Key Laboratory of Tropical Marine Bio-resourcesand Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; Southern Marine Science and Engineering Guangdong Laboratory, Guangzhou 511458, China; Institution of South China Sea Ecology and Environmental Engineering, Chinese Academy of Sciences, Guangzhou 510301, China.
Key Laboratory of Tropical Marine Bio-resourcesand Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; Southern Marine Science and Engineering Guangdong Laboratory, Guangzhou 511458, China; University of Chinese Academy of Science, Beijing 100049, China.
Aquat Toxicol. 2022 Jun;247:106180. doi: 10.1016/j.aquatox.2022.106180. Epub 2022 Apr 25.
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.
后鳔是硬骨鱼类的重要器官，主要维持其游泳和生存的浮力和活动性。在这项研究中，我们研究了镉 (Cd) 对斑马鱼鳔早期发育毒性的分子机制。当环境 Cd 浓度大于或等于 0.25mg/L 时，胚胎 Cd 暴露导致鳔无法充气。Cd 扰乱了表面活性剂脂质分布，并抑制了鳔的所有三层组织的形成。此外，过量的 Cd 下调了 Wnt（fzd3、nkd1、fzd7 和 axin2）和 Hedgehog（ihh、shh、ptc1 和 ptc2）信号通路。相反，Wnt 信号激活部分中和了 Cd 诱导的鳔发育缺陷。此外，ROS 清除剂有效减少了 Glutathione (GSH)，恢复了 Cd 诱导的鳔和 Wnt/Hedgehog 信号缺陷。综上所述，我们的研究结果首次揭示了 Cd 通过 ROS 介导的 Wnt 和 Hedgehog 通路抑制导致鳔发育缺陷。这些结果为未来 Cd 的毒理学研究和风险评估提供了重要数据。
