Exposure of embryonic cells to alcohol: contrasting effects during preimplantation and postimplantation development

Alcohol is a known teratogen that causes a broad variety of developmental anomalies, including fetal growth retardation, craniofacial anomalies, and neurological disorders. The etiology of this multiple defect syndrome, known as fetal alcohol syndrome, has been studied in animal models that reproduce many of the attributes of the human disease. These studies show that ethanol is most teratogenic during organogenesis and development of the nervous system. The molecular basis of fetal alcohol effects has been further investigated using embryo and cell culture systems. Recent studies show that signal transduction pathways controlling cell proliferation are perturbed during ethanol exposure. Ethanol can induce the release of intracellular calcium stores, which stimulates the cell cycle, and it also up-regulates the expression of myc proteins associated with cell proliferation. Increased proliferation is advantageous during the preimplantation period, but ethanol interference with terminal differentiation events within developing tissues during organogenesis may underlie alcohol teratogenicity.