ReviewAntioxidants (Basel, Switzerland)2020
Methylmercury-Mediated Oxidative Stress and Activation of the Cellular Protective System.
Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- The preventive and carcinogenic effect of metals on cancer: a systematic review.BMC public health · 2024Pooled it
- Mercury Exposure and Risk of Type 2 Diabetes: A Systematic Review and Meta-Analysis.International journal of clinical practice · 2022Pooled it
- Trace Elements in the Pancreas: From Physiological Homeostasis to the Pathogenesis of Diabetes, Pancreatitis, and Cancer-A Review.Life (Basel, Switzerland) · 2026Review
- Genetic Modulation of Mercury Exposure on Perinatal and Birth Outcomes: A Systematic Review and Meta-Analysis of Gene-Environment Interactions.Journal of xenobiotics · 2026Review
- Early-life mercury exposure and allergic diseases in childhood: systematic review and meta-analysis.Frontiers in pediatrics · 2026Review
- Mitochondrial dysfunction mediates the association between mercury exposure and lipid metabolism in children and adolescents.Lipids in health and disease · 2025Article
- Thiamine Mitigates the Toxicity of Methylmercury in Cultured Fetal Fibroblast Cell Lines.Cell biochemistry and biophysics · 2025Article
- Mercuric Chloride Aggravates Hyperglycemia-Induced Anxiety and Depressive-Like Behaviors in Type 2 Diabetic Rats: Breakdown of the Antioxidant Defense System.Biological trace element research · 2025Article
- Therapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice.Archives of toxicology · 2025Article
- Review
- Methylmercury Induces Apoptosis in Mouse C17.2 Neural Stem Cells through the Induction of OSGIN1 Expression by NRF2.International journal of molecular sciences · 2024Article
- Association between blood total mercury and psoriasis: The NHANES 2005-2006 and 2013-2014: A cross-sectional study.PloS one · 2024Article
- KEAP1 polymorphisms and neurodevelopmental outcomes in children with exposure to prenatal MeHg from the Seychelles Child Development Study Nutrition Cohort 2.Neurotoxicology · 2023Article
- Maternal DHA intake in mice increased DHA metabolites in the pup brain and ameliorated MeHg-induced behavioral disorder.Journal of lipid research · 2023Article
- Article
- Environmental Exposure to Metals, Parameters of Oxidative Stress in Blood and Prostate Cancer: Results from Two Cohorts.Antioxidants (Basel, Switzerland) · 2022Article
- Dietary Selenomethionine Reduce Mercury Tissue Levels and Modulate Methylmercury Induced Proteomic and Transcriptomic Alterations in Hippocampi of Adolescent BALB/c Mice.International journal of molecular sciences · 2022Article
- Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity.International journal of molecular sciences · 2022Review
- Mercury-Induced Oxidative Stress Response in Benthic Foraminifera: An In Vivo Experiment onBiology · 2022Article
- Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study.Toxicology reports · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylmercury (MeHg) is a well-known neurotoxicant that causes severe intoxication in humans. In Japan, it is referred to as Minamata disease, which involves two characteristic clinical forms: fetal type and adult type depending on the exposed age. In addition to MeHg burden level, individual susceptibility to MeHg plays a role in the manifestation of MeHg toxicity. Research progress has pointed out the importance of oxidative stress in the pathogenesis of MeHg toxicity. MeHg has a high affinity for selenohydryl groups, sulfhydryl groups, and selenides. It has been clarified that such affinity characteristics cause the impairment of antioxidant enzymes and proteins, resulting in the disruption of antioxidant systems. Furthermore, MeHg-induced intracellular selenium deficiency due to the greater affinity of MeHg for selenohydryl groups and selenides leads to failure in the recoding of a UGA codon for selenocysteine and results in the degradation of antioxidant selenoenzyme mRNA by nonsense-mediated mRNA decay. The defect of antioxidant selenoenzyme replenishment exacerbates MeHg-mediated oxidative stress. On the other hand, it has also been revealed that MeHg can directly activate the antioxidant Keap1/Nrf2 signaling pathway. This review summarizes the incidence of MeHg-mediated oxidative stress from the viewpoint of the individual intracellular redox system interactions and the MeHg-mediated aforementioned intracellular events. In addition, the mechanisms of cellular stress pathways and neuronal cell death triggered by MeHg-mediated oxidative stress and direct interactions of MeHg with reactive residues of proteins are mentioned.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.