ArticleEMBO reports2022
Developmental arsenic exposure impairs cognition, directly targets DNMT3A, and reduces DNA methylation.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- The gut-brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives.Metabolic brain disease · 2026Review
- Arsenic Trioxide Underpins Delayed Neuroinflammation and Impaired Synaptic Integrity involving Integrative Stress Response Signaling.bioRxiv : the preprint server for biology · 2025Article
- How chronic inflammation fuels carcinogenesis as an environmental epimutagen.Discover oncology · 2025Review
- Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.International journal of molecular sciences · 2024Article
- Effect of Long-Term Low-Dose Arsenic Exposure on DNA Methylation and Gene Expression in Human Liver Cells.International journal of molecular sciences · 2023Article
- Developmental origins of adult diseases.Medical review (2021) · 2022Review
- Developmental arsenic exposure impairs cognition, directly targets DNMT3A, and reduces DNA methylation.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developmental arsenic exposure has been associated with cognitive deficits in epidemiological studies, but the underlying mechanisms remain poorly understood. Here, we establish a mouse model of developmental arsenic exposure exhibiting deficits of recognition and spatial memory in the offspring. These deficits are associated with genome-wide DNA hypomethylation and abnormal expression of cognition-related genes in the hippocampus. Arsenic atoms directly bind to the cysteine-rich ADD domain of DNA methyltransferase 3A (DNMT3A), triggering ubiquitin- and proteasome-mediated degradation of DNMT3A in different cellular contexts. DNMT3A degradation leads to genome-wide DNA hypomethylation in mouse embryonic fibroblasts but not in non-embryonic cell lines. Treatment with metformin, a first-line antidiabetic agent reported to increase DNA methylation, ameliorates the behavioral deficits and normalizes the aberrant expression of cognition-related genes and DNA methylation in the hippocampus of arsenic-exposed offspring. Our study establishes a DNA hypomethylation effect of developmental arsenic exposure and proposes a potential treatment against cognitive deficits in the offspring of pregnant women in arsenic-contaminated areas.
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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.