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Updated: Jul 18, 2025

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Involvement of antioxidant enzymes in Parkinson's disease
Amir Tahavvori1, Morad Kohandel Gargari2, Yalda Yazdani3
1M, D, Internal Department, Urmia University of Medical Sciences, Urmia, Iran.
Abstract:
Similar to many other diseases, the etiology of Parkinson's disease (PD) is multifactorial and includes both genetic and environmental factors. Exposure to pesticides and the production of reactive oxygen species (ROS) in the body, mainly in electron transporter complexes 1 and 2 in the inner mitochondrial membrane, are two primary environmental risk factors for this disease. Increased accumulation of ROS and oxidative stress (OS) trigger a series of reactions that can lead to the aggregation of misfolded proteins, DNA damage, autophagy, and apoptosis, which may adversely affect cell function. These processes cause diseases such as coronary artery disease (CAD), Alzheimer's disease (AD), and PD. As indicated in previous studies, ROS is considered a critical regulator in the progression of PD. The human body contains several antioxidant molecules, such as vitamin A, vitamin C, bilirubin, and uric acid, as well as antioxidant enzymes including paraoxonase (PON), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). Therefore, based on the canonical function of the antioxidant enzymes in PD, In the present review, we attempted to examine the function of antioxidant enzymes in PD.
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