Fisher S E, Atkinson M, Burnap J K, Jacobson S, Sehgal P K, Scott W, Van Thiel D H
Alcohol Clin Exp Res. 1982 Spring;6(2):197-201. doi: 10.1111/j.1530-0277.1982.tb04962.x.
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.
胎儿酒精谱系障碍(FAS)的发病机制,尤其是其典型的宫内生长受限(IUGR),可能部分归因于与乙醇相关的胎盘损伤。乙醇和/或乙醛可能会损害对生长至关重要的营养物质(如氨基酸)的胎盘转运。无论母体营养状况如何,这种限制都可能发生,即选择性胎儿营养不良。在胎儿器官发生的关键阶段,胎盘营养物质转运受损可能会加重乙醇或乙醛对胎儿的任何直接毒性作用。乙醇对人胎盘激素合成以及维生素、矿物质、葡萄糖和核酸前体转运的影响有待进一步研究。同样,乙醇与酗酒者常见滥用的其他外源化学物之间的潜在相互作用也需要阐明。