Rotenone, Paraquat, and Parkinson’s Disease
By C. Tanner, F. Kamel, G. Ross, J. Hoppin, M. Samuel, Goldman, M. Korell, C. Marras, Grace S. Bhudhikanok, M. Kasten and 12 more. Environmental Health Perspectives, 2011
1,403 citations recorded by the source corpus.
Background Mitochondrial dysfunction and oxidative stress are pathophysiologic mechanisms implicated in experimental models and genetic forms of Parkinson’s disease (PD). Certain pesticides may affect these mechanisms, but no pesticide has been definitively associated with PD in humans. Objectives Our goal was to determine whether pesticides that cause mitochondrial dysfunction or oxidative stress are associated with PD or clinical features of parkinsonism in humans. Methods We assessed lifetime use of pesticides selected by mechanism in a case–control study nested in the Agricultural Health Study (AHS). PD was diagnosed by movement disorders specialists. Controls were a stratified random sample of all AHS participants frequency-matched to cases by age, sex, and state at approximately three controls: one case. Results In 110 PD cases and 358 controls, PD was associated with use of a group of pesticides that inhibit mitochondrial complex I [odds ratio (OR) = 1.7; 95% confidence interval (CI), 1.0–2.8] including rotenone (OR = 2.5; 95% CI, 1.3–4.7) and with use of a group of pesticides that cause oxidative stress (OR = 2.0; 95% CI, 1.2–3.6), including paraquat (OR = 2.5; 95% CI, 1.4–4.7). Conclusions PD was positively associated with two groups of pesticides defined by mechanisms implicated experimentally—those that impair mitochondrial function and those that increase oxidative stress—supporting a role for these mechanisms in PD pathophysiology.
Subfields: Molecular Biology, Neurology, Surgery
View Paper: https://www.semanticscholar.org/paper/01f468fb2f5d504a241050a6ac9b20b45e9136c5
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Citations in the corpus
- Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “…reporting an increased risk of 10–fold (OR = 10.0, 95% CI, 2.9–34.3) in East Texas farmers (Dhillon et al., 2008), and 2.5-fold (OR = 2.5, 95% CI, 1.3–4.7) in PD cases (n = 110) compared with controls (n = 358) from professional pesticide applicators participants in the AHS (Tanner et al., 2011).”
- The SH-SY5Y cell line in Parkinson’s disease research: a systematic review (2017, background): “Exposure to rotenone, a highly lipophilic insecticide, has been linked to sporadic PD [55] and can”
- Parkinson Disease Epidemiology, Pathology, Genetics and Pathophysiology (2019, background): “Chronic exposure of rodents to rotenone, also a potent mitochondrial complex I inhibitor, also causes preferential degeneration of dopaminergic neurons(37), and exposure to pesticides (including rotenone) is a risk factor for PD(38).”
- Neuroactive insecticides: targets, selectivity, resistance, and secondary effects. (2013, background): “Some of the insecticides proposed to contribute to these changes and the incidence of Parkinson’s disease are the NADH oxidase inhibitors rotenone and deguelin (4, 17, 129), the PCCAs heptachlor and dieldrin (9, 12), and the pyrethroid permethrin (9, 52).”
- The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “increased risk of PD [210, 212–215], undergoes redox”
- Parkinson disease: from pathology to molecular disease mechanisms. (2013, background): “The closest has been the ability of the structurally related paraquat, a commercial weed killer, to destroy dopaminergic cells in rodents and this links nicely to the increased risk of developing PD that repeatedly emerges from epidemiological studies, although there is no association with any speci”