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Published on: July 30, 2015
Cadmium impairs zebrafish swim bladder development via ROS mediated inhibition of the Wnt / Hedgehog pathway
Ting Zhang1, Canchuan Zhang2, Jin Zhang3
1Key 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.
Abstract:
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.
