Publication: Zinc rescues dopaminergic SK-N-SH cell lines from methamphetamine-induced toxicity
Submitted Date
Received Date
Accepted Date
Issued Date
2008-12-16
Copyright Date
Announcement No.
Application No.
Patent No.
Valid Date
Resource Type
Edition
Resource Version
Language
File Type
No. of Pages/File Size
ISBN
ISSN
03619230
eISSN
Scopus ID
WOS ID
Pubmed ID
arXiv ID
Call No.
Other identifier(s)
2-s2.0-57149121900
Journal Title
Volume
Issue
item.page.oaire.edition
Start Page
End Page
Access Rights
Access Status
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Physical Location
Bibliographic Citation
Brain Research Bulletin. Vol.77, No.6 (2008), 361-366
Citation
Amornpan Ajjimaporn, Shaik Shavali, Manuchair Ebadi, Piyarat Govitrapong (2008). Zinc rescues dopaminergic SK-N-SH cell lines from methamphetamine-induced toxicity. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/19848.
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Zinc rescues dopaminergic SK-N-SH cell lines from methamphetamine-induced toxicity
Alternative Title(s)
Author's Affiliation
Author's E-mail
Editor(s)
Editor's Affiliation
Corresponding Author(s)
Creator(s)
Compiler
Advisor(s)
Illustrator(s)
Applicant(s)
Inventor(s)
Issuer
Assignee
Series
Has Part
Abstract
Methamphetamine (METH) is a potent inducer of dopamine (DA) release, and is toxic to DA neurons. It has been reported that the formation of free radicals is an early signaling event that mediates cell death caused by METH. Currently, studies suggest that the generation of free radicals by oxidative catabolism of DA and dysfunction of the mitochondrial respiration chain are important mediators of neuronal death in Parkinson's disease (PD) and one process may counter the effect of the other. In our previous study, we investigated the deleterious effects of METH-induced reactive oxygen species (ROS) and mitochondrial dysfunction in dopaminergic SK-N-SH cells in culture, and assessed whether zinc-metallothionein induction provided mitochondrial protection against METH-induced mitochondrial dysfunction. Our present data demonstrate that METH enhances lipid peroxidation and mitochondrial manganese superoxide dismutase (MnSOD) enzyme levels, and decreases the antioxidant-reduced glutathione (GSH) together with an inhibition of mitochondrial complex-I activity. Pre-treatment with zinc markedly prevents the increase of lipid peroxidation and provides mitochondrial protection by scavenging free radicals via metallothionein and by increasing mitochondrial GSH and complex-I levels, thus rescuing SK-N-SH cells from METH toxicity. It should be emphasized that, however, it is still not clear that effects of METH on cultured SK-N-SH reliably model the effects of METH in the intact animal. Further studies in the intact animal are needed. © 2008 Elsevier Inc. All rights reserved.