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Parental exposure to microcystin-LR induced thyroid endocrine disruption in zebrafish offspring, a transgenerational toxicity

文献类型： 外文期刊

作者： Cheng, Houcheng 1 ; Yan, Wei 3 ; Wu, Qin 1 ; Liu, Chunsheng 1 ; Gong, Xiuying 1 ; Hung, Tien-Chieh 4 ; 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, People

关键词： MCLR;Transgenerational toxicity;Thyroid endocrine disruption;Zebrafish;Embryo

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

ISSN：

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收录情况： SCI

摘要： Microcystin-LR is the most poisonous and commonly encountered hepatotoxin produced by cyanobacteria in an aquatic ecosystem, and it may cause thyroid dysfunction in fish. The present study aimed to reveal the effects of transgenerational toxicity of MCLR on the thyroid endocrine system under sub chronic exposure conditions. Adult zebrafish (FO) were exposed to environmentally relevant concentrations (1, 5 and 25 mu g/L) of MCLR for 45 days. The produced F1 embryos were then tested without further MCLR treatment. In the FO generation, exposure to 25 mu g/L MCLR reduced thyroxine (T4) but not 3, 5, 3'-triiodothyronine (T3) levels in females, while the T4 and T3 levels were unchanged in males. After parental exposure to MCLR, we observed a decreased hatching and growth retardation correlated with reduced thyroid hormone levels in the F1 offspring. The gene transcription and protein expression along the hypothalamic-pituitary-thyroid axis were detected to further investigate the possible mechanisms of MCLR-induced thyroid disruption. Our results indicated MCLR could disturb the thyroid endocrine system under environmentally relevant concentrations and the disrupting effects could be remarkably transmitted to its F1 offspring. We regard these adverse effects as a parental transgenerational toxicity of MCLR. (C) 2017 Elsevier Ltd. All rights reserved.

  • 相关文献

[1]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

[2]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

[3]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.

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

[5]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

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