Amornpan AjjimapornPansiri Phansuwan-PujitoManuchair EbadiPiyarat GovitrapongThe Institute of Science and Technology for Research and Development, Mahidol UniversitySrinakharinwirot UniversityUniversity of North DakotaMahidol University2018-08-242018-08-242007-05-23Neuroscience Letters. Vol.419, No.1 (2007), 59-63030439402-s2.0-34248206819https://repository.li.mahidol.ac.th/handle/123456789/25085Methamphetamine (METH) is a well-known drug of abuse and neurotoxin that may cause temporary or permanent disturbances in the dopaminergic systems of the brain, predisposing individuals to Parkinsonism. Previously, we have shown that METH causes dopaminergic cell death by increasing the production of reactive oxygen species (ROS) and by depleting cellular ATP levels. These effects were abolished by pretreatment with ZnCl2which enhanced expression of the zinc binding protein, metallothionein. In the present study, the effects of ZnCl2on α-synuclein expression were examined further in METH-treated SK-N-SH cells in culture. We show that METH significantly increased α-synuclein expression in a dose-dependent manner after inducing oxidative stress. Pretreatment with ZnCl2(50 μM) reversed this stimulatory effect. We propose that zinc mediates this neuroprotective response via the production of metallothionein. © 2007 Elsevier Ireland Ltd. All rights reserved.Mahidol UniversityNeuroscienceArticleSCOPUS10.1016/j.neulet.2007.03.073