article Open AccessTop 1% cited
Rotenone, Paraquat, and Parkinson’s Disease
Environmental Health Perspectives · 2011 · Vol. 119(6) · pp. 866–872
Caroline M. Tanner✉(Parkinson's Institute and Clinical Center)Freya Kamel(National Institutes of Health)G. Webster Ross(VA Pacific Islands Health Care System)Jane A. Hoppin(National Institutes of Health)Samuel M. Goldman(Parkinson's Institute and Clinical Center)Monica Korell(Parkinson's Institute and Clinical Center)Connie Marras(University of Toronto)Grace S. Bhudhikanok(Parkinson's Institute and Clinical Center)Meike Kasten(University of Lübeck)Anabel Chade(Favaloro University)Kathleen Comyns(Parkinson's Institute and Clinical Center)Marie Richards(National Institutes of Health)Cheryl Meng(Parkinson's Institute and Clinical Center)Benjamin Priestley(Parkinson's Institute and Clinical Center)Hubert H. Fernandez(Cleveland Clinic)Franca Cambi(University of Kentucky)David M. Umbach(National Institutes of Health)Aaron Blair(National Institutes of Health)Dale P. Sandler(National Institutes of Health)J. William Langston(Parkinson's Institute and Clinical Center)
Abstract
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.
Parkinson's Disease Mechanisms and TreatmentsBiochemical and biochemical processesParaquat toxicity studies and treatmentsRotenoneParkinson's diseaseParaquatMedicineDiseaseBiologyPathologyMitochondrionBiochemistry
MeSH terms
AgedFemaleHerbicidesHumansInsecticidesIowaMaleMiddle AgedMitochondriaNorth CarolinaParaquatParkinson DiseaseRotenoneCase-Control StudiesOccupational Exposure
Funding
- National Institutes of Health
- National Cancer Institute
- National Institute of Environmental Health Sciences
Citations
1,427
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62
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