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题名: A protective role of autophagy in TDCIPP-induced developmental neurotoxicity in zebrafish larvae
作者: Li, Ruiwen1, 2, 3; Zhang, Ling1, 2; Shi, Qipeng3; Guo, Yongyong3; Zhang, Wei4; Zhou, Bingsheng3
关键词: TDCIPP ; Developmental neurotoxicity ; Autophagy ; LC3 II ; Zebrafish larvae
刊名: AQUATIC TOXICOLOGY
发表日期: 2018-06-01
DOI: 10.1016/j.aquatox.2018.03.016
卷: 199, 页:46-54
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
类目[WOS]: Marine & Freshwater Biology ; Toxicology
研究领域[WOS]: Marine & Freshwater Biology ; Toxicology
英文摘要: Tris (1, 3-dichloro-2-propyl) phosphate (TDCIPP), an extensively used organophosphorus flame retardant, is frequently detected in various environmental media and biota, and has been demonstrated as neurotoxic. Autophagy has been proposed as a protective mechanism against toxicant-induced neurotoxicity. The purpose of the present study was to investigate the effect of TDCIPP exposure on autophagy, and its role in TDCIPP-induced developmental neurotoxicity. Zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TDCIPP (0, 5, 50 and 500 mu g/l) and a model neurotoxic chemical, chlorpyrifos (CPF, 100 mu g/l). The developmental endpoints, locomotive behavior, cholinesterase activities, gene and protein expression related to neurodevelopment and autophagy were measured in the larvae. Our results demonstrate that exposure to TDCIPP (500 mu g/l) and CPF causes developmental toxicity, including reduced hatching and survival rates and increased malformation rate (e.g., spinal curvature), as well as altered locomotor behavior. The expression of selected neurodevelopmental gene and protein markers (e.g., mbp, syn2a, and alpha 1-tubulitt) was significantly down-regulated in CPF and TDCIPP exposed zebrafish larvae. Treatment with CPF significantly inhibits AChE and BChE, while TDCIPP (0-500 mu g/l) exerts no effects on these enzymes. Furthermore, the conversion of microtubule-associated protein I (LC3 I) to LC3 II was significantly increased in TDCIPP exposed zebrafish larvae. In addition, exposure to TDCIPP also activates transcription of several critical genes in autophagy (e.g. Becn1, atg3, atg5, map1lc3b and sqstm1). To further investigate the role of autophagy in TDCIPP induced developmental neurotoxicity, an autophagy inducer (rapamycin, Rapa, 1 nM) and inhibitor (chloroquine, CQ, 1 mu M) were used. The results demonstrate that the hatching rate, survival rate, and the expression of mbp and a1-tubulin proteins were all significantly increased in larvae treated with TDCIPP (500 mu g/l) and Rapa compared to TDCIPP alone. In contrast, co-treatment with the autophagy inhibitor CQ results in exacerbated neurodevelopmental toxicity. Taken together, our results confirm that exposure to TDCIPP induces autophagy, which plays a protective role in TDCIPP-induced developmental neurotoxicity in zebrafish embryos and larvae.
关键词[WOS]: ORGANOPHOSPHORUS FLAME RETARDANTS ; THYROID ENDOCRINE DISRUPTION ; MAMMALIAN DEVELOPMENT ; PHOSPHATE TDCPP ; MOLECULAR-MECHANISMS ; EXPOSURE ; WATER ; PLASTICIZERS ; EXPRESSION ; TOXICITY
语种: 英语
项目资助者: National Natural Science Foundation of China(21737005) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14040103) ; State Key Laboratory of Freshwater Ecology and Biotechnology(2016FBZ11)
WOS记录号: WOS:000433271600005
ISSN号: 0166-445X
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内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/50872
Appears in Collections:水环境工程研究中心_期刊论文

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作者单位: 1.Wuhan Univ Sci & Technol, Sch Publ Hlth, Dept Nutr & Toxicol, Wuhan, Hubei, Peoples R China
2.Wuhan Univ Sci & Technol, Hubei Prov Key Lab Occupat Hazard Identificat & C, Wuhan, Hubei, Peoples R China
3.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Hubei, Peoples R China
4.East China Univ Sci & Technol, Sch Resource & Environm Engn, State Environm Protect Key Lab Environm Risk Asse, Shanghai 200237, Peoples R China
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