Exposure to Oxadiazon-Butachlor causes cardiac toxicity in zebrafish embryos
Exposure to Oxadiazon-Butachlor causes cardiac toxicity in zebrafish embryos
复制标题
接触恶草酮-丁草胺会导致斑马鱼胚胎心脏毒性
DOI：
10.1016/j.envpol.2020.114775
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发表时间：
2020-10-01
影响因子：
8.9
通讯作者：
Lu, Huiqiang
中科院分区：
文献类型：
--
作者：
Huang, Yong;Ma, Jinze;Lu, Huiqiang
恶草酮-丁草胺（OB）是一种广泛使用的防除水稻田一年生杂草的除草剂。然而，迄今为止尚未对其在水生生物中的潜在毒性进行评价。我们使用斑马鱼胚胎模型来评估OB的毒性，发现它影响早期心脏发育并引起广泛的心脏损伤。从机制上讲，OB通过抑制抗氧化酶显着增加胚胎的氧化应激，导致活性氧（ROS）的过量产生，最终导致心肌细胞凋亡。此外，OB还能抑制WNT信号通路，下调其靶基因lef 1、axin 2和beta-catenin。通过Wnt激活剂BML-284和抗氧化剂虾青素重新激活该途径，挽救了胚胎免受OB的心脏毒性作用，表明氧化应激和WNT靶基因的抑制是OB诱导斑马鱼损伤的机制基础。我们的研究表明，OB暴露会导致斑马鱼胚胎的心脏毒性，并可能对其他水生生物甚至人类产生潜在毒性。(C)2020由Elsevier Ltd.出版
Oxadiazon-Butachlor (OB) is a widely used herbicide for controlling most annual weeds in rice fields. However, its potential toxicity in aquatic organisms has not been evaluated so far. We used the zebrafish embryo model to assess the toxicity of OB, and found that it affected early cardiac development and caused extensive cardiac damage. Mechanistically, OB significantly increased oxidative stress in the embryos by inhibiting antioxidant enzymes that resulted in excessive production of reactive oxygen species (ROS), eventually leading to cardiomyocyte apoptosis. In addition, OB also inhibited the WNT signaling pathway and downregulated its target genes includinglef1, axin2 and beta-catenin. Reactivation of this pathway by the Wnt activator BML-284 and the antioxidant astaxanthin rescued the embryos form the cardiotoxic effects of OB, indicating that oxidative stress, and inhibition of WNT target genes are the mechanistic basis of OB-induced damage in zebrafish. Our study shows that OB exposure causes cardiotoxicity in zebrafish embryos and may be potentially toxic to other aquatic life and even humans. (C) 2020 Published by Elsevier Ltd.