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BioMed Research International
Volume 2016 (2016), Article ID 2548792, 18 pages
Review Article

Potential Role of Epigenetic Mechanism in Manganese Induced Neurotoxicity

1Environmental Health Division, CSIR-National Environmental Engineering Research Institute, Nagpur 440020, India
2Visvesvaraya National Institute of Technology (VNIT), Nagpur 440010, India

Received 17 February 2016; Accepted 8 May 2016

Academic Editor: Andrei Surguchov

Copyright © 2016 Prashant Tarale et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Manganese is a vital nutrient and is maintained at an optimal level (2.5–5 mg/day) in human body. Chronic exposure to manganese is associated with neurotoxicity and correlated with the development of various neurological disorders such as Parkinson’s disease. Oxidative stress mediated apoptotic cell death has been well established mechanism in manganese induced toxicity. Oxidative stress has a potential to alter the epigenetic mechanism of gene regulation. Epigenetic insight of manganese neurotoxicity in context of its correlation with the development of parkinsonism is poorly understood. Parkinson’s disease is characterized by the -synuclein aggregation in the form of Lewy bodies in neuronal cells. Recent findings illustrate that manganese can cause overexpression of -synuclein. -Synuclein acts epigenetically via interaction with histone proteins in regulating apoptosis. -Synuclein also causes global DNA hypomethylation through sequestration of DNA methyltransferase in cytoplasm. An individual genetic difference may also have an influence on epigenetic susceptibility to manganese neurotoxicity and the development of Parkinson’s disease. This review presents the current state of findings in relation to role of epigenetic mechanism in manganese induced neurotoxicity, with a special emphasis on the development of Parkinson’s disease.