In the present study, we evaluated the zearalenone induced adverse effects in zebrafish embryos using various endpoints like embryo toxicity, heart rate, oxidative stress indicators (reactive oxygen species (ROS), lipid peroxidation (LPO), Nitric oxide (NO)), antioxidant responses (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase enzyme (GST) and reduced glutathione (GSH), metabolic biomarkers (lactate dehydrogenase (LDH) and Nitric oxide (NO)), neurotoxicity (acetylcholinesterase (AChE)), genotoxicity (comet assay and acridine orange staining (AO)) and histological analysis. In this study, four concentrations 350, 550, 750 and 950 μg/L of ZEA were chosen based on LC10 and LC50 values of the previous report. The results shows that ZEA induces developmental defects like pericardial edema, hyperemia, yolk sac edema, spine curvature and reduction in heart rate from above 550 μg/L exposure and the severity was increased with concentration and time dependent manner. Significant induction in oxidative stress indices (ROS, LPO and NO), reduction in antioxidant defence system (SOD, CAT, GPx, GST and GSH) and changes in metabolic biomarkers (LDH and AP) were observed at higher ZEA exposed concentration. Neurotoxic effects of ZEA were observed with significant inhibition of AChE activity at higher exposure groups (750 and 950 μg/L). Moreover, we also noticed DNA damage, apoptosis and histological changes in the higher ZEA treatments at 96 h post fertilization (hpf) embryos. Hence, in the present study we concluded that oxidative stress is the main culprit in ZEA induced developmental, genotoxicity and neurotoxicity in zebrafish embryos.

550μg/ L以上的暴露会导致卵黄囊水肿，脊柱弯曲和心率降低，严重程度随浓度和时间依赖性而增加。在较高的ZEA暴露浓度下，观察到氧化应激指数（ROS，LPO和NO）的显着诱导，抗氧化防御系统（SOD，CAT，GPx，GST和GSH）的降低以及代谢生物标志物（LDH和AP）的变化。在较高的暴露水平（750和950μg/ L）下，观察到ZEA的神经毒性具有明显的AChE活性抑制作用。此外，我们还注意到在受精（hpf）胚胎后96小时，较高ZEA处理中的DNA损伤，凋亡和组织学变化。因此，在本研究中，我们得出结论，氧化应激是ZEA诱导斑马鱼胚胎发育，遗传毒性和神经毒性的主要原因。