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Publication : Pathogenesis of ethanol-induced limb reduction defects in mice.

First Author  Kotch LE Year  1992
Journal  Teratology Volume  46
Issue  4 Pages  323-32
PubMed ID  1412063 Mgi Jnum  J:2709
Mgi Id  MGI:51231 Doi  10.1002/tera.1420460403
Citation  Kotch LE, et al. (1992) Pathogenesis of ethanol-induced limb reduction defects in mice. Teratology 46(4):323-32
abstractText  Acute administration of dosages of 2.5, 2.8, or 2.9 g/kg of ethanol to pregnant C57BL/6J mice on gestational day 9 1/4 resulted in major malformations of the forelimb including postaxial ectrodactyly, preaxial syndactyly, and reduction defects involving intermediate digits. The incidence and severity of these defects was positively correlated with dosage. Sidedness of the defects was also dose-dependent. In affected embryos, excessive amounts of cell death were notable within 5-9 hr of treatment initiation in selected cell populations. Cell death was primarily distributed in two regions of the developing limb bud--a ventrodistal ectodermal cell population (apical ectodermal ridge) and a proximal mesenchymal cell population. The patterns of cell death observed appear to be pathogenically related to the limb defects noted at later stages. In particular, it would appear that the deficiencies in the apical ectodermal ridge resulting from ethanol-induced cell death can account for virtually all the subsequent limb defects.
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