Metallobiology of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity

Hare, DJ; Adlard, PA; Doble, PA; Finkelstein, DI

Metallobiology of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity

Hare, DJ

Adlard, PA Doble, PA

Finkelstein, DI

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Publication Type:: Journal Article
Citation:: Metallomics, 2013, 5 (2), pp. 91 - 109
Issue Date:: 2013-02-01

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Field	Value	Language
dc.contributor.author	Hare, DJ https://orcid.org/0000-0002-5922-7643	en_US
dc.contributor.author	Adlard, PA	en_US
dc.contributor.author	Doble, PA https://orcid.org/0000-0002-8472-1301	en_US
dc.contributor.author	Finkelstein, DI	en_US
dc.date.issued	2013-02-01	en_US
dc.identifier.citation	Metallomics, 2013, 5 (2), pp. 91 - 109	en_US
dc.identifier.issn	1756-5901	en_US
dc.identifier.uri	http://hdl.handle.net/10453/23907
dc.description.abstract	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a potent toxin used to selectively destroy dopaminergic neurons in the substantia nigra and induce parkinsonism. MPTP is metabolised to the 1-methyl-4-phenylpyridinium ion (MPP+) in glia, after which it enters the neuron via the dopamine transporter and results in elevated levels of oxidative stress. The mechanism through which MPP+ causes cell death is thought to involve redox-active metals, particularly iron (Fe). This review will examine how cellular metal metabolism is altered following MPTP insult, and how this relates to metal dyshomeostasis in idiopathic Parkinson's disease. This includes both cell damage arising from increased metal concentration, and how metal-binding proteins respond to MPTP-induced neurotoxicity. Implications for using MPTP as a model for human Parkinson's disease will be discussed in terms of cell metallobiology. © 2013 The Royal Society of Chemistry.	en_US
dc.relation.ispartof	Metallomics	en_US
dc.relation.isbasedon	10.1039/c2mt20164j	en_US
dc.subject.classification	Analytical Chemistry	en_US
dc.subject.mesh	Substantia Nigra	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Parkinson Disease	en_US
dc.subject.mesh	MPTP Poisoning	en_US
dc.subject.mesh	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	en_US
dc.subject.mesh	Models, Biological	en_US
dc.title	Metallobiology of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity	en_US
dc.type	Journal Article
utslib.citation.volume	2	en_US
utslib.citation.volume	5	en_US
utslib.for	0301 Analytical Chemistry	en_US
utslib.for	03 Chemical Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Mathematical and Physical Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CFS - Centre for Forensic Science
utslib.copyright.status	open_access
pubs.issue	2	en_US
pubs.publication-status	Published	en_US
pubs.volume	5	en_US

Abstract:

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a potent toxin used to selectively destroy dopaminergic neurons in the substantia nigra and induce parkinsonism. MPTP is metabolised to the 1-methyl-4-phenylpyridinium ion (MPP+) in glia, after which it enters the neuron via the dopamine transporter and results in elevated levels of oxidative stress. The mechanism through which MPP+ causes cell death is thought to involve redox-active metals, particularly iron (Fe). This review will examine how cellular metal metabolism is altered following MPTP insult, and how this relates to metal dyshomeostasis in idiopathic Parkinson's disease. This includes both cell damage arising from increased metal concentration, and how metal-binding proteins respond to MPTP-induced neurotoxicity. Implications for using MPTP as a model for human Parkinson's disease will be discussed in terms of cell metallobiology. © 2013 The Royal Society of Chemistry.

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http://hdl.handle.net/10453/23907