Acetaldehyde production and transfer by the perfused human placental cotyledon

Fetal injury associated with maternal ethanol ingestion is a major cause of congenital anomalies and mental retardation. Studies with animals suggest that acedehyde, the primary hepatic oxidative metabolite ofethanol, may contribute to fetal damage. It is not known, however, whether acetaldehyde readies the human fetus, either by placental production or transfer. Studies utilizing the perfud human placental cotyledon show that the human placenta oxidizes ethanol to acetaldehyde, releasing it into the fetal perfusate. Moreover, when acldehyde is present in the maternal perfiusate, it is transferred to the fetal side, reaching approximately 50 percent of the maternal levd. These findings suggest that the human placenta may play a pivotal role in the pathophysiology of ethanol-associated fetal injury.