Exploring Cross-Talk Between Oxidative Damage and Excitotoxicity and the Effects of Riluzole in the Rat Cortex After Exposure to Methylmercury
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- 作者：Yu Deng (1)
Zhaofa Xu (1)
Bin Xu (1)
Wei Liu (1)
Yangang Wei (1)
Yuehui Li (1)
Shu Feng (1)
Tianyao Yang (1) - 关键词：Cross ; talk ; Oxidative damage ; Excitotoxicity ; Methylmercury ; Riluzole ; Cortex
- 刊名：Neurotoxicity Research
- 出版年：2014
- 出版时间：July 2014
- 年：2014
- 卷：26
- 期：1
- 页码：40-51
- 全文大小：
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Zhaofa Xu (1)
Bin Xu (1)
Wei Liu (1)
Yangang Wei (1)
Yuehui Li (1)
Shu Feng (1)
Tianyao Yang (1)
1. Department of Environmental Health, School of Public Health, China Medical University, North 2nd Road 92, Heping Ward, Shenyang, 110001, Liaoning, People’s Republic of China - ISSN：1476-3524
文摘
Methylmercury (MeHg) is a ubiquitous environmental toxin that causes neurologic and developmental diseases. Oxidative damage and excitotoxicity are putative mechanisms, which underlie MeHg-induced neurotoxicity. In this study, the cross-talk between the oxidative damage and excitotoxicity pathways and the protective effects of riluzole in the rat cortex were explored. Rats were injected with MeHg and/or riluzole, and cold vapor atomic fluorescence spectrometry, hematoxylin and eosin staining, flow cytometry, fluorescence assays, spectrophotometry, real-time PCR, and Western blotting were used to evaluate neurotoxicity. The present study showed that (1) MeHg accumulated in the cerebral cortex and caused pathology. (2) MeHg caused oxidative damage by inducing glutathione (GSH) depletion, reactive oxygen species (ROS) production, inhibition of antioxidant enzyme activity, and alteration of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. (3) MeHg disrupted the glutamate transporters (GluTs), glutamate–glutamine cycle, and N-methyl-d-aspartate receptor expression and induced excitotoxicity. (4) Excitotoxicity resulted in disruption of GSH synthesis, calcium overloading, oxidative damage, and excessive ROS production. (5) Pretreatment with riluzole antagonized MeHg neurotoxicity by down regulating cross-talk between the oxidative damage and excitotoxicity pathways. In conclusion, the cross-talk between the oxidative damage and excitotoxicity pathways caused by MeHg exposure was linked by GluTs and calcium and inhibited by riluzole treatment.