ArticleToxicology and applied pharmacology2010
Toxicogenomic profiling in maternal and fetal rodent brains following gestational exposure to chlorpyrifos.
Article in Toxicology and applied pharmacology, 2010. 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, 45 citations in OpenAlex.
- Modulation of CREB and its associated upstream signaling pathways in pesticide-induced neurotoxicity.Molecular and cellular biochemistry · 2022Review
- Developmental and social deficits and enhanced sensitivity to prenatal chlorpyrifos in PON1-/- mouse pups and adults.PloS one · 2020Article
- Impaired innate and conditioned social behavior in adult C57Bl6/J mice prenatally exposed to chlorpyrifos.Behavioral and brain functions : BBF · 2019Article
- The Role of Omics in the Application of Adverse Outcome Pathways for Chemical Risk Assessment.Toxicological sciences : an official journal of the Society of Toxicology · 2017Review
- Prenatal chlorpyrifos leads to autism-like deficits in C57Bl6/J mice.Environmental health : a global access science source · 2017Article
- Differential epigenetic effects of chlorpyrifos and arsenic in proliferating and differentiating human neural progenitor cells.Reproductive toxicology (Elmsford, N.Y.) · 2016Article
- Prenatal exposure to a common organophosphate insecticide delays motor development in a mouse model of idiopathic autism.PloS one · 2015Article
- Article
- Repeated gestational exposure of mice to chlorpyrifos oxon is associated with paraoxonase 1 (PON1) modulated effects in maternal and fetal tissues.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Genomic and phenotypic alterations of the neuronal-like cells derived from human embryonal carcinoma stem cells (NT2) caused by exposure to organophosphorus compounds paraoxon and mipafox.International journal of molecular sciences · 2014Article
- Toxicogenomic studies of human neural cells following exposure to organophosphorus chemical warfare nerve agent VX.Neurochemical research · 2013Article
- Repeated developmental exposure of mice to chlorpyrifos oxon is associated with paraoxonase 1 (PON1)-modulated effects on cerebellar gene expression.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Dose-related gene expression changes in forebrain following acute, low-level chlorpyrifos exposure in neonatal rats.Toxicology and applied pharmacology · 2010Article
- Paraoxonase-1 and Early-Life Environmental Exposures.Annals of global healthReview
- Neuronal connectivity as a convergent target of gene × environment interactions that confer risk for Autism Spectrum Disorders.Neurotoxicology and teratologyReview
- Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Considering the wide variety of effects that have been reported to occur in the developmental neurotoxicity of chlorpyrifos (CP) and the lack of consensus on their dependence of brain acetylcholinesterase (AChE) activity inhibition, we applied microarray technology to explore dose-dependent alterations in transcriptional response in the fetal and maternal C57BL/6 mouse brain after daily gestational exposure (days 6 to 17) to CP (2, 4, 10, 12 or 15 mg/kg, sc). We identified significantly altered genes across doses and assessed for overrepresentation of Gene Ontology (GO) biological processes and KEGG pathways. We further clustered genes based on their expression profiles across doses and repeated the GO/pathways analysis for each cluster. The dose-effect relationship of CP on gene expression, both at the gene and pathway levels was non-monotonic and not necessarily related to brain AChE inhibition. The largest impact was observed in the 10mg/kg dose group which was also the LOAEL for brain AChE inhibition. In the maternal brain, lower doses (4 mg/kg) influenced GO categories and pathways such as cell adhesion, behavior, lipid metabolism, long-term potentiation, nervous system development, neurogenesis, synaptic transmission. In the fetal brain, lower doses (2 and/or 4 mg/kg) significantly altered cell division, translation, transmission of nerve impulse, chromatin modification, long-term potentiation. In addition, some genes involved in nervous system development and signaling were shown to be specifically influenced by these lower CP doses. Our approach was sensitive and reflected the diversity of responses known to be disrupted by CP and highlighted possible additional consequences of CP neurotoxicity, such as disturbance of the ubiquitin proteasome system.
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Registered trials
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