Nodularin (NOD) is a kind of cyanobacterial toxins. It is of concern due to elicit severe genotoxicity in humans and animals. The comprehensive evaluation of NOD-induced adverse effects in living organisms is urgently needed. This study is aimed to report the developmental toxicity and molecular mechanism using zebrafish embryos exposed to NOD. The embryonic toxicity induced by NOD is demonstrated by inhibition of embryo hatching, increase in mortality rate, abnormal heart rate, embryonic malformation as well as defects in angiogenesis and common cardinal vein remodeling. NOD triggered a decreased rate of angiogenesis through inhibiting endothelial cells migration. NOD induced embryonic cell apoptosis and DNA damage, which can be alleviated by antioxidant N-acetyl-L-cysteine. NOD significantly caused oxidative damage as indicated by changes in reactive oxygen species, superoxide dismutase, catalase, glutathione and malondialdehyde. NOD also altered the expression of vascular development-genes (DLL4, CDH5, VEGFA, VEGFC) and apoptosis-related genes (BAX, BCL-2, P53, CASPASE 3). Taken together, NOD induced adverse effect on zebrafish embryos development, which may be associated with oxidative stress and apoptosis through the activation of P53-BAX/BCL-2-CASPASE 3-mediated pathway.

结核菌素（NOD）是一种蓝细菌毒素。由于在人和动物中引起严重的遗传毒性，因此引起关注。迫切需要对NOD在生物体内引起的不良反应进行综合评估。这项研究旨在报告使用暴露于NOD的斑马鱼胚胎的发育毒性和分子机制。NOD诱导的胚胎毒性通过抑制胚胎孵化，死亡率增加，心率异常，胚胎畸形以及血管生成和常见的主静脉重构缺陷来证明。NOD通过抑制内皮细胞迁移而触发了血管生成速率的降低。NOD诱导胚胎细胞凋亡和DNA损伤，可通过抗氧化剂N-乙酰基-L-半胱氨酸缓解。如活性氧，超氧化物歧化酶，过氧化氢酶，谷胱甘肽和丙二醛的变化所表明，NOD显着引起氧化损伤。NOD还改变了血管发育基因的表达（DLL4，CDH5，VEGFA，VEGFC）和凋亡相关基因（BAX，BCL-2，P53，CASPASE 3）。两者合计，NOD诱导对斑马鱼胚胎发育的不利影响，这可能与P53 - BAX / BCL-2 - CASPASE 3介导的途径的激活与氧化应激和细胞凋亡有关。