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Related Experiment Videos

Homocysteine interference in neurulation: a chick embryo model.

L A Afman1, H J Blom, N M J Van der Put

  • 1Department of Pediatrics, University Medical Center Nijmegen, The Netherlands. L.Afman@cukz.umcn.nl

Birth Defects Research. Part A, Clinical and Molecular Teratology
|September 10, 2003
PubMed
Summary

Elevated homocysteine levels may disrupt embryonic neural tube closure. An in vitro chick embryo model showed homocysteine transiently delays neural tube closure, suggesting a role in neurulation defects.

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Area of Science:

  • Developmental biology
  • Teratology
  • Embryology

Background:

  • Neural tube defects (NTDs) are reduced by folic acid.
  • Elevated plasma homocysteine is linked to NTDs.
  • Homocysteine may be teratogenic, interfering with neural tube closure.

Purpose of the Study:

  • To establish a chick embryo model for studying homocysteine's interference with neural tube closure.
  • To investigate the teratogenic potential of homocysteine on embryonic development.

Main Methods:

  • Chick embryos were treated with homocysteine or saline in ovo and in vitro.
  • In vitro treatment occurred during a specific somite window (4-6 somites).
  • Embryos were monitored for malformations and neural tube closure.

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Main Results:

  • In ovo homocysteine caused malformations but not increased NTDs.
  • In vitro homocysteine induced dose-dependent widening and closure delay of neural pores.
  • Neural tube closure was eventually completed after 16 hours in vitro.

Conclusions:

  • The in vitro chick embryo model is suitable for studying homocysteine's effects on neurulation.
  • Disturbed homocysteine metabolism may interfere with normal neural tube development.