ArticleToxicology2017
In vitro models reveal differences in the developmental neurotoxicity of an environmental polycylic aromatic hydrocarbon mixture compared to benzo[a]pyrene: Neuronotypic PC12 Cells and embryonic neural stem cells.
Article in Toxicology, 2017. 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, 53 citations in OpenAlex.
- Evidence from three taxonomically distinct species for a non-AhR mechanism of developmental neurotoxicity of an environmentally derived mixture of polycyclic aromatic hydrocarbons.bioRxiv : the preprint server for biology · 2026Article
- Article
- Association between polycyclic aromatic hydrocarbons exposure and metabolic dysfunction-associated steatotic liver disease in US adults.Frontiers in public health · 2025Article
- The role of DNA methylation on gene expression in the vertebrae of ancestrally benzo[a]pyrene exposed F1 and F3 male medaka.Epigenetics · 2023Article
- Aluminum Induced Necroptosis of PC12 Cells via TNFR1-RIP1/RIP3 Signalling Pathway.Neurochemical research · 2022Article
- The Ability of Probiotic Lactobacillus Strains in Removal of Benzo[a]pyrene: a Response Surface Methodology Study.Probiotics and antimicrobial proteins · 2022Article
- Understanding exposures and latent disease risk within the National Institute of Environmental Health Sciences Superfund Research Program.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Benzo[a]pyrene impairs the migratory pattern of human gonadotropin-releasing-hormone-secreting neuroblasts.European journal of histochemistry : EJH · 2021Article
- Regulation of mGluR1 on the Expression of PKC and NMDAR in Aluminum-Exposed PC12 Cells.Neurotoxicity research · 2021Article
- Single neonatal dexamethasone administration has long-lasting outcome on depressive-like behaviour, Bdnf, Nt-3, p75ngfr and sorting receptors (SorCS1-3) stress reactive expression.Scientific reports · 2021Article
- Endocrine disruptors also function as nervous disruptors and can be renamed endocrine and nervous disruptors (ENDs).Toxicology reports · 2021Review
- Effects of environmental stressors on stem cells.World journal of stem cells · 2019Review
- Systematic developmental neurotoxicity assessment of a representative PAH Superfund mixture using zebrafish.Toxicology and applied pharmacology · 2018Article
- Developmental neurotoxicity resulting from pharmacotherapy of preterm labor, modeled in vitro: Terbutaline and dexamethasone, separately and together.Toxicology · 2018Article
- Article
- Embryonic exposures to cadmium and PAHs cause long-term and interacting neurobehavioral effects in zebrafish.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
In addition to their carcinogenic activity, polycyclic aromatic hydrocarbons (PAHs) are suspected to be developmental neurotoxicants. We evaluated the effects of PAHs with two in vitro models that assess distinct "decision nodes" in neurodifferentiation: neuronotypic PC12 cells, which characterize the transition from cell replication to neurodifferentiation, neurite outgrowth and neurotransmitter specification; and embryonic neural stem cells (NSCs), which evaluate the origination of neurons and glia from precursors. We compared an environmentally-derived PAH mixture from a Superfund contamination site (Elizabeth River Sediment Extract, ERSE) to those of a single PAH, benzo[a]pyrene (BaP). In PC12 cells, BaP impaired the transition from cell replication to neurodifferentiation, resulting in higher numbers of cells, but with reduced cell size and deficits in all indices of neuronal features (neurite formation, development of dopamine and acetylcholine phenotypes). ERSE was far less effective, causing only modest changes in cell numbers and size and no impairment of neurite formation or neurotransmitter specification; in fact, ERSE evoked a slight increase in emergence of the acetylcholine phenotype. In the NSC model, this relationship was entirely reversed, with far greater sensitivity to ERSE than to BaP. Furthermore, ERSE, but not BaP, enhanced NSC differentiation into neurons, whereas both ERSE and BaP suppressed the glial phenotype. Our studies provide a cause-and-effect relationship for the observed association of developmental PAH exposure to behavioral deficits. Further, PAH sensitivity occurs over developmental stages corresponding to rudimentary brain formation through terminal neurodifferentiation, suggesting that vulnerability likely extends throughout fetal brain development and into early childhood.
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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.