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Related Concept Videos

In vitro Mutagenesis01:16

In vitro Mutagenesis

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To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
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Teratogenicity01:07

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Related Experiment Video

Updated: Apr 23, 2026

Developmental Toxicity Assay Based on Real-Time Monitoring of Fibroblast Growth Factor Signal Disruption in Human Induced Pluripotent Stem Cells
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Evaluating Thiram-Induced Embryotoxicity Using Integrated In Silico, In Vitro, and Transcriptomic Approaches.

Chia-Chi Ho1, Chun-Wei Tung2, B Linju Yen3

  • 1National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan, Taiwan.

Environmental Toxicology
|April 22, 2026
PubMed
Summary
This summary is machine-generated.

Thiram, a chemical found in food contact materials, significantly disrupts early embryonic development, particularly neural crest differentiation. This finding highlights potential risks and aids in assessing developmental toxicity of chemicals.

Keywords:
embryotoxicityhuman pluripotent embryonal carcinoma cells (NT2)mouse embryonic stem cells (mESCs)neural crest differentiationthiram

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Area of Science:

  • Toxicology
  • Developmental Biology
  • Computational Toxicology

Background:

  • Food contact materials (FCMs) exposure raises concerns for developmental toxicity.
  • A computational model identified 127 high-concern FCMs for developmental toxicity.

Purpose of the Study:

  • To evaluate the embryotoxicity of selected FCMs using the mouse embryonic stem cell test (mEST).
  • To investigate the mechanism of thiram-induced embryotoxicity in mouse embryonic stem cells (mESCs) and human NT2 cells.

Main Methods:

  • Weight-of-evidence computational modeling to prioritize FCMs.
  • Mouse embryonic stem cell test (mEST) for embryotoxicity screening.
  • Transcriptome analysis to identify disrupted pathways.

Main Results:

  • Thiram most potently inhibited cardiac differentiation in mEST.
  • Thiram suppressed markers for three germ layers but increased neurectoderm markers in mESCs.
  • Thiram disrupted neural crest differentiation pathway in mESCs and NT2 cells.

Conclusions:

  • Disruption of neural crest differentiation is a key mechanism in thiram-induced embryotoxicity.
  • This study provides a framework for mechanism-based biomarker identification for chemical safety assessment.