Selective fetal malnutrition: the effect of in vivo ethanol exposure upon in vitro placental uptake of amino acids in the non-human primate.

In vitro uptake (45 and 90 minutes) of amino acids, alpha-amino isobutyric (AIB) and valine (VAL), was measured in six placentae from the nonhuman primate, Macacca fascicularis. Three of the pregnant primates were chronically treated with ethanol before and throughout pregnancy (CHR); one during the last trimester only (LT); and two were controls (C). Compared to the C placentae, the LT placenta had significantly decreased uptake only for AIB at 45 min: 33.4 +/- 6.8% reduction (mean +/- S.E.) (P less than 0.05). In contrast, the CHR placentae demonstrated significantly reduced uptake (P less than 0.01) for both amino acids at both time points. Percent reduction at 45 and 90 min: AIB, 35.2 +/- 6.5% and 32.6 +/- 5.6% and VAL, 38.7 +/- 2.9% and 22.1 +/- 4.1%. The results indicate that chronic in vivo ethanol exposure impairs the in vitro placental uptake of two actively transported amino acids, using an animal with a placenta almost identical to the human.

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.