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Related Experiment Video

Updated: Feb 13, 2026

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

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

Published on: March 6, 2018

Association and Toxic Mechanism Between Foodborne OTA Exposure and Embryonic Development.

Teng Yao¹, Xingyun Zhu¹, Jiaolong Ma^1,2,3,4

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

Journal of Applied Toxicology : JAT

|February 12, 2026

Summary

This summary is machine-generated.

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.

Keywords:

bioinformatics embryotoxicity in vivo experiments ochratoxin A oxidative stress

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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.