Chlorpyrifos

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  Subject Areas on Research

  • Adverse benzo[a]pyrene effects on neurodifferentiation are altered by other neurotoxicant coexposures: interactions with dexamethasone, chlorpyrifos, or nicotine in PC12 cells. 
  • Alpha7 nicotinic acetylcholine receptors targeted by cholinergic developmental neurotoxicants: nicotine and chlorpyrifos. 
  • Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. 
  • Alterations in serotonin transporter expression in brain regions of rats exposed neonatally to chlorpyrifos. 
  • Ameliorating the developmental neurotoxicity of chlorpyrifos: a mechanisms-based approach in PC12 cells. 
  • Amyloid precursor protein 96-110 and beta-amyloid 1-42 elicit developmental anomalies in sea urchin embryos and larvae that are alleviated by neurotransmitter analogs for acetylcholine, serotonin and cannabinoids. 
  • An invertebrate model of the developmental neurotoxicity of insecticides: effects of chlorpyrifos and dieldrin in sea urchin embryos and larvae. 
  • Behavioral alterations in adolescent and adult rats caused by a brief subtoxic exposure to chlorpyrifos during neurulation. 
  • Benzo[a]pyrene impairs neurodifferentiation in PC12 cells. 
  • Brain anomalies in children exposed prenatally to a common organophosphate pesticide. 
  • Cellular mechanisms for developmental toxicity of chlorpyrifos: targeting the adenylyl cyclase signaling cascade. 
  • Chlorpyrifos affects phenotypic outcomes in a model of mammalian neurodevelopment: critical stages targeting differentiation in PC12 cells. 
  • Chlorpyrifos developmental neurotoxicity: interaction with glucocorticoids in PC12 cells. 
  • Chlorpyrifos elicits mitotic abnormalities and apoptosis in neuroepithelium of cultured rat embryos. 
  • Chlorpyrifos exposure during a critical neonatal period elicits gender-selective deficits in the development of coordination skills and locomotor activity. 
  • Chlorpyrifos exposure during neurulation: cholinergic synaptic dysfunction and cellular alterations in brain regions at adolescence and adulthood. 
  • Chlorpyrifos exposure of developing zebrafish: effects on survival and long-term effects on response latency and spatial discrimination. 
  • Chlorpyrifos interferes with cell development in rat brain regions. 
  • Chlorpyrifos oxon binds directly to muscarinic receptors and inhibits cAMP accumulation in rat striatum. 
  • Chlorpyrifos oxon interacts with the mammalian multidrug resistance protein, P-glycoprotein. 
  • Chlorpyrifos releases norepinephrine from adult and neonatal rat brain synaptosomes. 
  • Chlorpyrifos targets developing glia: effects on glial fibrillary acidic protein. 
  • Cholinergic synaptic signaling mechanisms underlying behavioral teratogenicity: effects of nicotine, chlorpyrifos, and heroin converge on protein kinase C translocation in the intermedial part of the hyperstriatum ventrale and on imprinting behavior in an avian model. 
  • Contamination of rural surface and ground water by endosulfan in farming areas of the Western Cape, South Africa. 
  • Critical duration of exposure for developmental chlorpyrifos-induced neurobehavioral toxicity. 
  • Critical periods for chlorpyrifos-induced developmental neurotoxicity: alterations in adenylyl cyclase signaling in adult rat brain regions after gestational or neonatal exposure. 
  • Critical periods for the role of oxidative stress in the developmental neurotoxicity of chlorpyrifos and terbutaline, alone or in combination. 
  • Determination of diazinon, chlorpyrifos, and their metabolites in rat plasma and urine by high-performance liquid chromatography. 
  • Development of a high-performance liquid chromatographic method for the quantification of chlorpyrifos, pyridostigmine bromide, N,N-diethyl-m-toluamide and their metabolites in rat plasma and urine. 
  • Developmental chlorpyrifos effects on hatchling zebrafish swimming behavior. 
