Avian Genetic Background Modulates the Neural Crest Apoptosis Induced by Ethanol Exposure

Authors

  • Katherine A. Debelak,

    1. Department of Nutritional Sciences and the Program for Environmental Toxicology, University of Wisconsin-Madison, Wisconsin.
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  • Susan M. Smith

    Corresponding author
    1. Department of Nutritional Sciences and the Program for Environmental Toxicology, University of Wisconsin-Madison, Wisconsin.
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  • This work was supported by the National March of Dimes Birth Defects Foundation, Awards #96-0915 and #98-0402, NIH Award #AA11085, and EHS Center Grant Award #ES09090.

Reprint requests: Susan M. Smith, Ph.D., Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Drive, Madison, WI 53706; Fax: 608-262-5860; E-mail: suesmith@nutrisci.wisc.edu

Abstract

Background: Ethanol-induced neural crest apoptosis likely contributes to the distinctive craniofacial phenotype that results from prenatal alcohol exposure. The mechanism responsible for this apoptosis is incompletely understood. A serendipitous change in poultry production flocks led to the discovery that, in chick, the embryo's genetic background modulates its susceptibility to ethanol-induced apoptosis.

Methods: We examined the level of ethanol-induced neural crest apoptosis in 11 chick layer strains or crosses, using acridine orange uptake.

Results: Holding the ethanol dose and exposure stage constant, strains were classified into very sensitive (Babcock ISA, HyLine W98, Babcock B300/Hampshire Red cross [BxHR]), moderately sensitive (Spafas, HyLine W36, Babcock B300), and nonresponsive (DeKalb White and Black, Shaver White and 2000, DeKalb White/Hampshire Red cross). Detailed examination of two susceptible strains (W98, BxHR) and a resistant strain (DeKalb White) revealed that the DeKalb's nonresponse was not caused by a shift in; timing of apoptosis, or to a lower alcohol exposure at either time of injection or time of death. Strains had identical stage distributions at the time of injection and at apoptosis; housing and diet were held constant.

Conclusions: Factors within the embryo and/or egg environment can affect the susceptibility to ethanol-induced apoptosis. These sensitive and resistant strains will be important tools to dissect the molecular mechanism of ethanol-induced apoptosis, and for understanding how these losses affect subsequent development.

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