Influence of developmental lead exposure on expression of DNA methyltransferases and methyl cytosine-binding proteins in hippocampus
Open accessAbstract
Developmental exposure to lead (Pb) has adverse effects on cognitive functioning and behavior that can persist into adulthood. Exposures that occur during fetal or early life periods may produce changes in brain related to physiological re-programming from an epigenetic influence such as altered DNA methylation status. Since DNA methylation is regulated by DNA methyltransferases and methyl cytosine-binding proteins, this study assessed the extent to which developmental Pb exposure might affect expression of these proteins in the hippocampus. Long Evans dams were fed chow with or without added Pb acetate (0, 150, 375, 750 ppm) prior to breeding and remained on the same diet through weaning (perinatal exposure group). Other animals were exposed to the same doses of Pb but exposure started on postnatal day 1 and continued through weaning (early postnatal exposure group). All animals were euthanized on day 55 and hippocampi were removed. Western blot analyses showed significant effects of Pb exposure on DNMT1, DNMT3a, and MeCP2 expression, with effects often seen at the lowest level of exposure and modified by sex and developmental window of Pb exposure. These data suggest potential epigenetic effects of developmental Pb exposure on DNA methylation mediated at least in part through dysregulation of methyltransferases.
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Exposure to lead (150, 375, 750 ppm) in utero and throughout lactation significantly reduced DNMT1 protein abundance by ∼25% uniquely in the female P55 Long Evans rat hippocampus.
“Exposure to lead (150, 375, 750 ppm) in utero and throughout lactation significantly reduced DNMT1 protein abundance by ∼25% uniquely in the female P55 Long Evans rat hippocampus [ 42 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [42]
Lactational exposure only (P1-21) had no effect on DNMT1 abundance in the female P55 hippocampus.
“In contrast, lactational exposure only (P1-21) had no effect on DNMT1 abundance in the female P55 hippocampus.”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [42]
In the male P55 hippocampus, lactational exposure to lead diminished DNMT1 expression by 18-23% at the lower doses of 150, 375 ppm and enhanced DNMT1 expression by 20% at the highest dose of 750 ppm.
“However, in the male P55 hippocampus, lactational exposure to lead diminished DNMT1 expression by 18–23% at the lower doses of 150, 375 ppm and enhanced DNMT1 expression by 20% at the highest dose of 750 ppm [ 42 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [42]
Sex- and stage-specific changes are also observed for DNMT3A and methyl CpG binding Protein 2 (MECP2).
“Sex- and stage-specific changes are also observed for DNMT3A and methyl CpG binding Protein 2 (MECP2) [ 42 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [42]
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References 46 · Cited by 115
- Authors
- Schneider, J. S., Kidd, S. K., & Anderson, D. W.
- Affiliations
- Thomas Jefferson University (US)
- Corresponding author
- Schneider, J.S.
- ORCID
- Schneider, J.S.
- Venue
- Toxicology Letters
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 217
- Issue
- 1
- Pages
- 75-81
- ISSN
- 0378-4274 (ISSN-L)
- PMC
- PMC3545007
- OpenAlex
- W1970547929
- Cited by
- 115
- References
- 46
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 7 · 2023: 10 · 2022: 7 · 2021: 12 · 2020: 6 · 2019: 4 · 2018: 9 · 2017: 10 · 2016: 12 · 2015: 6 · 2014: 12 · 2013: 3
- FWCI
- 4.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Toxicology Letters (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (ES015295)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Keywords
- developmental lead exposure, lead acetate, DNA methyltransferases, DNMT1, DNMT3A, MeCP2, hippocampus, DNA methylation, epigenetics, perinatal exposure, postnatal exposure, sex differences, developmental windows, brain development
- MeSH terms
- DNA (Cytosine-5-)-Methyltransferase 1, DNA Methyltransferase 3A, Animals, Child, Disease Models, Animal, DNA (Cytosine-5-)-Methyltransferases, Dose-Response Relationship, Drug, Female, Hippocampus, Humans, Lactation, Male, Nerve Tissue Proteins, Neurons, Organometallic Compounds, Pregnancy, Prenatal Exposure Delayed Effects, Sex Characteristics, Maternal Exposure, Lead Poisoning, Nervous System, Childhood, Rats, Long-Evans, Rats, Methyl-CpG-Binding Protein 2
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