Oxidative stress is a key factor in the pathogenesis of Parkinson's disease (PD), contributing to both the initiation and progression of the neurodegenerative disorder. PD is characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor symptoms such as tremor, rigidity, and bradykinesia. Oxidative stress arises from the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which damage cellular components, including lipids, proteins, and DNA. In PD, oxidative stress is linked to the formation of Lewy bodies and neuroinflammation, which exacerbate neuronal damage. Experimental models, such as the MPTP mouse model, show that oxidative stress can directly or indirectly kill dopaminergic neurons by activating cell death pathways. However, oxidative stress is not the sole contributor to neuronal death, as other factors, including genetic mutations and neuroinflammation, also play roles. The complex nature of PD suggests that a multifactorial approach may be necessary for effective treatment. Antioxidants, such as vitamin E and coenzyme Q10, have been tested in clinical trials, but their efficacy has been limited. This review highlights the importance of understanding oxidative stress in PD, including its sources, mechanisms, and potential therapeutic targets. It also emphasizes the need for further research to clarify the role of oxidative stress in PD and to develop more effective treatments.Oxidative stress is a key factor in the pathogenesis of Parkinson's disease (PD), contributing to both the initiation and progression of the neurodegenerative disorder. PD is characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor symptoms such as tremor, rigidity, and bradykinesia. Oxidative stress arises from the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which damage cellular components, including lipids, proteins, and DNA. In PD, oxidative stress is linked to the formation of Lewy bodies and neuroinflammation, which exacerbate neuronal damage. Experimental models, such as the MPTP mouse model, show that oxidative stress can directly or indirectly kill dopaminergic neurons by activating cell death pathways. However, oxidative stress is not the sole contributor to neuronal death, as other factors, including genetic mutations and neuroinflammation, also play roles. The complex nature of PD suggests that a multifactorial approach may be necessary for effective treatment. Antioxidants, such as vitamin E and coenzyme Q10, have been tested in clinical trials, but their efficacy has been limited. This review highlights the importance of understanding oxidative stress in PD, including its sources, mechanisms, and potential therapeutic targets. It also emphasizes the need for further research to clarify the role of oxidative stress in PD and to develop more effective treatments.