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Updated: Feb 13, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

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Association and Toxic Mechanism Between Foodborne OTA Exposure and Embryonic Development

Teng Yao1, Xingyun Zhu1, Jiaolong Ma1,2,3,4

  • 1Department of Preventive Medicine, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.

Journal of Applied Toxicology : JAT
|February 12, 2026
PubMed

Insights

Foodborne ochratoxin A (OTA) causes embryonic developmental toxicity by disrupting the PI3K/Akt/Nrf2/HO-1 pathway, leading to oxidative stress. This study integrates bioinformatics and in vivo experiments to elucidate OTA's toxic mechanisms.

Area of Science:

  • Toxicology
  • Developmental Biology
  • Bioinformatics

Background:

  • Foodborne ochratoxin A (OTA) is a prevalent mycotoxin with known toxicity.
  • Understanding OTA's specific mechanisms of embryonic developmental toxicity is crucial for public health.
  • Existing research necessitates further investigation into OTA's molecular pathways and in vivo effects.

Purpose of the Study:

  • To investigate the embryonic developmental toxicity of ochratoxin A (OTA).
  • To elucidate the specific molecular mechanisms underlying OTA-induced toxicity using bioinformatics and in vivo models.
  • To identify potential therapeutic targets and preventative strategies against foodborne contaminants.

Main Methods:

  • Bioinformatic analyses including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction (PPI) networks were used to identify key genes.
  • In vivo experiments involved establishing OTA exposure models in pregnant C57BL/6 mice to assess embryonic development and placental oxidative stress.
  • Key pathways, including PI3K/Akt/Nrf2/HO-1, were analyzed at the molecular and protein expression levels.

Main Results:

  • Bioinformatic analysis revealed enrichment of differentially expressed genes in PI3K/Akt pathways, identifying crucial hub genes.
  • OTA exposure in mice led to impaired maternal weight gain, reduced live fetus rates, and fetal malformations.
  • OTA exposure downregulated placental antioxidant capacity (glutathione) and upregulated oxidative stress markers (malondialdehyde), alongside suppressed PI3K/Akt and Nrf2/HO-1 pathway activation.

Conclusions:

  • Ochratoxin A suppresses PI3K/Akt phosphorylation, impacting the Nrf2/HO-1 signaling pathway.
  • This disruption inhibits the body's antioxidant capacity, inducing oxidative stress and causing embryonic developmental toxicity.
  • The findings provide evidence for OTA's teratogenic effects and highlight the PI3K/Akt/Nrf2/HO-1 pathway as a critical target.
Keywords:
bioinformaticsembryotoxicityin vivo experimentsochratoxin Aoxidative stress

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