Microcystin-LR exposure induced nephrotoxicity by triggering apoptosis in female zebrafish
文献类型： 外文期刊
作者： Wang, Zhikuan 1 ; Li, Guangyu 1 ; Wu, Qin 1 ; Liu, Chunsheng 1 ; Shen, JianZhong 1 ; Yan, Wei 2 ;
作者机构： 1.Huazhong Agr Univ, Coll Fisheries, Wuhan 430070, Hubei, Peoples R China
2.Hubei Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, Wuhan 430064, Hubei, Peoples R China
关键词： Microcystin-LR; Zebrafish; Nephrotoxicity; Apoptosis; Transcriptome
期刊名称：CHEMOSPHERE （ 2020影响因子：7.086； 五年影响因子：6.956 ）
ISSN： 0045-6535
年卷期： 2019 年 214 卷
收录情况： SCI
摘要： Recently, several studies showed that microcystin-LR (MCLR) can accumulate and induce toxicity in kidney. However, the exact mechanism is unknown. The aim of this study was to explore the mechanism of MCLR-induced nephrotoxicity. To this end, adult zebrafish were exposed to MCLR (0, 1, 5 and 25 mu g/L) for 60 days. Exposure to MCLR caused histopathological lesions, which were characterized by renal tubules filled with eosinophilic casts, abnormal renal tubules, intertubular space decrease, and blood infiltration in renal cells. RNA-Seq analysis indicated that exposure to MCLR significantly interfered with renal gene expressions, and these genes were enriched in various pathways, such as oxidative phosphorylation, cell cycle, and protein processing in endoplasmic reticulum, which were related to apoptosis. Furthermore, terminal deoxynucleotide transferase-mediated deoxy-UTP nick end labelling (TUNEL) assay showed that MCLR exposure induced renal cell apoptosis. In addition, negative changes of the reactive oxygen species (ROS) level as well as apoptotic-related gene, protein expressions and enzyme activities suggested that MCLR could induce production of ROS, subsequently triggering apoptosis via p53-bcl-2 and caspase-dependent pathway in the kidney of zebrafish. Therefore, it can be concluded that apoptosis is a primary case of MCLR-induced nephrotoxicity. (C) 2018 Elsevier Ltd. All rights reserved.
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