ZFIN ID: ZDB-PUB-160329-9
Developmental exposure of zebrafish larvae to organophosphate flame retardants causes neurotoxicity
Sun, L., Xu, W., Peng, T., Chen, H., Ren, L., Tan, H., Xiao, D., Qian, H., Fu, Z.
Date: 2016
Source: Neurotoxicology and teratology   55: 16-22 (Journal)
Registered Authors:
Keywords: Acetylcholinesterase (AChE) activity, Aquatic organism, Early life stage, Gene transcriptional analysis, Locomotor behavior, Nervous system
MeSH Terms:
  • Acetylcholinesterase/metabolism
  • Animals
  • Behavior, Animal/drug effects*
  • Chlorpyrifos/toxicity
  • Female
  • Flame Retardants/toxicity*
  • Insecticides/toxicity*
  • Organophosphates/toxicity*
  • Organophosphorus Compounds/toxicity
  • Phosphines/toxicity
  • Pregnancy
  • Prenatal Exposure Delayed Effects/metabolism*
  • Prenatal Exposure Delayed Effects/psychology*
  • Swimming
  • Transcription, Genetic/drug effects
  • Zebrafish/genetics
  • Zebrafish/physiology
PubMed: 27018022 Full text @ Neurotoxicol. Teratol.
With the gradual ban on brominated flame retardants (FRs), the application of organophosphate flame retardants (OPFRs) has increased remarkably. Considering the structural similarity between OPFRs and organophosphate pesticides, hypotheses that OPFRs may interfere with neurodevelopment as organophosphate pesticides are reasonable. In this study, the neurotoxicity of three OPFRs, including tri-n-butyl phosphate (TNBP), tris (2-butoxyethyl) phosphate (TBOEP) and tris (2-chloroethyl) phosphate (TCEP), was evaluated in zebrafish larvae and then compared with the neurotoxicity of organophosphate pesticide chlorpyrifos (CPF). The results showed that similar to CPF, exposure to OPFRs for 5days resulted in significant changes in locomotor behavior, either in free swimming or in photomotor response. However, given the transcriptional changes that occur in nervous system genes in response to OPFRs and CPF, as well as the altered enzyme activity of AChE and its mRNA level, the underlying mechanisms for neurotoxicity among these organophosphate chemicals might be varied. In summary, the results confirm the potential neurodevelopmental toxicity of OPFRs and underscore the importance of identifying the mechanistic targets of the OPFRs with specific moieties. Furthermore, as the neurobehavioral responses are well conserved among vertebrates and the exposure of children to OPFRs is significant, a thorough assessment of the risk of OPFRs exposure during early development should be highly emphasized in future studies.