ArticleNeurotoxicology2011
Role of oxidative stress and the mitochondrial permeability transition in methylmercury cytotoxicity.
Article in Neurotoxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis 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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- DNA methylation changes associated with prenatal mercury exposure: A meta-analysis of prospective cohort studies from PACE consortium.Environmental research · 2022Pooled it
- Mitochondrial dysfunction mediates the association between mercury exposure and lipid metabolism in children and adolescents.Lipids in health and disease · 2025Article
- Associations of Prenatal Mercury Exposure and PUFA with Telomere Length and mtDNA Copy Number in 7-Year-Old Children in the Seychelles Child Development Nutrition Cohort 2.Environmental health perspectives · 2025Article
- Effective Analysis of Alzheimer's Disease and Mechanisms of Methyl-4- Hydroxybenzoate using Network Toxicology, Molecular Docking, and Machine Learning Strategies.Current Alzheimer research · 2025Article
- Article
- Effect of methylmercury on fetal neurobehavioral development: an overview of the possible mechanisms of toxicity and the neuroprotective effect of phytochemicals.Archives of toxicology · 2022Review
- Ghrelin attenuates methylmercury-induced oxidative stress in neuronal cells.Molecular neurobiology · 2022Article
- Acute Methylmercury Exposure and the Hypoxia-InducibleEnvironmental health perspectives · 2019Article
- Curcumin protects against methylmercury-induced cytotoxicity in primary rat astrocytes by activating the Nrf2/ARE pathway independently of PKCδ.Toxicology · 2019Article
- Post-translational modifications in MeHg-induced neurotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- The Putative Role of Environmental Mercury in the Pathogenesis and Pathophysiology of Autism Spectrum Disorders and Subtypes.Molecular neurobiology · 2018Review
- Effect of thimerosal on thyroid hormones metabolism in rats.Endocrine connections · 2017Article
- Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans.DNA repair · 2017Article
- Low-Dose Methylmercury-Induced Apoptosis and Mitochondrial DNA Mutation in Human Embryonic Neural Progenitor Cells.Oxidative medicine and cellular longevity · 2016Article
- A novel synthetic activator of Nurr1 induces dopaminergic gene expression and protects against 6-hydroxydopamine neurotoxicity in vitro.Neuroscience letters · 2015Article
- A hypothesis about how early developmental methylmercury exposure disrupts behavior in adulthood.Behavioural processes · 2015Review
- MeHg Developing Exposure Causes DNA Double-Strand Breaks and Elicits Cell Cycle Arrest in Spinal Cord Cells.Journal of toxicology · 2015Article
- Exploring cross-talk between oxidative damage and excitotoxicity and the effects of riluzole in the rat cortex after exposure to methylmercury.Neurotoxicity research · 2014Article
- Phytoremediation potential of Maná-Cubiu (Solanum sessiliflorum Dunal) for the deleterious effects of methylmercury on the reproductive system of rats.BioMed research international · 2014Article
- Rescue of neuronal migration deficits in a mouse model of fetal Minamata disease by increasing neuronal Ca2+ spike frequency.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress has been implicated in the pathogenesis of methylmercury (MeHg) neurotoxicity. Studies of mature neurons suggest that the mitochondrion may be a major source of MeHg-induced reactive oxygen species and a critical mediator of MeHg-induced neuronal death, likely by activation of apoptotic pathways. It is unclear, however, whether the mitochondria of developing and mature neurons are equally susceptible to MeHg. Murine embryonal carcinoma (EC) cells, which differentiate into neurons following exposure to retinoic acid, were used to compare the differentiation-dependent effects of MeHg on ROS production and mitochondrial depolarization. EC cells and their neuronal derivatives were pre-incubated with the ROS indicator 2',7'-dichlorofluoroscein diacetate or tetramethylrhodamine methyl ester, an indicator of mitochondrial membrane potential, with or without cyclosporin A (CsA), an inhibitor of mitochondrial permeability transition pore opening, and examined by laser scanning confocal microscopy in the presence of 1.5 μM MeHg. To examine consequences of mitochondrial perturbation, immunohistochemical localization of cytochrome c (cyt c) was determined after incubation of cells in MeHg for 4 h. MeHg treatment induced earlier and significantly higher levels of ROS production and more extensive mitochondrial depolarization in neurons than in undifferentiated EC cells. CsA completely inhibited mitochondrial depolarization by MeHg in EC cells but only delayed this response in the neurons. In contrast, CsA significantly inhibited MeHg-induced neuronal ROS production. Cyt c release was also more extensive in neurons, with less protection afforded by CsA. These data indicate that neuronal differentiation state influences mitochondrial transition pore dynamics and MeHg-stimulated production of ROS.
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