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Developmental toxicity of glyceryl trinitrate in quail embryos

Ghalib K Bardai1, Barbara F Hales, Geoffrey I Sunahara

  • 1Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.

Birth Defects Research. Part A, Clinical and Molecular Teratology
|April 8, 2011
PubMed
Abstract

Insights

Glyceryl trinitrate (GTN) exposure caused dose-dependent birth defects in quail embryos, including eye, heart, and neural tube malformations. This suggests GTN may disrupt embryonic development through reactive nitrogen species.

Area of Science:

  • Developmental toxicology
  • Embryology
  • Pharmacology

Background:

  • Glyceryl trinitrate (GTN) is widely used for angina and heart failure.
  • Its effects on embryonic development, particularly during organogenesis, are largely unknown.
  • Quail embryos provide a model to study GTN's teratogenic potential.

Purpose of the Study:

  • To investigate the developmental toxicity of GTN in quail embryos.
  • To determine dose-dependent effects and critical developmental stages for GTN exposure.
  • To explore the molecular mechanisms underlying GTN-induced malformations.

Main Methods:

  • Fertilized quail eggs were exposed to varying GTN concentrations at different developmental stages (Hamburger-Hamilton stages 0, 9, 19).
  • Embryos were examined for malformations at 7 days post-exposure.
  • Specific tissues were analyzed for nitrated proteins following ex ovo exposure.

Main Results:

  • GTN exposure resulted in a dose-dependent increase in embryo malformations, most pronounced at HH stage 9.
  • Observed defects included microphthalmia, craniofacial, heart, and neural tube abnormalities.
  • Nitrated proteins were detected in the developing eye, indicating reactive nitrogen species formation.

Conclusions:

  • GTN induces significant developmental abnormalities in quail embryos.
  • The formation of nitrated proteins suggests GTN generates reactive nitrogen species.
  • GTN's disruption of embryonic redox status may be responsible for its developmental toxicity.

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