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Updated: Jun 8, 2025

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Pesticide Exposure and Its Association with Parkinson's Disease: A Case-Control Analysis
Ali Samareh1,2,3, Hossein Pourghadamyari1,3, Mohammad Hadi Nemtollahi1,3
1Applied Cellular and Molecular Research Center, Kerman University of Medical Sciences, Kerman, Iran.
Abstract:
Parkinson's disease (PD) is a complex disorder that arises from genetic and environmental factors. The current investigation endeavors to investigate the role of exposure to organochlorine (OCPs) and organophosphate pesticides (OPPs), recognized as the main environmental elements, in the genesis of PD. In this case-control study, 29 PD patients and 51 healthy subjects were involved. Gas chromatography was performed to measure the serum levels of organochlorine chemicals (2,4-DDT, 4,4-DDT, 2,4-DDE, 4,4-DDE, α-HCH, β-HCH, and γ-HCH). Furthermore, acetylcholinesterase (AChE) activity, arylesterase activity of paraoxonase-1 (PON-1), and several oxidative stress (OS) markers were assessed. The levels of OCPs in the PD patients were significantly higher than in the control subjects. In addition, AChE activity, arylesterase activity of PON-1, catalase activity, and superoxide dismutase 3 activity in PD patients were significantly less than controls. However, the levels of carbonyl protein, total antioxidant capacity, malondialdehyde, and nitric oxide in PD patients were higher than the controls. The findings of this investigation have indicated that OCPs and OPPs exposure could contribute to the development of Parkinson's disease. This potential linkage could either be established through the direct impact of these pesticides on the nervous system, leading to neurotoxicity, or via an indirect route through the triggering of OS.
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