Understanding Rotenone and the link to Parkinson's disease

Below are just a few of the relevant online scientific papers describing the overwhelming body of evidence exposing the role that rotenone and other toxins in the environment play in developing Parkinson's disease (PD). These are all available online through the PubMed database or just by doing a search. I have provided citations as well for your convenience to the full papers for your own scrutiny. I have taken small snippets of the papers and posted here, and have underlined in bold pertinent statements. Otherwise these are unchanged as published online as you may verify for yourself and are encouraged to do so.

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Environ Health Perspect. 2011 Jun; 119(6): 866–872.

PMCID: PMC3114824

Rotenone, Paraquat, and Parkinson’s Disease

Caroline M. Tanner,1 Freya Kamel,2 G. Webster Ross,3 Jane A. Hoppin,2 Samuel M. Goldman,1 Monica Korell,1 Connie Marras,4 Grace S. Bhudhikanok,1 Meike Kasten,5 Anabel R. Chade,6 Kathleen Comyns,1 Marie Barber Richards,2,7 Cheryl Meng,1 Benjamin Priestley,1 Hubert H. Fernandez,8 Franca Cambi,9 David M. Umbach,10 Aaron Blair,11 Dale P. Sandler,2 and J. William Langston1

The pathogenesis of PD is thought to involve several critical abnormalities, each of which can be the result of genetic or environmental factors. Chief among these abnormalities are dysfunction of the mitochondrial respiratory chain, particularly complex I, and the production of reactive oxygen species (Henchcliffe and Beal 2008). To our knowledge, we have performed the first analysis of pesticides classified by presumed mechanism, rather than by functional categories (e.g., herbicides) or chemical class (e.g., organochlorines). We found significant associations of PD with use of groups of pesticides classified as complex I inhibitors or as oxidative stressors, providing support in humans for findings from decades of experimental work. In particular, PD was strongly associated with rotenone and paraquat, two individual pesticides used extensively to model PD in the laboratory.

This study provides strong evidence of an association between rotenone use and PD in humans. PD developed 2.5 times as often in those who reported use of rotenone compared with nonusers, and an association of similar magnitude was observed even when exposure was truncated up to 15 years before PD diagnosis.

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Oxid Med Cell Longev. 2016; 2016: 6705621.

PMCID: PMC4684867

Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity

Kaige Peng, 1 Yuan Tao, 2 Jun Zhang, 2 Jian Wang, 1 Feng Ye, 1 Guorong Dan, 1 Yuanpeng Zhao, 1 Ying Cai, 1 Jiqing Zhao, 1 Qiang Wu, 2 Zhongmin Zou, 1 Jia Cao, 1 and Yan Sai 1 , *

PD is the second most common neurodegenerative disease, characterized by a progressive loss of DA neurons in the substantia nigra (SN) [8]. Although the etiology of dopaminergic neurodegeneration remains unknown, it has been accepted that PD-related neurodegeneration is the result of environmental and genetic interactions [8]. Rotenone, one of the most widely used pesticides, has been suggested as the primary environmental risk factor for PD [9, 10]. Long-term and low-dose exposure to rotenone leads to a systemic defect in mitochondrial complex I and oxidative stress, the main contributors to the etiology of PD [9, 11]. Therefore, mitochondria are believed to play an important role in rotenone-induced dopaminergic neurodegeneration [12].

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