Diclofop-methyl (DM) is one of the most widely used herbicides in agriculture production and has been frequently detected in both freshwater and environments, even agricultural products. However, the potential toxic effects of DM on organisms and the underlying mechanisms are still poorly understood. In this study, we utilized zebrafish to evaluate the toxicity of DM during the cardiovascular developmental process. Exposure of zebrafish embryos to 0.75, 1.0 and 1.25 mg/L DM induced cardiac defects, such as pericardial edema, slow heart rate and long SV-BA distance but the vascular development in zebrafish larvae was not influenced by DM treatment. The expression of cardiac-related genes were disordered and DM exposure initiated disordering cardiogenesis from the period of precardiac mesoderm formation. Moreover, the apoptosis and proliferation of cardiomyocytes were not influenced but the levels of oxidative stress were upregulated by DM exposure. Fullerenes and astaxanthin was able to rescue cardiac defects caused by DM via downregulating oxidative stress. Wnt signaling was downregulated after DM treatment and activation of Wnt signaling could rescue cardiac defects. Therefore, our results suggest that DM has the potential to induce cardiac developmental toxicity through upregulation of Wnt-Mediated (reactive oxygen species) ROS generation in zebrafish larvae.

双氯芬（DM）是农业生产中使用最广泛的除草剂之一，在淡水和环境中，甚至在农产品中都经常被发现。然而，DM对生物体的潜在毒性作用及其潜在机制仍知之甚少。在这项研究中，我们利用斑马鱼来评估DM在心血管发育过程中的毒性。斑马鱼胚胎暴露于0.75、1.0和1.25 mg / L DM会诱发心脏缺陷，例如心包水肿，心律缓慢和SV-BA距离长，但是DM处理不会影响斑马鱼幼虫的血管发育。从心脏前中胚层形成时期开始，心脏相关基因的表达紊乱，而DM暴露引发了紊乱的心脏发生。此外，DM暴露不影响心肌细胞的凋亡和增殖，但氧化应激水平上调。富勒烯和虾青素能够通过下调氧化应激来挽救由DM引起的心脏缺陷。DM治疗后Wnt信号被下调，激活Wnt信号可以挽救心脏缺陷。因此，我们的结果表明，DM有可能通过上调斑马鱼幼虫中Wnt介导的（活性氧）ROS生成来诱导心脏发育毒性。DM治疗后Wnt信号被下调，激活Wnt信号可以挽救心脏缺陷。因此，我们的结果表明，DM有可能通过上调斑马鱼幼虫中Wnt介导的（活性氧）ROS生成来诱导心脏发育毒性。DM治疗后Wnt信号被下调，激活Wnt信号可以挽救心脏缺陷。因此，我们的结果表明，DM有可能通过上调斑马鱼幼虫中Wnt介导的（活性氧）ROS生成来诱导心脏发育毒性。