ZFIN ID: ZDB-PUB-161231-3
Developmental Neurotoxicity of Methamidophos in the Embryo-Larval Stages of Zebrafish
He, X., Gao, J., Dong, T., Chen, M., Zhou, K., Chang, C., Luo, J., Wang, C., Wang, S., Chen, D., Zhou, Z., Tian, Y., Xia, Y., Wang, X.
Date: 2016
Source: International Journal of Environmental Research and Public Health   14(1): (Journal)
Registered Authors: Wang, Chao
Keywords: developmental neurotoxicity, methamidophos, toxicology, zebrafish
MeSH Terms:
  • Animals
  • Apoptosis/drug effects
  • Embryo, Nonmammalian
  • Gene Expression Regulation, Developmental
  • Insecticides/pharmacology*
  • Larva/drug effects*
  • Neurotoxicity Syndromes/embryology*
  • Organophosphorus Compounds/pharmacology*
  • Organothiophosphorus Compounds/pharmacology*
  • RNA, Messenger/genetics
  • Zebrafish/embryology*
PubMed: 28036051 Full text @ Int. J. Environ. Res. Public Health
Methamidophos is a representative organophosphate insecticide. The knowledge of its developmental neurotoxicity is limited, especially for zebrafish in the early stages of their life. Four hour post-fertilization (hpf) zebrafish embryos were exposed to several environmentally relevant concentrations of methamidophos (0, 25, and 500 μg/L) for up to 72 hpf. Locomotor behavior was then studied in the zebrafish larvae at this timepoint. Acridine orange (AO) staining was carried out in the zebrafish larvae, and the mRNA levels of genes associated with neural development (mbp and syn2a) were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). The number of escape responders for mechanical stimulation was significantly decreased in exposed groups. AO staining showed noticeable signs of apoptosis mainly in the brain. In addition, the mRNA levels of mbp and syn2a were both significantly down-regulated in exposed groups. Our study provides the first evidence that methamidophos exposure can cause developmental neurotoxicity in the early stages of zebrafish life, which may be caused by the effect of methamidophos on neurodevelopmental genes and the activation of cell apoptosis in the brain.