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Transplacental genotoxicity of diethylstilbestrol

A Gladek1, J G Liehr

  • 1Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77550-2782.

Carcinogenesis
|May 1, 1991
PubMed

Insights

Diethylstilbestrol (DES) is a transplacental carcinogen. This study shows DES is genotoxic in fetal organs, indicating it crosses the placenta and damages fetal DNA, potentially causing cancer.

Area of Science:

  • Toxicology
  • Carcinogenesis
  • Molecular Biology

Background:

  • Diethylstilbestrol (DES) is a known human transplacental carcinogen.
  • Understanding the genotoxic mechanisms of transplacental carcinogens is crucial for risk assessment.
  • Previous studies have established DES's carcinogenic potential in various species.

Purpose of the Study:

  • To investigate the transplacental genotoxicity of diethylstilbestrol (DES).
  • To identify DNA adducts formed by DES and its metabolites in maternal and fetal tissues.
  • To elucidate the role of fetal metabolism in DES-induced genotoxicity.

Main Methods:

  • Pregnant hamsters were administered a single dose of DES (200 mg/kg) on day 10 of gestation.
  • Maternal organs and fetal tissues (heart, kidney, liver) were collected 5 and 24 hours post-treatment.
  • DNA was extracted and analyzed for adducts using 32P-postlabeling analysis.

Main Results:

  • DES-DNA adduct patterns, attributed to the genotoxic metabolite diethylstilbestrol-4',4'-quinone (DES Q), were detected in maternal organs.
  • Similar DES Q-related adducts were found in fetal heart and kidney DNA.
  • A novel major DNA adduct was identified in fetal liver, suggesting the involvement of unknown DES metabolites.

Conclusions:

  • Diethylstilbestrol (DES) is a transplacentally active genotoxic agent.
  • Fetal tissues can metabolize DES to the genotoxic DES Q.
  • Evidence suggests the existence of other, yet unidentified, genotoxic DES metabolites that can reach fetal organs.

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