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Teratogenicity of cytochalasin D in the mouse

Teratology
|October 1, 1977
PubMed

Insights

Cytochalasin D, a mold metabolite, caused birth defects in mice, including exencephaly and skeletal abnormalities. This teratogenic compound also increased embryo resorption rates across all tested mouse strains.

Area of Science:

  • Toxicology
  • Developmental Biology
  • Teratology

Background:

  • Cytochalasin D is a mycotoxin found in food.
  • Its effects on embryonic development require further investigation.

Purpose of the Study:

  • To evaluate the teratogenic potential of Cytochalasin D in mice.
  • To identify specific birth defects and sensitive developmental periods.

Main Methods:

  • Administration of Cytochalasin D via intraperitoneal injection and oral gavage to pregnant mice on gestational days 7-11.
  • Assessment of fetal development, including external and skeletal examinations.
  • Evaluation of embryo resorption rates.

Main Results:

  • Intraperitoneal Cytochalasin D (0.4-0.9 mg/kg) induced teratogenicity in C57BL/6J and BALB/c mice, causing exencephaly, hypognathia, and axial skeletal defects.
  • No defects were observed in the Swiss Webster strain, but all strains showed increased resorption rates.
  • Oral administration (approx. 7.0 mg/kg) in BALB/c mice also resulted in exencephaly.
  • Autoclaved Cytochalasin D retained its teratogenic properties.

Conclusions:

  • Cytochalasin D is a potent teratogen in susceptible mouse strains, affecting multiple developmental processes.
  • Embryo resorption is a common outcome of Cytochalasin D exposure, regardless of genetic background.
  • The teratogenic potential of Cytochalasin D is heat-stable.

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