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Palatal development and the arachidonic acid cascade.

R L Piddington, A S Goldman

    Progress in Clinical and Biological Research
    |January 1, 1985
    PubMed
    Summary

    Glucocorticoids and phenytoin can cause cleft palate by interfering with programmed cell death in developing palates. This interference is linked to the glucocorticoid receptor and arachidonic acid release, impacting embryonic development.

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    Area of Science:

    • Developmental biology
    • Pharmacology
    • Immunogenetics

    Background:

    • Cleft palate can be induced by glucocorticoids and phenytoin, involving complex genetic and biochemical pathways.
    • The H-2 histocompatibility region influences susceptibility to drug-induced cleft palate and glucocorticoid receptor levels.
    • Phenytoin acts as an alternate ligand for the glucocorticoid receptor, affecting prostaglandin and thromboxane production.

    Purpose of the Study:

    • To investigate the mechanisms underlying glucocorticoid- and phenytoin-induced cleft palate.
    • To explore the role of the glucocorticoid receptor and arachidonic acid metabolism in teratogenesis.
    • To understand the genetic factors influencing susceptibility to drug-induced developmental abnormalities.

    Main Methods:

    • Analysis of gene expression and receptor levels in maternal and embryonic tissues.
    • Investigating the effects of glucocorticoids and phenytoin on prostaglandin and thromboxane production in thymocytes.
    • Administering exogenous arachidonic acid and indomethacin to pregnant rodents to assess their impact on teratogenic effects.

    Main Results:

    • Glucocorticoid and phenytoin exposure delays palatal shelf elevation.
    • These drugs interfere with programmed cell death in medial edge epithelial cells.
    • The teratogenic effects are mediated by the glucocorticoid receptor, require protein synthesis, and involve arachidonic acid release.

    Conclusions:

    • Glucocorticoid- and phenytoin-induced cleft palate involves interference with programmed cell death, mediated by the glucocorticoid receptor.
    • Arachidonic acid metabolism and prostaglandin/thromboxane production are key pathways in these teratogenic effects.
    • Genetic factors, including the H-2 and H-3 loci, influence individual susceptibility to drug-induced cleft palate.

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