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dc.contributor.authorAmornpan Ajjimapornen_US
dc.contributor.authorShaik Shavalien_US
dc.contributor.authorManuchair Ebadien_US
dc.contributor.authorPiyarat Govitrapongen_US
dc.contributor.otherThe Institute of Science and Technology for Research and Development, Mahidol Universityen_US
dc.contributor.otherUniversity of North Dakota School of Medicine & Health Sciencesen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-07-12T02:49:24Z-
dc.date.available2018-07-12T02:49:24Z-
dc.date.issued2008-12-16en_US
dc.identifier.citationBrain Research Bulletin. Vol.77, No.6 (2008), 361-366en_US
dc.identifier.issn03619230en_US
dc.identifier.other2-s2.0-57149121900en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=57149121900&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/19848-
dc.description.abstractMethamphetamine (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.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=57149121900&origin=inwarden_US
dc.subjectNeuroscienceen_US
dc.titleZinc rescues dopaminergic SK-N-SH cell lines from methamphetamine-induced toxicityen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1016/j.brainresbull.2008.09.006en_US
Appears in Collections:Scopus 2006-2010

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