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Cited by 29Toxic Organic Pollutants ImpactPharmacogenetics and Drug MetabolismImmunotoxicology and immune responses

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PAH Particles Perturb Prenatal Processes and Phenotypes: Protection from Deficits in Object Discrimination Afforded by Dampening of Brain Oxidoreductase Following In Utero Exposure to Inhaled Benzo(a)pyrene

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Li, Zhu, Chadalapaka, Gayathri, Ramesh, Aramandla, Khoshbouei, Habibeh, Maguire, Mark, Safe, Stephen, Rhoades, Raina E., Clark, Ryan, Jules, George, McCallister, Monique, Aschner, Michael, Hood, Darryl B.·2012·Toxicological Sciences
DOI 10.1093/toxsci/kfr261PMC PMC3243744
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Abstract

The wild-type (WT) Cpr(lox/lox) (cytochrome P(450) oxidoreductase, Cpr) mouse is an ideal model to assess the contribution of P(450) enzymes to the metabolic activation and disposition of environmental xenobiotics. In the present study, we examined the effect of in utero exposure to benzo(a)pyrene [B(a)P] aerosol on Sp4 and N-methyl-D-aspartate (NMDA)-dependent systems as well as a resulting behavioral phenotype (object discrimination) in Cpr offspring. Results from in utero exposure of WT Cpr(lox/lox) mice were compared with in utero exposed brain-Cpr-null offspring mice. Null mice were used as they do not express brain cytochrome P(450)1B1-associated NADPH oxidoreductase (CYP1B1-associated NADPH oxidoreductase), thus reducing their capacity to produce neural B(a)P metabolites. Subsequent to in utero (E14-E17) exposure to B(a)P (100 μg/m(3)), Cpr(lox/lox) offspring exhibited: (1) elevated B(a)P metabolite and F(2)-isoprostane neocortical tissue burdens, (2) elevated concentrations of cortical glutamate, (3) premature developmental expression of Sp4, (4) decreased subunit ratios of NR2B:NR2A, and (5) deficits in a novelty discrimination phenotype monitored to in utero exposed brain-Cpr-null offspring. Collectively, these findings suggest that in situ generation of metabolites by CYP1B1-associated NADPH oxidoreductase promotes negative effects on NMDA-mediated signaling processes during the period when synapses are first forming as well as effects on a subsequent behavioral phenotype.

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  • Reactive metals and PAHs play a role in eliciting pathology and behavioral dysfunction after PM exposure, versus the elemental carbon fraction alone.

    “Studies teasing apart the critical components of PM responsible for adverse cognitive effects highlight the role of reactive metals, as well as PAHs [122], in eliciting pathology and behavioral dysfunction, versus the elemental carbon fraction alone [118].”

    From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [122]

    The Methods compare prenatal exposure to benzo(a)pyrene (a PAH) on carbon-black particles with carbon black alone, and ‘Rescue of Discrimination Deficit Phenotype’ reports impaired object discrimination in exposed offspring. The Discussion reports neurotoxicity but says there were no observable pathologies in neocortical cytoarchitecture, so the behavioral claim is supported while the claim of elicited pathology is not established by this study. Reactive metals are not the part of the sentence attributed to this citation. (LLM, conf=0.84)

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Metadata

Authors
Li, Z., Chadalapaka, G., Ramesh, A., Khoshbouei, H., Maguire, M., Safe, S., Rhoades, R. E., Clark, R., Jules, G., McCallister, M., Aschner, M., & Hood, D. B.
Affiliations
  • Meharry Medical College (US)
  • Texas A&M Health Science Center (US)
  • Vanderbilt University (US)
Corresponding author
Hood, Darryl B.
ORCID
Venue
Toxicological Sciences
Publisher
Oxford University Press (OUP)
Published
2011-10-10
Volume
125
Issue
1
Pages
233-247
ISSN
  • 1096-0929 (ISSN-L)
  • 1096-6080
DOI
10.1093/toxsci/kfr261
PMC
PMC3243744
OpenAlex
W2139965181
Cited by
29
References
5
Citations by year
2024: 2 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 5 · 2014: 3 · 2013: 1 · 2012: 1
FWCI
1.16
Type
journal article
Language
en
Open access
Locations
  • Toxicological Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • New York State Department of Health
  • New York State Department of Health - Wadsworth Center
  • National Institutes of Health
  • National Institute of Mental Health (T32MH065782)
  • National Institute on Drug Abuse (R01DA026947)
  • National Cancer Institute (R01CA142845)
  • National Institute of Neurological Disorders and Stroke (U54NS041071, R01NS071122)
  • National Institute of Environmental Health Sciences (R56ES017448, S11ES014156)
  • National Center for Research Resources (G12RR003032)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords
benzo[a]pyrene, polycyclic aromatic hydrocarbons, prenatal exposure, cytochrome P450 oxidoreductase, CYP1B1, NADPH oxidoreductase, NMDA receptor, Sp4, object discrimination, glutamate, F2-isoprostanes, prenatal neurodevelopment, behavioral phenotypes
MeSH terms
Aerosols, Animals, Behavior, Animal, Benzo(a)pyrene, Brain, Discrimination Learning, Female, Mice, Inbred C57BL, NADPH-Ferrihemoprotein Reductase, Neurons, Oxidation-Reduction, Particle Size, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, Tissue Distribution, Receptors, N-Methyl-D-Aspartate, Mice, Knockout, Glutamic Acid, Inhalation Exposure, Mice, Soot

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