ArticleEnvironmental and molecular mutagenesis2016
Transcriptional profiling of the mouse hippocampus supports an NMDAR-mediated neurotoxic mode of action for benzo[a]pyrene.
Article in Environmental and molecular mutagenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
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- Integrated transcriptomics and proteomics reveal ferroptosis induced by B[a]P and BPDE in mouse hippocampal neurons.Scientific reports · 2025Article
- Plin4 modulates lipid droplet accumulation and ferroptosis in neurons exposed to benzo[a]pyrene.Cell death discovery · 2025Article
- Pathways to the Brain: Impact of Fine Particulate Matter Components on the Central Nervous System.Antioxidants (Basel, Switzerland) · 2025Review
- The Effects of Air Pollution on Neurological Diseases: A Narrative Review on Causes and Mechanisms.Toxics · 2025Review
- Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms.Toxics · 2022Review
- Whole Genome Sequencing of the Mutamouse Model Reveals Strain- and Colony-Level Variation, and Genomic Features of the Transgene Integration Site.Scientific reports · 2019Article
- Postnatal Subacute Benzo(a)Pyrene Exposure Caused Neurobehavioral Impairment and Metabolomic Changes of Cerebellum in the Early Adulthood Period of Sprague-Dawley Rats.Neurotoxicity research · 2018Article
- Article
- Recommended approaches in the application of toxicogenomics to derive points of departure for chemical risk assessment.Archives of toxicology · 2017Article
- Polycyclic aromatic hydrocarbons and child mental health: is the effect modified by exposure to environmental nitrous oxide?Environmental science and pollution research international · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Benzo[a]pyrene (BaP) is a genotoxic carcinogen and a neurotoxicant. The neurotoxicity of BaP is proposed to arise from either genotoxicity leading to neuronal cell death, or perturbed expression of N-methyl-d-aspartate receptor (NMDAR) subunits. To explore these hypotheses, we profiled hippocampal gene expression of adult male Muta(™) Mouse administered 0, 1, 35, or 70 mg BaP/kg bw per day by oral gavage for 3 days. Transcriptional profiles were examined by RNA-sequencing (RNA-seq), DNA microarrays, and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). BaP-DNA adducts in the cerebellum were quantified by (32) P-post-labeling to measure genotoxicity. RNA-seq revealed altered expression of 0, 260, and 219 genes (P-value < 0.05, fold-change ≥ ± 1.5) following exposure to the low, medium, and high doses, respectively; 54 genes were confirmed by microarrays. Microarray and RT-PCR analysis showed increased expression of NMDAR subunits Grina and Grin2a. In contrast, no effects on DNA-damage response genes were observed despite comparable BaP-DNA adduct levels in the cerebellum and in the lungs and livers of mice at similar BaP doses in previous studies. The results suggest that DNA-damage response does not play a major role in BaP-induced adult neurotoxicity. Meta-analysis revealed that BaP-induced transcriptional profiles are highly correlated with those from the hippocampus of transgenic mice exhibiting similar neurotoxicity outcomes to BaP-exposed mice and rats (i.e., defects in learning and memory). Overall, we suggest that BaP-induced neurotoxicity is more likely to be a consequence of NMDAR perturbation than genotoxicity, and identify other important genes potentially mediating this adverse outcome. Environ. Mol. Mutagen. 57:350-363, 2016. © 2016 Her Majesty the Queen in Right of Canada. Environmental and Molecular Mutagenesis © 2016 Environmental Mutagen Society.
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