|ZFIN ID: ZDB-PUB-210106-17|
Effects of acetochlor on neurogenesis and behaviour in zebrafish at early developmental stages
Wang, H., Meng, Z., Zhou, L., Cao, Z., Liao, X., Ye, R., Lu, H.
|Source:||Chemosphere 220: 954-964 (Journal)|
|Registered Authors:||Lu, Huiqiang|
|Keywords:||AChE, Acetochlor, Apoptosis, Neurotoxicity, Oxidative stress, Zebrafish|
|PubMed:||33395817 Full text @ Chemosphere|
Wang, H., Meng, Z., Zhou, L., Cao, Z., Liao, X., Ye, R., Lu, H. (2019) Effects of acetochlor on neurogenesis and behaviour in zebrafish at early developmental stages. Chemosphere. 220:954-964.
ABSTRACTThe herbicide acetochlor is used in most parts of the world and is frequently detected in agricultural land and surface water; however, knowledge on the neurotoxicity of acetochlor is limited. Here, to test the effects of acetochlor on zebrafish development and behaviour, zebrafish embryos were exposed to acetochlor from 6 h post-fertilization (hpf) to 24 hpf, and larvae at 6 days post-fertilization (dpf) were exposed to acetochlor for 24 h. Both were exposed to 5, 10, or 20 mg/L acetochlor. We found that acetochlor induced developmental abnormalities, locomotion variations and changes in the physiology and gene expression in the embryos and larvae. The abnormalities included spinal curvature, brain abnormalities, and the decreased formation of newborn neurons. Larval locomotion was decreased with increases in the absolute turn angle and sinuosity. Acetylcholinesterase activity reduced in both embryos and larvae, and the expression of genes that are involved in neurodevelopment and the neurotransmitter system altered. Acetochlor increased the production of ROS and the accumulation of MDA but decreased CAT activity in the embryonic brain. Additionally, acetochlor induced cell death in the brain and tail spinal cord, and the expression of the apoptosis-related genes Bcl2 and caspase 3 were significantly upregulated. Collectively, this is the first study to examine the molecular and physiological effects of acetochlor on neuronal development, and the potential mechanisms appear to be associated with oxidative stress and decreased AChE activity, which disrupt the expression of nervous system genes and apoptosis-related genes and finally lead to apoptosis and morphological malformations.
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