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J Neural Transm (Vienna). 2016 Feb;123(2):113-23. doi: 10.1007/s00702-015-1386-4. Epub 2015 Mar 7.

Mitochondrial mechanisms of redox cycling agents implicated in Parkinson's disease.

Author information

1
University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
2
University of Colorado Anschutz Medical Campus, Aurora, CO, USA. manisha.patel@ucdenver.edu.

Abstract

Environmental agents have been implicated in Parkinson's disease (PD) based on epidemiological studies and the ability of toxicants to replicate features of PD. However, the precise mechanisms by which toxicants induce dopaminergic toxicity observed in the idiopathic form of PD remain to be fully understood. The roles of ROS and mitochondria are strongly suggested in the mechanisms by which these toxicants exert dopaminergic toxicity. There are marked differences and similarities shared by the toxicants in increasing steady-state levels of mitochondrial ROS. Furthermore, toxicants increase steady-state mitochondrial ROS levels by stimulating the production, inhibiting the antioxidant pathways of both. This review will focus on the role of mitochondria and ROS in PD associated with environmental exposures to redox-based toxicants.

KEYWORDS:

Antioxidants; Mitochondria; Parkinson's disease; Pesticides; Reactive oxygen species; Redox-cycling

PMID:
25749885
PMCID:
PMC5049695
DOI:
10.1007/s00702-015-1386-4
[Indexed for MEDLINE]
Free PMC Article

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