Interactions between Oxidative Stress and Mitochondrial Dysfunction in Parkinson’s Disease: Potential of Natural Antioxidants

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective degeneration of dopaminergic neurons in the substantia nigra pars compacta, resulting in a spectrum of motor and non-motor symptoms. Among the critical pathological mechanisms in PD, oxidative stress and mitochondrial dysfunction have emerged as significant contributors to neuronal death. Reactive oxygen species (ROS), produced during dopamine metabolism and mitochondrial respiration, lead to oxidative damage, while mitochondrial dysfunction exacerbates energy deficits and disrupts cellular homeostasis. The interplay between these processes engenders a detrimental cycle of neurodegeneration. Recent investigations have concentrated on the potential of antioxidants, including polyphenols, flavonoids, and certain vitamins, for their potential to mitigate both oxidative stress and mitochondrial dysfunction. These compounds exhibit neuroprotective properties by scavenging ROS, preserving mitochondrial integrity, and promoting mitophagy. Notably, antioxidants such as curcumin, resveratrol, and quercetin have demonstrated efficacy in experimental models of PD, reducing ROS levels, restoring mitochondrial function, and preventing neuronal loss. Furthermore, advancements in delivery systems have enhanced the bioavailability of these antioxidants, amplifying their therapeutic potential. This review delves into the dual pathological roles of oxidative stress and mitochondrial dysfunction in PD, elucidating the multifaceted protective effects of natural antioxidants. In this review, we summarize the current literature on natural antioxidants’ role in oxidative stress and mitochondrial dysfunction in PD and discuss possible therapeutic approaches targeting this interaction