Neurodevelopmental toxicity of bromoacetamide on zebrafish embryo

• 1、School of Public Health,Soochow University,Suzhou 215123

Abstract： [Objective]To study the neurodevelopmental toxicity and its mechanism caused by bromoacetamide on zebrafish embryo. [Methods]The zebrafish embryos were randomly divided into 6 groups (30 in each group) for exposure, namely the control group and the BAcAm exposure group (0.625, 1.25, 2.5, 5, 10 mg/L). The exposure period is 2-96 hours of post-fertilization (2-96 hpf). The motility, hatching, malformation and body length of zebrafish embryos were detected. The motor ability of zebrafish was tested at 120 hpf. 2,7-Dichlorodi -hydrofluorescein diacetate (DCFH-DA) was used as a probe to detect ROS levels in zebrafish. The expression of neurodevelopment-related genes and ROS-related genes were detected by fluorescence quantitative PCR. [Results]At 72 hpf, compared with the control group, the hatching of zebrafish embryos was delayed in the 10 mg/L BAcAm exposure group (P<0.05). At 96 hpf, compared with the control group, the zebrafish embryos have increased motility rate and malformation rate and shorten body length in the 5 mg/L and 10 mg/L BAcAm exposure groups (P<0.05). Motor ability test found that compared with the control group, the BAcAm exposure group showed a decreasing in exercise distance and exercise time. ROS detection revealed that the expression of ROS in the head area of zebrafish embryos increased after exposure to bromoacetamide (P < 0.05). Quantitative PCR results showed that neurodevelopment-related genes (dlx2, ngn1, elavl3, Shha, mbp, syn2a) were all down-regulated to varying degrees, and ROS-related genes (Cu/Zn sod, gpx, cat, nrf2, ho-1) were all up-regulation to varying degrees, the difference was statistically significant (P < 0.05). [Conclusion]Bromoacetamide induced neurodevelopmental toxicity on zebrafish by causing oxidative stress.

Keywords： Bromoacetamide Zebrafish Neurodevelopmental toxicity Oxidative stress