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2'-Deoxyadenosine causes cell death in embryonic chicken sympathetic ganglia and brain

Z Zhao1, W J Crossland, J S Kulkarni

  • 1Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI 48202, USA.

Insights

2'-deoxyadenosine (2'-dAdo) causes developmental toxicity and cell loss in chick embryos, particularly affecting the sympathetic ganglion and optic tectum by inhibiting cell proliferation. Its in vivo toxicity at low concentrations limits its use in later developmental stages.

Area of Science:

  • Developmental biology
  • Neuroscience
  • Toxicology

Background:

  • Nucleosides are known to induce apoptosis in sympathetic ganglion (SG) cells in vitro.
  • Understanding nucleoside effects on embryonic development is crucial for identifying potential teratogens and developmental disruptions.

Purpose of the Study:

  • To investigate the in vivo effects of adenosine and 2 -deoxyadenosine (2 -dAdo) on chick embryo development, focusing on the sympathetic ganglion (SG) and optic tectum.
  • To determine the developmental toxicity and teratogenic potential of 2 -dAdo at different embryonic stages.

Main Methods:

  • Administration of adenosine and 2 -dAdo to chick embryos at various developmental stages (E3, E6 1/2, E11) in the presence of an adenosine deaminase inhibitor.
  • Dosage experiments to assess toxicity and teratogenicity of 2 -dAdo in E6 1/2 embryos.
  • Histological examination of SG and optic tectum in E6 1/2 and E10 embryos exposed to sublethal doses of 2 -dAdo to quantify cell loss and volume changes.

Main Results:

  • 2 -dAdo exhibited differential toxicity, being toxic at early (E3) and later (E6 1/2, E11) stages, whereas adenosine was toxic only at E3.
  • Sublethal doses of 2 -dAdo were teratogenic and caused significant neuron loss (83%) and volume reduction (65%) in the E6 1/2 SG, and cell loss in the optic tectum's ventricular zone.
  • At later stages (E10), 2 -dAdo showed minimal cell loss in the SG and optic tectum, suggesting an effect on cell proliferation rather than cell death in actively developing tissues.
  • In vivo lethality of 2 -dAdo at 30 microM was observed, which is lower than concentrations causing apoptosis in vitro.

Conclusions:

  • 2 -dAdo significantly impacts early embryonic development, leading to cell loss and teratogenicity by inhibiting cell proliferation in the developing nervous system.
  • The developmental stage is critical, with 2 -dAdo primarily affecting actively proliferating tissues.
  • The lower in vivo toxicity threshold of 2 -dAdo compared to in vitro studies highlights the complexity of nucleoside metabolism in embryonic development and its role in purine and pyrimidine pathways.

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