  • Developmental cholinotoxicants: nicotine and chlorpyrifos. 
  • Developmental effects of chlorpyrifos extend beyond neurotoxicity: critical periods for immediate and delayed-onset effects on cardiac and hepatic cell signaling. 
  • Developmental exposure of rats to chlorpyrifos elicits sex-selective hyperlipidemia and hyperinsulinemia in adulthood. 
  • Developmental exposure of rats to chlorpyrifos leads to behavioral alterations in adulthood, involving serotonergic mechanisms and resembling animal models of depression. 
  • Developmental exposure to chlorpyrifos elicits sex-selective alterations of serotonergic synaptic function in adulthood: critical periods and regional selectivity for effects on the serotonin transporter, receptor subtypes, and cell signaling. 
  • Developmental exposure to organophosphates triggers transcriptional changes in genes associated with Parkinson's disease in vitro and in vivo. 
  • Developmental exposure to terbutaline alters cell signaling in mature rat brain regions and augments the effects of subsequent neonatal exposure to the organophosphorus insecticide chlorpyrifos. 
  • Developmental exposure to terbutaline and chlorpyrifos, separately or sequentially, elicits presynaptic serotonergic hyperactivity in juvenile and adolescent rats. 
  • Developmental exposure to terbutaline and chlorpyrifos: pharmacotherapy of preterm labor and an environmental neurotoxicant converge on serotonergic systems in neonatal rat brain regions. 
  • Developmental neurotoxic effects of chlorpyrifos on acetylcholine and serotonin pathways in an avian model. 
  • Developmental neurotoxicants target neurodifferentiation into the serotonin phenotype: Chlorpyrifos, diazinon, dieldrin and divalent nickel. 
  • Developmental neurotoxicity elicited by gestational exposure to chlorpyrifos: when is adenylyl cyclase a target? 
  • Developmental neurotoxicity elicited by prenatal or postnatal chlorpyrifos exposure: effects on neurospecific proteins indicate changing vulnerabilities. 
  • Developmental neurotoxicity of chlorpyrifos in vivo and in vitro: effects on nuclear transcription factors involved in cell replication and differentiation. 
  • Developmental neurotoxicity of chlorpyrifos modeled in vitro: comparative effects of metabolites and other cholinesterase inhibitors on DNA synthesis in PC12 and C6 cells. 
  • Developmental neurotoxicity of chlorpyrifos: cellular mechanisms. 
  • Developmental neurotoxicity of chlorpyrifos: delayed targeting of DNA synthesis after repeated administration. 
  • Developmental neurotoxicity of chlorpyrifos: what is the vulnerable period? 
  • Developmental neurotoxicity of organophosphates targets cell cycle and apoptosis, revealed by transcriptional profiles in vivo and in vitro. 
  • Developmental neurotoxicity targeting hepatic and cardiac sympathetic innervation: effects of organophosphates are distinct from those of glucocorticoids. 
  • Differential acetylcholinesterase inhibition of chlorpyrifos, diazinon and parathion in larval zebrafish. 
  • Disparate developmental neurotoxicants converge on the cyclic AMP signaling cascade, revealed by transcriptional profiles in vitro and in vivo. 
  • Diverse neurotoxicants converge on gene expression for neuropeptides and their receptors in an in vitro model of neurodifferentiation: effects of chlorpyrifos, diazinon, dieldrin and divalent nickel in PC12 cells. 
  • Does pharmacotherapy for preterm labor sensitize the developing brain to environmental neurotoxicants? Cellular and synaptic effects of sequential exposure to terbutaline and chlorpyrifos in neonatal rats. 
  • Does the developmental neurotoxicity of chlorpyrifos involve glial targets? Macromolecule synthesis, adenylyl cyclase signaling, nuclear transcription factors, and formation of reactive oxygen in C6 glioma cells. 
  • Does thyroid disruption contribute to the developmental neurotoxicity of chlorpyrifos? 
