The role of apoptosis in MCLR-induced developmental toxicity in zebrafish embryos

文献类型： 外文期刊

第一作者： Zeng, Cheng

作者： Zeng, Cheng;Wang, Jianghua;Zhang, Guirong;Chen, Nan;Li, Guangyu;Sun, Hong;Xie, Ping;Li, Guangyu;Yan, Wei

作者机构：

关键词： MCLR;Zebrafish;Embryo;Apoptosis;Developmental toxicity

期刊名称：AQUATIC TOXICOLOGY （ 影响因子：4.964； 五年影响因子：5.071 ）

ISSN： 0166-445X

年卷期： 2014 年 149 卷

页码：

收录情况： SCI

摘要： We previously demonstrated that cyanobacteria-derived microcystin-leucine-arginine (MCLR) is able to induce developing toxicity, such as malformation, growth delay and also decreased heart rates in zebrafish embryos. However, the molecular mechanisms by which MCLR induces its toxicity during the development of zebrafish remain largely unknown. Here, we evaluate the role of apoptosis in MCLRinduced developmental toxicity. Zebrafish embryos were exposed to various concentrations of MCLR (0, 0.2, 0.5, 2, and 5.0 mg L-1) for 96 h, at which time reactive oxygen species (ROS) was significantly induced in the 2 and 5.0 mg L-1 MCLR exposure groups. Acridine orange (AO) staining and terminal deoxynucleotide transferase-mediated deoxy-UTP nick end labelling (TUNEL) assay showed that MCLR exposure resulted in cell apoptosis. To test the apoptotic pathway, the expression pattern of several apoptoticrelated genes was examined for the level of enzyme activity, gene and protein expression, respectively. The overall results demonstrate that MCLR induced ROS which consequently triggered apoptosis in the heart of developing zebrafish embryos. Our results also indicate that the p53-Bax-Bc1-2 pathway and the caspase-dependent apoptotic pathway play major roles in MCLR-induced apoptosis in the developing embryos. (C) 2014 Elsevier B.V. All rights reserved.

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