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Copper impairs zebrafish swimbladder development by down-regulating Wnt signaling.

JiangPing Xu1, RuiTao Zhang1, Ting Zhang1

  • 1College of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, 430070, China.

Aquatic Toxicology (Amsterdam, Netherlands)
|September 29, 2017
PubMed
Summary

Copper nanoparticles (CuNPs) and copper ions (Cu2+) disrupt zebrafish swimbladder development by inhibiting its formation and inflation. These effects are stage-specific and linked to the downregulation of Wnt signaling pathways.

Keywords:
BIOCu(2+)CuNPsSwimbladderWnt signaling

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Area of Science:

  • Environmental toxicology
  • Developmental biology
  • Nanomaterial safety

Background:

  • Copper nanoparticles (CuNPs) exhibit antimicrobial properties but their developmental toxicity in aquatic organisms remains understudied.
  • Understanding the molecular mechanisms of CuNP toxicity is crucial for assessing environmental risks.

Purpose of the Study:

  • To investigate the effects of CuNPs and copper (II) ions (Cu2+) on zebrafish swimbladder development.
  • To elucidate the molecular mechanisms underlying CuNP-induced developmental toxicity, focusing on Wnt signaling.

Main Methods:

  • Zebrafish embryos were exposed to CuNPs and Cu2+ at different developmental stages.
  • Swimbladder morphology and inflation were assessed.
  • Wnt signaling pathway activity was evaluated.
  • The effect of a Wnt agonist (BIO) was tested to determine its role in mitigating toxicity.

Main Results:

  • Both CuNPs and Cu2+ inhibited swimbladder layer specification, formation, and inflation in a stage-specific manner.
  • CuNPs and Cu2+ significantly downregulated Wnt signaling in zebrafish embryos.
  • Wnt agonist BIO treatment rescued the swimbladder developmental defects caused by CuNPs and Cu2+.

Conclusions:

  • CuNPs and Cu2+ interfere with zebrafish swimbladder development by disrupting Wnt signaling.
  • This study provides the first evidence of CuNP and Cu2+ toxicity on swimbladder formation and inflation via Wnt pathway modulation.