ArticleNeurotoxicity research2014
Exploring cross-talk between oxidative damage and excitotoxicity and the effects of riluzole in the rat cortex after exposure to methylmercury.
Article in Neurotoxicity research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Imperatorin as an activator of Nrf2/ARE in mercury-induced brain damage based on rat model study, molecular docking, and molecular simulation approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Neurotoxicity mechanism of aconitine in HT22 cells studied by microfluidic chip-mass spectrometry.Journal of pharmaceutical analysis · 2023Article
- Article
- Acute Methylmercury Exposure and the Hypoxia-InducibleEnvironmental health perspectives · 2019Article
- Human-induced pluripotent stems cells as a model to dissect the selective neurotoxicity of methylmercury.Biochimica et biophysica acta. General subjects · 2019Review
- Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice.Oxidative medicine and cellular longevity · 2018Article
- Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.Antioxidants & redox signaling · 2017Review
- Neurotoxicity of Methylmercury in Isolated Astrocytes and Neurons: the Cytoskeleton as a Main Target.Molecular neurobiology · 2017Article
- Impaired cross-talk between the thioredoxin and glutathione systems is related to ASK-1 mediated apoptosis in neuronal cells exposed to mercury.Redox biology · 2017Article
- Memantine, a Low-Affinity NMDA Receptor Antagonist, Protects against Methylmercury-Induced Cytotoxicity of Rat Primary Cultured Cortical Neurons, Involvement of CaMolecular neurobiology · 2017Article
- The catecholaminergic neurotransmitter system in methylmercury-induced neurotoxicity.Advances in neurotoxicology · 2017Article
- Biomarkers of mercury toxicity: Past, present, and future trends.Journal of toxicology and environmental health. Part B, Critical reviews · 2017Review
- Role of autophagy in methylmercury-induced neurotoxicity in rat primary astrocytes.Archives of toxicology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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