Neurotoxicity and transcriptome changes in embryonic zebrafish induced by halobenzoquinone exposure

Halobenzoquinones (HBQs) are emerging disinfection byproducts (DBPs) with a widespread presence in drinking water that exhibit much higher cytotoxicity than regulated DBPs. However, the developmental neurotoxicity of HBQs has not been studied in vivo. In this work, we studied the neurotoxicity of HBQs on zebrafish embryos, after exposure to varying concentrations (0-8 mu mol/L) of three HBQs, 2,5-dichloro-1,4-benzoquinone (2,5-DCBQ), 2,6-dichloro-1,4-benzoquinone (2,6-DCBQ), and 2,5-dibromo-1,4-benzoquinone (2,5-DBBQ) for 4 to 120 hr post fertilization (hpf). HBQ exposure significantly decreased the locomotor activity of larvae, accompanied by significant reduction of neurotransmitters (dopamine and gamma-aminobutyric acid) and acetylcholinesterase activity. Furthermore, the expression of genes involved in neuronal morphogenesis (gfap, alpha 1-tubulin, mbp, and syn-2 alpha) were downregulated by 4.4-, 5.2-, 3.0-, and 4.5-fold in the 5 mu mol/L 2,5-DCBQ group and 2.0-, 1.6-, 2.1-, and 2.3-fold in the 5 mu mol/L 2,5-DBBQ group, respectively. Transcriptomic analysis revealed that HBQ exposure affected the signaling pathways of neural development. This study demonstrates the significant neurotoxicity of HBQs in embryonic zebrafish and provides molecular evidence for understanding the potential mechanisms of HBQ neurotoxicity. (C) 2022 The Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences. Published by Elsevier B.V.

Automated summary

This study investigated the neurotoxicity of halobenzoquinones (HBQs) on zebrafish embryos. The results showed that HBQs could decrease the locomotor activity of zebrafish larvae, reduce neurotransmitters and acetylcholinesterase activity, and inhibit the expression of genes involved in neuronal morphogenesis. Transcriptomic analysis revealed that HBQ exposure affected the signaling pathways of neural development.