ArticleToxicology letters2013
Microglial disruption in young mice with early chronic lead exposure.
Article in Toxicology letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Regulatory role of GLUT1 in lead-induced neurotoxicity and the neuroprotective effect ofiScience · 2026Article
- Neuroprotective Potential ofInternational journal of molecular sciences · 2026Article
- Article
- The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR TInternational journal of molecular sciences · 2023Article
- Microglia and Astroglia-The Potential Role in Neuroinflammation Induced by Pre- and Neonatal Exposure to Lead (Pb).International journal of molecular sciences · 2023Article
- Improving Equitability and Inclusion for Testing and Detection of Lead Poisoning in US Children.The Milbank quarterly · 2023Article
- Neuroendocrine-Immune Crosstalk Shapes Sex-Specific Brain Development.Endocrinology · 2020Review
- Persistent Effects on Cardiorespiratory and Nervous Systems Induced by Long-Term Lead Exposure: Results from a Longitudinal Study.Neurotoxicity research · 2020Article
- Early chronic low-level lead exposure reduced C-C chemokine receptor 7 in hippocampal microglia.Toxicology letters · 2019Article
- Long-term consequences of early postnatal lead exposure on hippocampal synaptic activity in adult mice.Brain and behavior · 2019Article
- Loss of IL-10 Promotes Differentiation of Microglia to a M1 Phenotype.Frontiers in cellular neuroscience · 2019Article
- Intraventricular infusion of quinolinic acid impairs spatial learning and memory in young rats: a novel mechanism of lead-induced neurotoxicity.Journal of neuroinflammation · 2018Article
- Environmental Mechanisms of Neurodevelopmental Toxicity.Current environmental health reports · 2018Review
- Early chronic lead exposure reduces exploratory activity in young C57BL/6J mice.Journal of applied toxicology : JAT · 2015Article
- Early chronic low-level lead exposure produces glomerular hypertrophy in young C57BL/6J mice.Toxicology letters · 2014Article
- δ-Aminolevulinic acid dehydratase single nucleotide polymorphism 2 (ALAD2) and peptide transporter 2*2 haplotype (hPEPT2*2) differently influence neurobehavior in low-level lead exposed children.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The mechanisms by which early chronic lead (Pb) exposure alter brain development have not been identified. We examined neuroimmune system effects in C57BL/6J mice with Pb exposure, including levels that may be common among children in lower socioeconomic income environments. Pups were exposed via dams' drinking water from birth to post-natal day 28 to low, high or no Pb conditions. We compared gene expression of neuroinflammatory markers (study 1); and microglial mean cell body volume and mean cell body number in dentate gyrus, and dentate gyrus volume (study 2). Blood Pb levels in exposed animals at sacrifice (post-natal day 28) ranged from 2.66 to 20.31μg/dL. Only interleukin-6 (IL6) differed between groups and reductions were dose-dependent. Microglia cell body number also differed between groups and reductions were dose-dependent. As compared with controls, microglia cell body volume was greater but highly variable in only low-dose animals; dentate gyri volumes in low- and high-dose animals were reduced. The results did not support a model of increased neuroinflammation. Instead, early chronic exposure to Pb disrupted microglia via damage to, loss of, or lack of proliferation of microglia in the developing brains of Pb-exposed animals.
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Registered trials
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