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Microcystin-LR exposure induces developmental neurotoxicity in zebrafish embryo

文献类型： 外文期刊

作者： Wu, Qin 1 ; Yan, Wei 2 ; Liu, Chunsheng 1 ; Li, Li 1 ; Yu, Liqin 1 ; Zhao, Sujuan 4 ; Li, Guangyu 1 ;

作者机构： 1.Huazhong Agr Univ, Coll Fisheries, Wuhan 430070, Peoples R China

2.Hubei Acad Agr Sci, Inst Agr Qual Stand & Testing Technol, Wuhan 430064, Peoples R China

3.Minist Agr, Key Lab Freshwater Anim Breeding, Wuhan 430070, Peoples R China

4.Anhui Med Univ, Sch Publ Hlth, Hefei 230032, Peoples R China

关键词： MCLR;Zebrafish embryo;Developmental neurotoxicity;Acetylcholine;Dopamine

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：8.071； 五年影响因子：8.35 ）

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收录情况： SCI

摘要： Microcystin-LR (MCLR) is a commonly acting potent hepatotoxin and has been pointed out of potentially causing developmental neurotoxicity, but the exact mechanism is little known. In this study, zebrafish embryos were exposed to 0, 0.8, 1.6 or 3.2 mg/L MCLR for 120 h. MCLR exposure through submersion caused serious hatching delay and body length decrease. The content of MCLR in zebrafish larvae was analyzed and the results demonstrated that MCLR can accumulate in zebrafish larvae. The locomotor speed of zebrafish larvae was decreased. Furthermore, the dopamine and acetylcholine (ACh) content were detected to be significantly decreased in MCLR exposure groups. And the acetylcholinesterase (AChE) activity was significantly increased after exposure to 1.6 and 3.2 mg/L MCLR. The transcription pattern of manf, chrn alpha 7 and ache gene was consistent with the change of the dopamine content, ACh content and AChE activity. Gene expression involved in the development of neurons was also measured. a1-tubulin and shha gene expression were down-regulated, whereas mbp and gap43 gene expression were observed to be significantly up-regulated upon exposure to MCLR. The above results indicated that MCLR-induced developmental toxicity might attribute to the disorder of cholinergic system, dopaminergic signaling, and the development of neurons. (C) 2016 Elsevier Ltd. All rights reserved.

  • 相关文献

[1]Parental transfer of microcystin-LR induced transgenerational effects of developmental neurotoxicity in zebrafish offspring. Wu, Qin,Cheng, Houcheng,Liu, Chunsheng,Li, Guangyu,Wu, Qin,Cheng, Houcheng,Li, Guangyu,Yan, Wei,Hung, Tien-Chieh,Li, Guangyu,Li, Guangyu,Guo, Xiaochun. 2017

[2]Parental exposure to microcystin-LR induced thyroid endocrine disruption in zebrafish offspring, a transgenerational toxicity. Cheng, Houcheng,Wu, Qin,Liu, Chunsheng,Gong, Xiuying,Li, Guangyu,Cheng, Houcheng,Wu, Qin,Gong, Xiuying,Li, Guangyu,Yan, Wei,Hung, Tien-Chieh,Li, Guangyu,Li, Guangyu.

[3]Microcystin-LR induces changes in the GABA neurotransmitter system of zebrafish. Yan, Wei,Li, Li,Li, Guangyu,Zhao, Sujuan.

[4]The role of apoptosis in MCLR-induced developmental toxicity in zebrafish embryos. Zeng, Cheng,Wang, Jianghua,Zhang, Guirong,Chen, Nan,Li, Guangyu,Sun, Hong,Xie, Ping,Li, Guangyu,Yan, Wei. 2014

[5]Waterborne exposure to microcystin-LR alters thyroid hormone levels and gene transcription in the hypothalamic-pituitary-thyroid axis in zebrafish larvae. Chen, Jun,Yan, Wei,Zhou, Youxiang,Yang, Jie,Li, Shuqian,Hu, Dingjin,Wang, Jianghua,Li, Guangyu. 2012

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