  • Early biochemical detection of delayed neurotoxicity resulting from developmental exposure to chloropyrifos. 
  • Effects of sub-chronic in vivo chlorpyrifos exposure on muscarinic receptors and adenylate cyclase of rat striatum. 
  • Exposure to organophosphates reduces the expression of neurotrophic factors in neonatal rat brain regions: similarities and differences in the effects of chlorpyrifos and diazinon on the fibroblast growth factor superfamily. 
  • Fetal chlorpyrifos exposure: adverse effects on brain cell development and cholinergic biomarkers emerge postnatally and continue into adolescence and adulthood. 
  • Fetal nicotinic overload, blunted sympathetic responsivity, and obesity. 
  • Imbalances emerge in cardiac autonomic cell signaling after neonatal exposure to terbutaline or chlorpyrifos, alone or in combination. 
  • In utero exposure to nicotine and chlorpyrifos alone, and in combination produces persistent sensorimotor deficits and Purkinje neuron loss in the cerebellum of adult offspring rats. 
  • In vitro effect of chlorpyrifos oxon on muscarinic receptors and adenylate cyclase. 
  • Increased expression of glial fibrillary acidic protein in cerebellum and hippocampus: differential effects on neonatal brain regional acetylcholinesterase following maternal exposure to combined chlorpyrifos and nicotine. 
  • Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. 
  • Inhibition and recovery of maternal and fetal cholinesterase enzymes following a single oral dose of chlorpyrifos in rats. 
  • Inhibition of cholinesterase enzymes following a single dermal dose of chlorpyrifos and methyl parathion, alone and in combination, in pregnant rats. 
  • Is fipronil safer than chlorpyrifos? Comparative developmental neurotoxicity modeled in PC12 cells. 
  • Is oxidative stress involved in the developmental neurotoxicity of chlorpyrifos? 
  • Maternal exposure to nicotine and chlorpyrifos, alone and in combination, leads to persistently elevated expression of glial fibrillary acidic protein in the cerebellum of the offspring in late puberty. 
  • Modeling the developmental neurotoxicity of chlorpyrifos in vitro: macromolecule synthesis in PC12 cells. 
  • Modeling the developmental neurotoxicity of chlorpyrifos in vitro: macromolecule synthesis in PC12 cells. 
  • Morphologic effects of subtoxic neonatal chlorpyrifos exposure in developing rat brain: regionally selective alterations in neurons and glia. 
  • Neonatal chlorpyrifos administration elicits deficits in immune function in adulthood: a neural effect? 
  • Neonatal chlorpyrifos exposure alters synaptic development and neuronal activity in cholinergic and catecholaminergic pathways. 
  • Neonatal chlorpyrifos exposure targets multiple proteins governing the hepatic adenylyl cyclase signaling cascade: implications for neurotoxicity. 
  • Nicotine is a developmental neurotoxicant and neuroprotectant: stage-selective inhibition of DNA synthesis coincident with shielding from effects of chlorpyrifos. 
  • Nonenzymatic functions of acetylcholinesterase splice variants in the developmental neurotoxicity of organophosphates: chlorpyrifos, chlorpyrifos oxon, and diazinon. 
  • Organophosphate exposure during a critical developmental stage reprograms adenylyl cyclase signaling in PC12 cells. 
  • Oxidative and excitatory mechanisms of developmental neurotoxicity: transcriptional profiles for chlorpyrifos, diazinon, dieldrin, and divalent nickel in PC12 cells. 
  • Oxidative mechanisms contributing to the developmental neurotoxicity of nicotine and chlorpyrifos. 
  • Oxidative stress from diverse developmental neurotoxicants: antioxidants protect against lipid peroxidation without preventing cell loss. 
  • Perinatal exposure to environmental tobacco smoke upregulates nicotinic cholinergic receptors in monkey brain. 
  • Persistent behavioral consequences of neonatal chlorpyrifos exposure in rats. 
  • Persistent cholinergic presynaptic deficits after neonatal chlorpyrifos exposure. 
