Ethanol-associated selective fetal malnutrition: a contributing factor in the fetal alcohol syndrome.
The pathogenesis of the FAS, particularly the characteristic IUGR, may be due in part to ethanol-related placental injury. Ethanol and/ or acetaldehyde may impair placental transfer of nutrients essential for growth, e.g., amino acids. Such restriction could occur regardless of maternal nutritional status: selective fetal malnutrition. Impairment of placental nutrient transport at critical phases of fetal organogenesis could compound any direct fetotoxic effects of ethanol or acetaldehyde. The effect of ethanol upon human placental hormone synthesis and transport of vitamins, minerals, glucose, and nucleic acid precursors awaits further investigation. Similarly, potential interactions between ethanol and other xenobiotics commonly abused by alcoholics require clarification.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D000431:Ethanol / Q000009:adverse effects*; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000503:physiopathology*; D005317:Fetal Growth Retardation / Q000139:chemically induced; D006728:Hormones / Q000096:biosynthesis; D006801:Humans; D010920:Placenta / Q000378:metabolism; D010922:Placenta Diseases / Q000139:chemically induced*; D010927:Placental Insufficiency / Q000139:chemically induced*; D011247:Pregnancy; D012907:Smoking; D013045:Species Specificity; D019966:Substance-Related Disorders / Q000150:complications
D000596:Amino Acids; D006728:Hormones; D000431:Ethanol