Shows dose-dependent disruption of maturation and cell junctions in ethanol-exposed cardiac myocytes, indicating mechanisms underlying alcohol teratogenicity during heart organogenesis.
Alteration of growth and development of cells exposed to ethanol during embryogenesis contributes to dysmorphism. The mechanism(s) of these alterations remains an enigma. This paper describes studies of an in vitro cardiac myocyte model in which the major effort was to investigate growth and development parameters in an obligate interacting multicellular system. The well defined events of in vitro myogenesis allow for documentation or dysgenesis and altered growth in the presence of the taratogen, ethanol. The cells exposed to ethanol did not mature morphologically or functionally compared with controls. Increasing concentrations of ethanol appear to have a graded damaging effect. The greater the concentration of ethanol the more profound the dyssynchronous growth. The morphologic correlates were multinucleation, and alteration in the ultrastructural organization of cell-cell contacts and myofilaments. Correlation of these findings with those observed in dysgenic muscle of human infants and rat pups exposed to ethanol in utero, may provide at least a partial understanding of the teratogenic manifestation of ethanol in embryogenesis and organogenesis.
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Adickes et al. (1990) studied this question.
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