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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Hydroxyurea embryotoxicity is enhanced in P53-deficient mice.

Nazem El Husseini1, Barbara F Hales1

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

Reproductive Toxicology (Elmsford, N.Y.)
|June 26, 2018
PubMed
Summary

The P53 gene suppresses hydroxyurea

Area of Science:

  • Developmental toxicology
  • Teratology
  • Molecular genetics

Background:

  • Hydroxyurea is a teratogen causing birth defects.
  • Hydroxyurea exposure triggers embryonic stress and P53 activation.
  • The role of P53 in hydroxyurea embryotoxicity is unknown.

Purpose of the Study:

  • To investigate if P53 suppresses hydroxyurea-induced embryotoxicity.
  • To determine the impact of P53 genotype on fetal development after hydroxyurea exposure.

Main Methods:

  • Trp53+/- mice were treated with hydroxyurea on gestation day 9.
  • Fetal viability and malformations were assessed on gestation day 18.
  • Comparison of outcomes between wildtype and Trp53-/- fetuses.
Keywords:
Birth defectsDevelopmental toxicityHydroxyureaOrganogenesisP53Teratogen

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Main Results:

  • Hydroxyurea did not significantly affect fetal growth.
  • Trp53-/- fetuses showed a trend towards decreased weight.
  • Hydroxyurea caused more malformations and resorptions in Trp53-/- fetuses than wildtype.

Conclusions:

  • Fetal P53 genotype is a key factor in hydroxyurea's effects on developing embryos.
  • P53 appears to protect against hydroxyurea-induced developmental toxicity.
  • This study clarifies the role of P53 in teratogenesis.