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University of Washington: Dataset Details, ID=GSE58103

Superfund Research Program

Effects-Related Biomarkers of Environmental Neurotoxic Exposures

Center Director: Evan P. Gallagher
Grant Number: P42ES004696
Funding Period: 1987-2023
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Title: Repeated gestational exposure of mice to chlorpyrifos oxon is associated with paraoxonase 1 (PON1)-modulated effects in maternal and fetal tissues

Accession Number: GSE58103

Link to Dataset:

Repository: Gene Expression Omnibus (GEO)

Data Type(s): Gene Expression

Experiment Type(s): Expression profiling by array

Organism(s): Mus musculus

Summary: Chlorpyrifos oxon (CPO), the toxic metabolite of the organophosphorus (OP) insecticide chlorpyrifos, causes developmental neurotoxicity in humans and rodents. CPO is hydrolyzed by paraoxonase-1 (PON1), with protection determined by PON1 levels and the human Q192R polymorphism. To examine how the Q192R polymorphism influences fetal toxicity associated with gestational CPO exposure, we measured biomarker inhibition and fetal-brain gene expression in wild-type (PON1+/+), PON1-knockout (PON1-/-), and tgHuPON1R192 and tgHuPON1Q192 transgenic mice. Pregnant mice exposed dermally to 0, 0.50, 0.75 or 0.85 mg/kg/d CPO from gestational days (GD) 6 through 17 were sacrificed on GD18. Biomarkers of CPO exposure inhibited in maternal tissues included brain acetylcholinesterase (AChE), RBC acylpeptide hydrolase (APH), plasma butyrylcholinesterase (BChE) and carboxylesterase (CES). Fetal plasma BChE was inhibited in PON1-/- and tgHuPON1Q192, but not PON1+/+ or tgHuPON1R192 mice. Fetal brain AChE and plasma CES were inhibited in PON1-/- mice, but not in other genotypes.

Publication(s) associated with this dataset:
  • Cole TB, Li WF, Co AL, Hay AM, MacDonald JW, Bammler TK, Farin FM, Costa LG, Furlong CE. 2014. Repeated gestational exposure of mice to chlorpyrifos oxon is associated with paraoxonase 1 (PON1) modulated effects in maternal and fetal tissues. Toxicol Sci 141(2):409-422. doi:10.1093/toxsci/kfu144 PMID:25070982 PMCID:PMC4271046
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