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Transplacentally induced anorectal malformations in rats.

Y Hirai1, N Kuwabara

  • 1Department of Surgery, Juntendo University School of Medicine, Tokyo, Japan.

Journal of Pediatric Surgery
|July 1, 1990
PubMed
Summary

Ethylenethiourea (ETU) exposure during pregnancy in rats caused significant external and anorectal malformations in fetuses, with males more severely affected. Histological analysis revealed muscle abnormalities in the anorectal region.

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Area of Science:

  • Developmental toxicology
  • Teratology
  • Reproductive toxicology

Background:

  • Ethylenethiourea (ETU) is a known teratogen.
  • Prenatal exposure to ETU can induce developmental abnormalities in fetuses.
  • Anorectal malformations are serious congenital defects requiring detailed study.

Purpose of the Study:

  • To investigate the teratogenic effects of ethylenethiourea (ETU) on prenatal development in rats.
  • To characterize the types and incidences of externally visible and anorectal malformations induced by ETU.
  • To examine the histological changes in the anorectal region of affected fetuses.

Main Methods:

  • Pregnant Wistar-Imamichi rats were administered single intragastric doses of ETU (100-200 mg/kg) on gestation day 11.
  • Cesarean sections were performed on gestation day 20 to collect fetuses.

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  • External malformations were recorded, and fetuses were processed for sagittal serial sectioning and light microscopy.
  • Histological examination focused on the anorectal region to identify malformations and muscle abnormalities.

    • Main Results:

    • ETU induced a high incidence of external malformations, including absent/kinked tails and spina bifida/myeloschisis, with significantly higher rates in males.
    • Various anorectal anomalies were observed, such as rectourethral fistula, rectocloacal fistula, covered anus, anoperineal fistula, and anal membrane stenosis.
    • The incidence of anorectal anomalies was significantly higher in male fetuses compared to females.
    • Histological examination revealed hypertrophy of the inner circular smooth muscle layer at the rectum end and hypoplasia of the external sphincter muscle complex in severely deformed fetuses.

    Conclusions:

    • A dose of 125 mg/kg ETU was suggested as optimal for inducing malformations in this study.
    • ETU is a potent teratogen causing a spectrum of external and anorectal malformations in rat fetuses, with a notable sex-specific difference in incidence.
    • The observed muscle abnormalities in the anorectal region provide insights into the pathogenesis of ETU-induced anorectal defects.