Neurodevelopmental toxicity of bromadiolone to early-staged zebrafish

Yuanzhao WU; Anhui Zhang; Fan XU; Zhongyu Zheng; Jianbo Ying; Binjie Wang; Jiye Wang; Weixuan Yao

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Neurodevelopmental toxicity of bromadiolone to early-staged zebrafish

VernacularTitle:溴敌隆对斑马鱼早期发育阶段的神经毒性作用
Author: Yuanzhao WU ¹ ; Anhui ZHANG ¹ ; Fan XU ¹ ; Zhongyu ZHENG ¹ ; Jianbo YING ² ; Binjie WANG ¹ ; Jiye WANG ¹ ; Weixuan YAO ³
Author Information

1. Key Laboratory of Drug Prevention and Control Technology of Zhejiang Province, Zhejiang Police College, Hangzhou, Zhejiang 310051, China.
2. Institute of Criminal Science and Technology, Public Security Bureau of Hangzhou, Hangzhou, Zhejiang 310004, China.
3. .
Publication Type:Experiment
Keywords: anticoagulant rodenticide; bromadiolone; zebrafish; neurodevelopmental toxicity
From: Journal of Environmental and Occupational Medicine 2022;39(10):1154-1159
CountryChina
Language:Chinese
Abstract: Background Bromadiolone is the second-generation anticoagulant rodenticide widely used all over the world. Exposure to bromadiolone in early life stage can lead to neurodevelopmental toxicity, but its toxic mechanism of neurodevelopment is not clear so far. Objective To investigate the developmental neurotoxicity and mechanism of bromadiolone to zebrafish embryos. Methods Zebrafish embryos were randomly divided into four groups: a solvent control group (dimethylsulphoxide) and three bromadiolone exposure groups (0.39, 0.78, and 1.18 mg·L⁻¹). The exposure period was from 4 h to 120 h post-fertilization. The number of spontaneous movement per minute was recorded at 24 h post-treatment. The locomotor ability of zebrafish larvae and the activity of acetylcholinesterase (AChE) were tested at 120 h post-treatment. The relative expression levels of neurodevelopment-related genes (elavl3, gap43, mbp, and syn2a) were measured by fluorescence quantitative PCR. Results Compared with the control group, the number of spontaneous movement per minute at 24 h decreased significantly in the 1.18 mg·L⁻¹ bromadiolone exposure group (P<0.05). Compared with the control group, the total distance travelled of the zebrafish larvae in the 0.78 and 1.18 mg·L⁻¹ bromadiolone exposure groups decreased by 60% and 69% respectively (P<0.05, P<0.01), and the total movement time decreased by 34% and 65% respectively (P<0.05, P<0.01). The AChE activity in the 1.18 mg·L⁻¹ bromadiolone exposure group increased by 36% when compared with the control group (P<0.05). The fluorescence quantitative PCR results showed that compared with the control group, the expression levels of neurodevelopment-related genes elavl3, syn2a, and mbp were significantly down-regulated by 66%, 69%, and 65% in the 1.18 mg·L⁻¹ bromadiolone exposure group respectively (P<0.01), the expression level of gap43 was up-regulated by 56% in the 0.78 mg·L⁻¹ bromadiolone exposure group (P<0.01) and down-regulated by 34% in the 1.18 mg·L⁻¹ bromadiolone exposure group (P<0.05). Conclusion Bromadiolone exposure could inhibit spontaneous movement and locomotive behavior, down-regulate the expression levels of neurodevelopment-related genes, hinder the release of neurotransmitters, and result in neurodevelopmental toxicity in the early-staged zebrafish.