Riluzole-Triggered GSH Synthesis via Activation of Glutamate Transporters to Antagonize Methylmercury-Induced Oxidative Stress in Rat Cerebral Cortex
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- Yu Deng
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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- Zhao-Fa Xu
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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- Wei Liu
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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- Bin Xu
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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- Hai-Bo Yang
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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- Yan-Gang Wei
- Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China
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説明
<jats:p><jats:italic>Objective</jats:italic>. This study was to evaluate the effect of riluzole on methylmercury- (MeHg-) induced oxidative stress, through promotion of glutathione (GSH) synthesis by activating of glutamate transporters (GluTs) in rat cerebral cortex.<jats:italic>Methods</jats:italic>. Eighty rats were randomly assigned to four groups, control group, riluzole alone group, MeHg alone group, and riluzole + MeHg group. The neurotoxicity of MeHg was observed by measuring mercury (Hg) absorption, pathological changes, and cell apoptosis of cortex. Oxidative stress was evaluated via determining reactive oxygen species (ROS), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDAs), carbonyl, sulfydryl, and GSH in cortex. Glutamate (Glu) transport was studied by measuring Glu, glutamine (Gln), mRNA, and protein of glutamate/aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1).<jats:italic>Result</jats:italic>. (1) MeHg induced Hg accumulation, pathological injury, and apoptosis of cortex; (2) MeHg increased ROS, 8-OHdG, MDA, and carbonyl, and inhibited sulfydryl and GSH; (3) MeHg elevated Glu, decreased Gln, and downregulated GLAST and GLT-1 mRNA expression and protein levels; (4) riluzole antagonized MeHg-induced downregulation of GLAST and GLT-1 function and expression, GSH depletion, oxidative stress, pathological injury, and apoptosis obviously.<jats:italic>Conclusion</jats:italic>. Data indicate that MeHg administration induced oxidative stress in cortex and that riluzole could antagonize this situation through elevation of GSH synthesis by activating of GluTs.</jats:p>
収録刊行物
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- Oxidative Medicine and Cellular Longevity
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Oxidative Medicine and Cellular Longevity 2012 1-12, 2012
Wiley