  • Pharmacokinetic profile and placental transfer of a single intravenous injection of [(14)C]chlorpyrifos in pregnant rats. 
  • Prenatal chlorpyrifos exposure elicits presynaptic serotonergic and dopaminergic hyperactivity at adolescence: critical periods for regional and sex-selective effects. 
  • Prenatal chlorpyrifos exposure in rats causes persistent behavioral alterations. 
  • Prenatal dexamethasone augments the neurobehavioral teratology of chlorpyrifos: significance for maternal stress and preterm labor. 
  • Prenatal dexamethasone augments the sex-selective developmental neurotoxicity of chlorpyrifos: implications for vulnerability after pharmacotherapy for preterm labor. 
  • Prenatal dexamethasone, as used in preterm labor, worsens the impact of postnatal chlorpyrifos exposure on serotonergic pathways. 
  • Prenatal drug exposures sensitize noradrenergic circuits to subsequent disruption by chlorpyrifos. 
  • Prenatal nicotine alters the developmental neurotoxicity of postnatal chlorpyrifos directed toward cholinergic systems: better, worse, or just "different?". 
  • Prenatal nicotine changes the response to postnatal chlorpyrifos: Interactions targeting serotonergic synaptic function and cognition. 
  • Protein kinase C is a target for diverse developmental neurotoxicants: transcriptional responses to chlorpyrifos, diazinon, dieldrin and divalent nickel in PC12 cells. 
  • Quantification of nicotine, chlorpyrifos and their metabolites in rat plasma and urine using high-performance liquid chromatography. 
  • Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. 
  • Response to the letter of Hanley et al. ([1999] Teratology 59:323-324), concerning the article by Roy et al. ([1998] Teratology 58:62-68) 
  • Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by allographic transplantation of adult subventricular zone-derived neural stem cells. 
  • Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by nicotine administration and neural stem cell transplantation. 
  • Sensorimotor deficits and increased brain nicotinic acetylcholine receptors following exposure to chlorpyrifos and/or nicotine in rats. 
  • Serotonergic systems targeted by developmental exposure to chlorpyrifos: effects during different critical periods. 
  • Silver impairs neurodevelopment: studies in PC12 cells. 
  • Simultaneous determination of chlorpyrifos, permethrin, and their metabolites in rat plasma and urine by high-performance liquid chromatography. 
  • Targeting of neurotrophic factors, their receptors, and signaling pathways in the developmental neurotoxicity of organophosphates in vivo and in vitro. 
  • The alterations in CNS serotonergic mechanisms caused by neonatal chlorpyrifos exposure are permanent. 
  • The organophosphate pesticide chlorpyrifos affects form deprivation myopia. 
  • The sea urchin embryo, an invertebrate model for mammalian developmental neurotoxicity, reveals multiple neurotransmitter mechanisms for effects of chlorpyrifos: therapeutic interventions and a comparison with the monoamine depleter, reserpine. 
  • Transcriptional biomarkers distinguish between vulnerable periods for developmental neurotoxicity of chlorpyrifos: Implications for toxicogenomics. 
  • Transcriptional profiles for glutamate transporters reveal differences between organophosphates but similarities with unrelated neurotoxicants. 
  • Transcriptional profiles reveal similarities and differences in the effects of developmental neurotoxicants on differentiation into neurotransmitter phenotypes in PC12 cells. 
  • Ultraviolet photolysis of chlorpyrifos: developmental neurotoxicity modeled in PC12 cells. 
  • Zebrafish as a neurotoxicological model. 
  • Zebrafish provide a sensitive model of persisting neurobehavioral effects of developmental chlorpyrifos exposure: comparison with nicotine and pilocarpine effects and relationship to dopamine deficits. 
  • [Cholinergic regulation of the sea urchin embryonic and larval development]. 
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  Keywords of People

  • Ferguson, P. Lee, Associate Professor of Civil and Environmental Engineering, Civil and Environmental Engineering