ArticleToxicological sciences : an official journal of the Society of Toxicology2011
Repeated developmental exposure of mice to chlorpyrifos oxon is associated with paraoxonase 1 (PON1)-modulated effects on cerebellar gene expression.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Mitochondria as a target of organophosphate and carbamate pesticides: Revisiting common mechanisms of action with new approach methodologies.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Low doses of chlorpyrifos interfere with spermatogenesis of rats through reduction of sex hormones.Environmental science and pollution research international · 2017Article
- Paraoxonases-1, -2 and -3: What are their functions?Chemico-biological interactions · 2016Article
- 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
- A sensitive LC-MS/MS method for measurement of organophosphorus pesticides and their oxygen analogs in air sampling matrices.Journal of environmental science and health. Part. B, Pesticides, food contaminants, and agricultural wastes · 2014Article
- Comparison of polyurethane foam and XAD-2 sampling matrices to measure airborne organophosphorus pesticides and their oxygen analogs in an agricultural community.Chemosphere · 2013Article
- Paraoxonase 1 (PON1) as a genetic determinant of susceptibility to organophosphate toxicity.Toxicology · 2013Review
- Gestational age-dependent changes in gene expression of metabolic enzymes and transporters in pregnant mice.Drug metabolism and disposition: the biological fate of chemicals · 2013Article
- Presence of organophosphorus pesticide oxygen analogs in air samples.Atmospheric environment (Oxford, England : 1994) · 2013Article
- Is autism a disease of the cerebellum? An integration of clinical and pre-clinical research.Frontiers in systems neuroscience · 2013Article
- Chlorpyrifos-, diisopropylphosphorofluoridate-, and parathion-induced behavioral and oxidative stress effects: are they mediated by analogous mechanisms of action?Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Exposure to triaryl phosphates: metabolism and biomarkers of exposure.Journal of biological physics and chemistry : JBPC · 2011Article
- Paraoxonase-1 and Early-Life Environmental Exposures.Annals of global healthReview
- Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon.Neurotoxicology and teratologyArticle
- Neuronal connectivity as a convergent target of gene × environment interactions that confer risk for Autism Spectrum Disorders.Neurotoxicology and teratologyReview
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Authors and funding
7 authors at 3 institutions in 3 countries.
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Abstract
Microarray analysis was used to examine effects of repeated postnatal exposure to chlorpyrifos oxon (CPO) on gene expression in the cerebellum of genetically modified mice. The high-density lipoprotein-associated enzyme paraoxonase 1 (PON1) plays a significant role in the detoxication of CPO, which is present in exposures and generated from chlorpyrifos (CPF) in vivo following exposure. Two factors are important in modulating toxicity of CPO, the Q192R PON1 polymorphism and PON1 plasma level, which is low at birth and increases throughout postnatal development. Mice used in these studies included wild type (PON1(+/+)), PON1 knockout (PON1(-/-)), and two transgenic lines (tgHuPON1(Q192), tgHuPON1(R192)) expressing either human PON1(Q192) or PON1(R192) on the PON1(-/-) background. PON1(R192) hydrolyzes CPO more efficiently than PON1(Q192). All four genotypes exposed to CPO (0.35 or 0.50 mg/kg/day) daily from postnatal day (PND) 4 to PND 21 showed significant differences in gene expression on PND 22 compared with controls. Pathway analysis and Gene Set Analysis revealed multiple pathways and gene sets significantly affected by CPO exposure, including genes involved in mitochondrial dysfunction, oxidative stress, neurotransmission, and nervous system development. Comparison between genotypes revealed specific genes, gene sets, and pathways differentially affected between tgHuPON1(Q192) and tgHuPON1(R192) mice and between PON1(-/-) and PON1(+/+) mice following CPO exposure. Repeated CPO exposure also resulted in a dose-related decrease in brain acetylcholinesterase activity during postnatal development in PON1(-/-) and tgHuPON1(Q192) mice but not in PON1(+/+) or tgHuPON1(R192) mice. These findings indicate that PON1 status plays a critical role in modulating the effects of neonatal CPO exposure in the developing brain.
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