzheimer’s and Parkinson’s disease. ROS production plays a part in cardiovascular diseases by causing endothelial dysfunction, low-density lipoprotein (LDL) oxidation, and nitric oxide (NO) dysregulation, which promotes atherosclerosis, hypertension, and heart failure. Recombinant enzyme treatments, which enhance antioxidant enzyme activity, are a promising technique for combating oxidative stress-related damage. Advances in protein engineering, gene therapy, and nanotechnology have increased enzyme stability, specificity, and targeted delivery. These therapies have potential for treating oxidative stress-related disorders by minimizing cellular damage and restoring equilibrium. However, immunogenicity, high production costs, and regulatory barriers impede their clinical adoption. Future advances in gene-editing technologies such as CRISPR, precision medicine, and bioprocessing developments could improve the efficacy and accessibility of recombinant enzyme therapy. As research advances, these medicines have the potential to transform treatment approaches for oxidative stress-related disorders by providing focused and individualized interventions that improve patient outcomes.