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Disruption of liver development and coagulation pathway by ochratoxin A in embryonic zebrafish

Ting-Shuan Wu1, Yu-Ting Lin1, Ying-Tzu Huang1

  • 1Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Toxicology and Applied Pharmacology
|December 25, 2017
PubMed

Insights

Ochratoxin A (OTA) exposure in zebrafish embryos impairs liver development, leading to smaller livers and reduced blood clotting factors. This mycotoxin disrupts key gene expression and cell proliferation necessary for liver formation.

Area of Science:

  • Toxicology
  • Developmental Biology
  • Genomics

Background:

  • Ochratoxin A (OTA) is a prevalent mycotoxin in food and feed.
  • Molecular mechanisms of OTA's effects on developing organisms, particularly liver and teratogenicity, are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying OTA-induced hepatotoxicity and teratogenicity in developing zebrafish embryos.
  • To investigate the impact of OTA on liver development, gene expression, and related pathways.

Main Methods:

  • Transcriptomic profiling of zebrafish embryos exposed to OTA.
  • Quantitative analysis of gene and microRNA expression (e.g., f7, f9b, cp, vtna, miR-122).
  • Immunohistochemical staining for cell proliferation markers (phosphorylated histone H3) and in vitro studies using zebrafish liver (ZFL) cells.

Main Results:

  • OTA significantly affected hemostasis and blood coagulation pathways.
  • Decreased expression of coagulation factors (f7, f9b) and liver markers (cp, vtna) was observed.
  • OTA reduced embryonic liver size, suppressed key developmental genes (hhex, prox1), and impaired hepatocyte proliferation.

Conclusions:

  • OTA exposure disrupts zebrafish liver development by suppressing critical transcriptional factors and inhibiting hepatocyte proliferation.
  • The resulting small livers lead to deficiencies in essential coagulation factors, highlighting OTA's developmental toxicity.

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