The environmental effects of additives have attracted increasing attention. Sodium dehydroacetate (DHA-S), as an approved preservative, is widely added in processed foods, cosmetics and personal care products. However, DHA-S has been recently reported to induce hemorrhage and coagulation aberration in rats. Yet little is known about the ecotoxicological effect and underlying mechanisms of DHA-S. Here, we utilized the advantage of zebrafish model to evaluate such effects. DHA-S induced cerebral hemorrhage, mandibular dysplasia and pericardial edema in zebrafish after 24 h exposure (48–72 hpf) at 50 mg/L. We also observed the defective heart looping and apoptosis in DHA-S-treated zebrafish through o-dianisidine and acridine orange staining. Meanwhile, DHA-S induced the deficiency of Ca²⁺ and vitamin D3 in zebrafish. We further demonstrated that DHA-S stimulated Ca²⁺ influx resulting in Ca²⁺-dependent mitochondrial damage in cardiomyocytes. Additionally, DHA-S inhibited glucose uptake and repressed the biosynthesis of amino acids. Finally, we identified that sodium bicarbonate could rescue zebrafish from DHA-S induced cardiovascular toxicity. Altogether, our results suggest that DHA-S is a potential risk for cardiovascular system.

添加剂对环境的影响已引起越来越多的关注。脱氢乙酸钠（DHA-S）作为批准的防腐剂，被广泛添加到加工食品，化妆品和个人护理产品中。然而，最近有报道说DHA-S会引起大鼠出血和凝血异常。关于DHA-S的生态毒理作用及其潜在机理，人们所知甚少。在这里，我们利用斑马鱼模型的优势来评估这种效果。DHA-S在50 mg / L暴露24 h（48–72 hpf）后，引起斑马鱼脑出血，下颌发育不良和心包水肿。我们还观察到通过O-dianisidine和Acridine橙染色在DHA-S处理的斑马鱼中有缺陷的心脏循环和细胞凋亡。同时，DHA-S引起Ca ²⁺缺乏和斑马鱼中的维生素D3。我们进一步证明DHA-S刺激Ca ^2+内流，导致心肌细胞中Ca ²⁺依赖性线粒体损伤。此外，DHA-S抑制了葡萄糖的摄取并抑制了氨基酸的生物合成。最后，我们确定了碳酸氢钠可以从DHA-S诱导的心血管毒性中拯救斑马鱼。总之，我们的结果表明DHA-S是心血管系统的潜在风险。