ArticleNeurotoxicology2006
Methylmercury elicits rapid inhibition of cell proliferation in the developing brain and decreases cell cycle regulator, cyclin E.
Article in Neurotoxicology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 85 citations in OpenAlex.
- The Threat Posed by Environmental Contaminants on Neurodevelopment: What Can We Learn from Neural Stem Cells?International journal of molecular sciences · 2023Review
- Prenatal Mercury Exposure and Infant Weight Trajectories in a UK Observational Birth Cohort.Toxics · 2022Article
- Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Single cell RNA sequencing detects persistent cell type- and methylmercury exposure paradigm-specific effects in a human cortical neurodevelopmental model.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Characterizing the Low-Dose Effects of Methylmercury on the Early Stages of Embryo Development Using Cultured Human Embryonic Stem Cells.Environmental health perspectives · 2021Article
- Environmentally relevant developmental methylmercury exposures alter neuronal differentiation in a human-induced pluripotent stem cell model.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation.International journal of molecular sciences · 2021Review
- Tissue-specific Nrf2 signaling protects against methylmercury toxicity in Drosophila neuromuscular development.Archives of toxicology · 2020Article
- Human-induced pluripotent stems cells as a model to dissect the selective neurotoxicity of methylmercury.Biochimica et biophysica acta. General subjects · 2019Review
- Article
- Methylmercury alters proliferation, migration, and antioxidant capacity in human HTR8/SV-neo trophoblast cells.Reproductive toxicology (Elmsford, N.Y.) · 2018Article
- MeHg Causes Ultrastructural Changes in Mitochondria and Autophagy in the Spinal Cord Cells of Chicken Embryo.Journal of toxicology · 2018Article
- Low-Dose Methylmercury-Induced Genes Regulate Mitochondrial Biogenesis via miR-25 in Immortalized Human Embryonic Neural Progenitor Cells.International journal of molecular sciences · 2016Article
- Methylmercury and brain development: A review of recent literature.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2016Review
- Effect ofExperimental and therapeutic medicine · 2016Article
- Is Low Non-Lethal Concentration of Methylmercury Really Safe? A Report on Genotoxicity with Delayed Cell Proliferation.PloS one · 2016Article
- Early Developmental Low-Dose Methylmercury Exposure Alters Learning and Memory in Periadolescent but Not Young Adult Rats.BioMed research international · 2016Article
- Hippocampal developmental vulnerability to methylmercury extends into prepubescence.Frontiers in neuroscience · 2015Article
- MeHg Developing Exposure Causes DNA Double-Strand Breaks and Elicits Cell Cycle Arrest in Spinal Cord Cells.Journal of toxicology · 2015Article
- Neural stem cell apoptosis after low-methylmercury exposures in postnatal hippocampus produce persistent cell loss and adolescent memory deficits.Developmental neurobiology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The developing brain is highly sensitive to methylmercury (MeHg). Still, the initial changes in cell proliferation that may contribute to long-term MeHg effects are largely undefined. Our previous studies with growth factors indicate that acute alterations of the G1/S-phase transition can permanently affect cell numbers and organ size. Therefore, we determined whether an environmental toxicant could also impact brain development with rapid (6-7h) effects on DNA synthesis and cell cycle machinery in neuronal precursors. In vivo studies in newborn rat hippocampus and cerebellum, two regions of postnatal neurogenesis, were followed by in vitro analysis of two precursor models, cortical and cerebellar cells, focusing on the proteins that regulate the G1/S transition. In postnatal day 7 (P7) pups, a single subcutaneous injection of MeHg (3microg/g) acutely (7h) decreased DNA synthesis in the hippocampus by 40% and produced long-term (2 weeks) reductions in total cell number, estimated by DNA quantification. Surprisingly, cerebellar granule cells were resistant to MeHg effects in vivo at comparable tissue concentrations, suggesting region-specific differences in precursor populations. In vitro, MeHg altered proliferation and cell viability, with DNA synthesis selectively inhibited at an early timepoint (6h) corresponding to our in vivo observations. Considering that G1/S regulators are targets of exogenous signals, we used a well-defined cortical cell model to examine MeHg effects on relevant cyclin-dependent kinases (CDK) and CDK inhibitors. At 6h, MeHg decreased by 75% levels of cyclin E, a cell cycle regulator with roles in proliferation and apoptosis, without altering p57, p27, or CDK2 nor levels of activated caspase 3. In aggregate, our observations identify the G1/S transition as an early target of MeHg toxicity and raise the possibility that cyclin E degradation contributes to both decreased proliferation and eventual cell death.
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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.