This review explores the role of oxidative stress in Parkinson's disease (PD) and its potential as a therapeutic target. PD is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor and non-motor symptoms. Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is implicated in the pathogenesis of PD. Key contributors to oxidative stress include mitochondrial dysfunction, neuroinflammation, and environmental factors. ROS accumulation leads to oxidative damage to DNA, proteins, and lipids, contributing to neuronal death. Mitochondrial dysfunction is a central factor in PD, with complex I deficiencies in the mitochondrial respiratory chain being a major cause of ROS overproduction. Genes such as Parkin, PINK1, and DJ-1 are closely associated with oxidative stress and mitochondrial dysfunction in PD. Additionally, iron accumulation in the substantia nigra is linked to oxidative stress and neuronal damage. Neuroinflammation, driven by microglial and astrocytic activation, further exacerbates oxidative stress and neuronal loss. Antioxidant therapies, including vitamins, coenzyme Q10, and phytochemicals, are being investigated as potential treatments for PD. However, challenges remain in delivering antioxidants effectively to the brain and in identifying biomarkers for oxidative stress. While some antioxidant compounds show promise in preclinical studies, clinical trials have yielded mixed results, highlighting the need for further research to determine their efficacy and safety. The review also discusses the potential of nanocarriers and exosomes for targeted delivery of antioxidants to the brain, aiming to reduce oxidative stress and mitochondrial impairment in PD. Despite the complexity of PD, oxidative stress remains a promising therapeutic target, with ongoing research aimed at developing new strategies to prevent and treat the disease.This review explores the role of oxidative stress in Parkinson's disease (PD) and its potential as a therapeutic target. PD is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor and non-motor symptoms. Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is implicated in the pathogenesis of PD. Key contributors to oxidative stress include mitochondrial dysfunction, neuroinflammation, and environmental factors. ROS accumulation leads to oxidative damage to DNA, proteins, and lipids, contributing to neuronal death. Mitochondrial dysfunction is a central factor in PD, with complex I deficiencies in the mitochondrial respiratory chain being a major cause of ROS overproduction. Genes such as Parkin, PINK1, and DJ-1 are closely associated with oxidative stress and mitochondrial dysfunction in PD. Additionally, iron accumulation in the substantia nigra is linked to oxidative stress and neuronal damage. Neuroinflammation, driven by microglial and astrocytic activation, further exacerbates oxidative stress and neuronal loss. Antioxidant therapies, including vitamins, coenzyme Q10, and phytochemicals, are being investigated as potential treatments for PD. However, challenges remain in delivering antioxidants effectively to the brain and in identifying biomarkers for oxidative stress. While some antioxidant compounds show promise in preclinical studies, clinical trials have yielded mixed results, highlighting the need for further research to determine their efficacy and safety. The review also discusses the potential of nanocarriers and exosomes for targeted delivery of antioxidants to the brain, aiming to reduce oxidative stress and mitochondrial impairment in PD. Despite the complexity of PD, oxidative stress remains a promising therapeutic target, with ongoing research aimed at developing new strategies to prevent and treat the disease.