ArticleMolecular neurobiology2017
Sulforaphane Prevents Methylmercury-Induced Oxidative Damage and Excitotoxicity Through Activation of the Nrf2-ARE Pathway.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- Sulforaphane enhances locomotor recovery after spinal cord injury through antioxidant, anti-inflammatory, and JAK/STAT-modulating mechanisms.Current research in neurobiology · 2026Article
- Nrf2 and STAT3 Pathways in Protecting Against Methylmercury-Induced Oxidative Stress in Hypothalamic Neuronal GT1-7 Cells.Neurochemical research · 2026Article
- Modulation of the PI3K/AKT/mTOR and AMPK/TSC2/mTOR Pathways by N-Acetyl-L-Cysteine as a Protector of Embryonic Bodies from the Toxic Effect of Methylmercury.Brain sciences · 2026Review
- Dose-dependent effects of silver nanoparticles on cell death modes in mouse blastocysts induced via endoplasmic reticulum stress and mitochondrial apoptosis.Toxicology research · 2024Article
- Experimental verification about treatment of Bu-Shen-Yi-Jing-Fang in Alzheimer's disease by the analysis of the feasible signaling pathway of network pharmacology.BMC complementary medicine and therapies · 2024Article
- Prevention of methylmercury-triggered ROS-mediated impairment of embryo development by co-culture with adult adipose-derived mesenchymal stem cells.Toxicology research · 2024Article
- Role of activated p21-activated kinase 2 in methylmercury-induced embryotoxic effects on mouse blastocysts.Toxicology research · 2023Article
- Article
- Therapeutic potential of sulforaphane in liver diseases: a review.Frontiers in pharmacology · 2023Review
- Low-dose silver nanoparticles plus methyl mercury exert embryotoxic effects on mouse blastocysts via endoplasmic reticulum stress and mitochondrial apoptosis.Toxicology research · 2022Article
- Sulforaphane Induces Glioprotection After LPS Challenge.Cellular and molecular neurobiology · 2022Article
- Ghrelin attenuates methylmercury-induced oxidative stress in neuronal cells.Molecular neurobiology · 2022Article
- Nrf2/HO-1 Signaling Activator Acetyl-11-keto-beta Boswellic Acid (AKBA)-Mediated Neuroprotection in Methyl Mercury-Induced Experimental Model of ALS.Neurochemical research · 2021Article
- The antioxidant role of STAT3 in methylmercury-induced toxicity in mouse hypothalamic neuronal GT1-7 cell line.Free radical biology & medicine · 2021Article
- ROS‑associated mechanism of different concentrations of pinacidil postconditioning in the rat cardiac Nrf2‑ARE signaling pathway.Molecular medicine reports · 2021Article
- Drugs Based on NMDAR Hypofunction Hypothesis in Schizophrenia.Frontiers in neuroscience · 2021Review
- Tissue-specific Nrf2 signaling protects against methylmercury toxicity in Drosophila neuromuscular development.Archives of toxicology · 2020Article
- Redox toxicology of environmental chemicals causing oxidative stress.Redox biology · 2020Review
- LaInternational journal of nanomedicine · 2020Article
- Simultaneous exposure to vinylcyclohexene and methylmercury in Drosophila melanogaster: biochemical and molecular analyses.BMC pharmacology & toxicology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylmercury (MeHg) is a prominent environmental neurotoxicant, which induces oxidative damage and an indirect excitotoxicity caused by altered glutamate (Glu) metabolism. However, the interaction between oxidative damage and excitotoxicity in MeHg-exposed rats has not been fully recognized. Here, we explored the interaction between oxidative damage and excitotoxicity and evaluated the preventive effects of sulforaphane (SFN) on MeHg-induced neurotoxicity in rat cerebral cortex. Seventy-two rats were randomly assigned to four groups: control group, MeHg-treated groups (4 and 12 μmol/kg), and SFN pretreatment group. After treatment (28 days), the rats were killed and the cerebral cortex was analyzed. Then, Hg, glutathione (GSH), malondialdehyde (MDA), protein sulfhydryl, protein carbonyl, 8-hydroxy-2-deoxyguanosine (8-OHdG), and the levels of reactive oxygen species (ROS) and apoptosis were examined. Glu and glutamine (Gln) levels, glutamine synthetase (GS), phosphate-activated glutaminase (PAG), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na
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