Differential acetylcholinesterase inhibition of chlorpyrifos, diazinon and parathion in larval zebrafish
- Yen, J., Donerly, S., Levin, E.D., and Linney, E.A.
- Neurotoxicology and teratology 33(6): 735-41 (Journal)
- Registered Authors
- Donerly, Sue, Linney, Elwood
- chloropyrifos, zebrafish, AChE, behavior, neurodevelopment, organophosphates
- MeSH Terms
- Behavior, Animal/drug effects
- Cholinesterase Inhibitors/chemistry
- Cholinesterase Inhibitors/toxicity*
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/enzymology
- Embryonic Development/drug effects
- Neurotoxicity Syndromes/embryology*
- Neurotoxicity Syndromes/enzymology
- Neurotoxicity Syndromes/etiology
- Neurotoxicity Syndromes/physiopathology
- Structure-Activity Relationship
- 22036888 Full text @ Neurotoxicol. Teratol.
Yen, J., Donerly, S., Levin, E.D., and Linney, E.A. (2011) Differential acetylcholinesterase inhibition of chlorpyrifos, diazinon and parathion in larval zebrafish. Neurotoxicology and teratology. 33(6):735-41.
Zebrafish are increasingly used for developmental neurotoxicity testing because early embryonic events are easy to visualize, exposures are done without affecting the mother and the rapid development of zebrafish allows for high throughput testing. We used zebrafish to examine how exposures to three different organophosphorus pesticides (chlorpyrifos, diazinon and parathion) over the first five days of embryonic and larval development of zebrafish affected their survival, acetylcholinesterase (AChE) activity and behavior. We show that at non-lethal, equimolar concentrations, chlorpyrifos (CPF) is more effective at equimolar concentrations than diazinon (DZN) and parathion (PA) in producing AChE inhibition. As concentrations of DZN and PA are raised, lethality occurs before they can produce the degree of AChE inhibition observed with CPF at 300 nM. Because of its availability outside the mother at the time of fertilization, zebrafish provides a complementary model for studying the neurotoxicity of very early developmental exposures.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes