Bisphenol A Analogues Induce Neuroendocrine Disruption via Gut-Brain Regulation in Zebrafish
文献类型： 外文期刊
作者： Mu, Xiyan 1 ; Liu, Zaiteng 1 ; Zhao, Xiaoyu 1 ; Yuan, Lilai 2 ; Li, Yingren 2 ; Wang, Chengju 3 ; Xiao, Guohua 4 ; Mu, Jiandong 4 ; Qiu, Jing 1 ; Qian, Yongzhong 1 ;
作者机构： 1.Chinese Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, Beijing 100081, Peoples R China
2.Chinese Acad Fishery Sci, Fishery Resource & Environm Res Ctr, Beijing 214081, Peoples R China
3.China Agr Univ, Coll Sci, Beijing 100083, Peoples R China
4.Hebei Ocean & Fisheries Sci Res Inst, Qinhuangdao 066000, Peoples R China
5.Hebei Marine Living Resources & Environm Key Lab, Qinhuangdao 066004, Peoples R China
关键词： zebrafish; bisphenol analogues; neuroendocrinedisruption; gut-brain axis; vagal neuron
期刊名称：ENVIRONMENTAL SCIENCE & TECHNOLOGY （ 影响因子：11.4； 五年影响因子：12.0 ）
ISSN： 0013-936X
年卷期： 2024 年 58 卷 2 期
页码：
收录情况： SCI
摘要： There is epidemiological evidence in humans that exposure to endocrine-disrupting chemicals such as bisphenol A (BPA) is tied to abnormal neuroendocrine function with both behavioral and intestinal symptoms. However, the underlying mechanism of this effect, particularly the role of gut-brain regulation, is poorly understood. We exposed zebrafish embryos to a concentration series (including environmentally relevant levels) of BPA and its analogues. The analogue bisphenol G (BPG) yielded the strongest behavioral impact on zebrafish larvae and inhibited the largest number of neurotransmitters, with an effective concentration of 0.5 mu g/L, followed by bisphenol AF (BPAF) and BPA. In neurod1:EGFP transgenic zebrafish, BPG and BPAF inhibited the distribution of enteroendocrine cells (EECs), which is associated with decreased neurotransmitters level and behavioral activity. Immune staining of ace-alpha-tubulin suggested that BPAF inhibited vagal neural development at 50 and 500 mu g/L. Single-cell RNA-Seq demonstrated that BPG disrupted the neuroendocrine system by inducing inflammatory responses in intestinal epithelial cells via TNF alpha-trypsin-EEC signaling. BPAF exposure activated apoptosis and inhibited neural developmental pathways in vagal neurons, consistent with immunofluorescence imaging studies. These findings show that both BPG and BPAF affect the neuroendocrine system through the gut-brain axis but by different mechanisms, revealing new insights into the modes of bisphenol-mediated neuroendocrine disruption.
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