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Cadmium impairs zebrafish swim bladder development via ROS mediated inhibition of the Wnt / Hedgehog pathway
Aquatic Toxicology ( IF 4.5 ) Pub Date : 2022-04-25 , DOI: 10.1016/j.aquatox.2022.106180
Ting Zhang 1 , Canchuan Zhang 2 , Jin Zhang 3 , Jiangtian Lin 2 , Dongdong Song 2 , Peng Zhang 2 , Yang Liu 2 , Lizhao Chen 2 , Li Zhang 1
Affiliation  

The posterior swim bladder is an important organ in teleost fishes, that primarily maintains buoyancy and motility for swimming and survival. In this study, we examined the molecular mechanisms of the toxicity of cadmium (Cd) on the early development of the swim bladder in zebrafish. Embryonic Cd exposure resulted in the non-inflation of the swim bladder when the ambient Cd concentration was greater than or equal to 0.25 mg/L. Cd disturbed surfactant lipid distribution and inhibited the formation of all three tissue layers in the swim bladder. Additionally, excessive Cd down-regulated Wnt (fzd3, nkd1, fzd7 and axin2) and Hedgehog (ihh, shh, ptc1 and ptc2) signaling pathways. Conversely, Wnt signaling activation partially neutralized Cd-induced swim bladder developmental defects. Moreover, ROS scavenger reduced Glutathione (GSH) effectively recovered Cd induced defects in swim bladder and Wnt/Hedgehog signaling. Taken together, our results first revealed that Cd caused swim bladder developmental defects via ROS-mediated inhibition of the Wnt and Hedgehog pathways. These results herein provide important data for future toxicological studies and risk assessments of Cd.



中文翻译:

镉通过 ROS 介导的 Wnt / Hedgehog 通路抑制损害斑马鱼鳔发育

后鳔是硬骨鱼类的一个重要器官,主要维持浮力和运动性以供游泳和生存。在这项研究中,我们研究了镉 (Cd) 毒性对斑马鱼鱼鳔早期发育的分子机制。当环境 Cd 浓度大于或等于 0.25 mg/L 时,胚胎 Cd 暴露导致鱼鳔不膨胀。Cd 扰乱了表面活性剂脂质分布并抑制了鱼鳔中所有三个组织层的形成。此外,过量的 Cd 下调 Wn​​t(fzd3、nkd1、fzd7axin2)和 Hedgehog(ihh、shh、ptc1ptc2) 信号通路。相反,Wnt 信号激活部分中和了镉诱导的鱼鳔发育缺陷。此外,ROS 清除剂降低的谷胱甘肽 (GSH) 有效地恢复了 Cd 诱导的鱼鳔和 Wnt/Hedgehog 信号传导缺陷。总之,我们的研究结果首先表明,镉通过 ROS 介导的 Wnt 和 Hedgehog 通路抑制导致鱼鳔发育缺陷。本文的这些结果为未来的 Cd 毒理学研究和风险评估提供了重要数据。

更新日期:2022-04-28
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