对抗
斑马鱼
卵黄囊
毒性
孵化
心跳
锌
发育毒性
胚胎
化学
蛋黄
个体发育
内科学
生物
毒理
内分泌学
解剖
动物科学
基因
生物化学
遗传学
受体
医学
食品科学
胎儿
怀孕
计算机科学
计算机安全
有机化学
作者
Yongmeng Yang,Yue Yu,Rong Zhou,Yan Yang,Yuanqing Bu
摘要
Abstract Excessive accumulation of Zn 2+ or Ni 2+ can cause various problems to aquatic animals. In this study, the developmental toxicity induced by individual or combined exposure of Zn 2+ and Ni 2+ to zebrafish embryos and larvae were evaluated to better understand the interaction between Zn 2+ and Ni 2+ . Both of individual and combined exposure of Zn 2+ and Ni 2+ could cause obvious developmental toxicity, which mainly occurred after hatching, at a concentration‐dependent manner. The calculated 168‐h LC 50 were 2.79 mg/L for Zn 2+ and 7.44 mg/L for Ni 2+ . The interaction of Zn 2+ and Ni 2+ 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 Zn 2+ and Ni 2+ . Meanwhile, some genes related to cardiovascular development and bone formation were mainly down‐regulated by the individual and combined exposure of Zn 2+ and Ni 2+ . The individual exposure was more toxic than combined exposure because the interaction of Zn 2+ and Ni 2+ 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.
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