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Parental transfer of microcystin-LR induced transgenerational effects of developmental neurotoxicity in zebrafish offspring

文献类型: 外文期刊

作者: Wu, Qin 1 ; Yan, Wei 3 ; Cheng, Houcheng 1 ; Liu, Chunsheng 1 ; Hung, Tien-Chieh 4 ; Guo, Xiaochun 7 ; Li, Guangyu 1 ;

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

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

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

4.Univ Calif Davis, Dept Biol & Agr Engn, Davis, CA 95616 USA

5.Hubei Prov Engn Lab Pond Aquaculture, Wuhan 430070, Hubei, Peoples R China

6.Huazhong Agr Univ, Natl Demonstrat Ctr Expt Aquaculture Educ, Wuhan 430070, Hubei, Peoples R China

7.Chinese Res Inst Environm Sci, State Key Lab Environm Criteria & Risk Assessment, State Environm Protect Key Lab Lake Pollut Contro, Beijing 10001

关键词: MCLR;Zebrafish embryos;Transgenerational effects;Developmental neurotoxicity;Neurotransmitter

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

ISSN: 0269-7491

年卷期: 2017 年 231 卷

页码:

收录情况: SCI

摘要: Microcystin-LR (MCLR) has been reported to cause developmental neurotoxicity in zebrafish, but there are few studies on the mechanisms of MCLR-induced transgenerational effects of developmental neurotoxicity. In this study, zebrafish were exposed to 0, 1, 5, and 25 mu g/L MCLR for 60 days. The F1 zebrafish embryos from the above-mentioned parents were collected and incubated in clean water for 120 h for hatching. After examining the parental zebrafish and F1 embryos, MCLR was detected in the gonad of adults and F1 embryos, indicating MCLR could potentially be transferred from parents to offspring. The larvae also showed a serious hypoactivity. The contents of dopamine, dihydroxyphenylacetic acid (DOPAC), serotonin, gamma-aminobutyric acid (GABA) and acetylcholine (ACh) were further detected, but only the first three neurotransmitters showed significant reduction in the 5 and 25 a MCLR parental exposure groups. In addition, the acetylcholinesterase (AChE) activity was remarkably decreased in MCLR parental exposure groups, while the expression levels of manf, bdnf, ache, htr1ab, htr1b, htr2a, htr1aa, htr5a, DAT, TH1 and TH2 genes coincided with the decreased content of neurotransmitters (dopamine, DOPAC and serotonin) and the activity of AChE. Neuronal development related genes, ca-tubulin, syn2a, mbp, gfap, elavI3, shha and gap43 were also measured, but gap43 was the gene only up-regulated. Our results demonstrated MCLR could be transferred to offspring, and subsequently induce developmental neurotoxicity in F1 zebrafish larvae by disturbing the neurotransmitter systems and neuronal development.(C) 2017 Elsevier Ltd. All rights reserved.

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[1]Microcystin-LR exposure induces developmental neurotoxicity in zebrafish embryo. Wu, Qin,Liu, Chunsheng,Li, Li,Yu, Liqin,Li, Guangyu,Yan, Wei,Wu, Qin,Li, Li,Li, Guangyu,Zhao, Sujuan.

[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

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