LAUSR

Excessive accumulation of Zn2+ or Ni2+ can cause various problems to aquatic animals. In this study, the developmental toxicity induced by individual or combined exposure of Zn2+ and Ni2+ to zebrafish embryos and larvae were evaluated to better understand the interaction between Zn2+ and Ni2+. Both of individual and combined exposure of Zn2+ and Ni2+ could cause obvious developmental toxicity, which mainly occurred after hatching, at a concentration‐dependent manner. The calculated 168‐h LC50 were 2.79 mg/L for Zn2+ and 7.44 mg/L for Ni2+. The interaction of Zn2+ and Ni2+ based on mortality was found to be an antagonism. Various malformations, including tail curving, spinal curvature, pericardial edema, and yolk sac edema, were observed with significant effects on body length and heartbeat rates after exposure of Zn2+ and Ni2+. Meanwhile, some genes related to cardiovascular development and bone formation were mainly down‐regulated by the individual and combined exposure of Zn2+ and Ni2+. The individual exposure was more toxic than combined exposure because the interaction of Zn2+ and Ni2+ was determined to be an antagonism. The down‐regulation of genes related to cardiovascular development and bone formation may contribute to the observed malformation and decreases of body length and heartbeat rates.