Abstract
This chapter discusses the effects of alcohol and xenobiotics in placenta damage. The wide variety of cellular/biochemical effects of ethanol on placental and fetal tissues suggests that fetotoxic responses to ethanol reflect a multifactorial setting. The placenta, a temporary organ found only in eutherian mammals, is the site where physiological exchanges between the mother and the fetus occur. The events that characterize normal placental growth are considered to be important determinants of fetal growth and development. The most likely hypothesis whereby alcohol decreases prenatal growth is via hypoxia, which interferes with cellular processes that require oxygen to function adequately, such as placental transport and protein synthesis. Placental oxygenation is associated with oxygen tension in the uterine environment and this determines whether the cytotrophoblast proliferate or invade, thereby, regulating placental growth and cellular architecture. Impairment in fetal placental nutrient transport during critical phases of fetal organogenesis could compound any direct fetotoxic effects. Ethanol and/or acetaldehyde damage other tissues by inducing oxidative stress. Placental syncytiotrophoblast, while regulating the passage of nutrients from the maternal blood to the fetal circulation, exposes itself to the risk of oxidative attack by oxygen free radicals.
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