Effect of Ethanol on Human Placental Transport of Model Amino Acids and Glucose

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Abstract
Prior studies in rodents, sheep, and subhuman primates have shown that ethanol, especially atter chronic exposure, inhibits the transport of amino acids by the placenta. A small decrease in glucose transport by rat placenta chronically exposed to ethanol has also been noted. With human placental slices, however, only pharmacological (high) concentrations of ethanol impaired uptake of amino acids, and there are no data on glucose transport. In the present study, the effect of brief exposure to ethanol on human placental transport of model amino acids and glucose was studied by two techniques not previously jointly employed for this—the perfused human placental cotyledon and human placental vesicle systems. The nonmetabolizable amino acids, α-aminoisobutyric (AIB) acid and cycloleucine (CLEU), as well as d-glucose, and nonmetabolized glucose (3-O-methyl-d-glucose), were used as probes. AIB and CLEU are transferred normally by active transport and d-glucose by facilitated transport from maternal to fetal compartments. The pertused placental system was exposed to ethanol (300-500 mg%) for 2–4 hr and the vesicles to 200–400 mg% ethanol for times varying from 10 min to 48 hr. There was no impairment of AIB, d-glucose, or 3-O-methyl-d-glucose transfer by ethanol using these techniques. Normally, about 60% of AIB transport by human placenta is sodium dependent. This component (using the vesicle system) was also not impaired by ethanol. Ethanol caused a very small decrease of CLEU clearance by the perfused human placenta (p= 0.05) but not using vesicles. We conclude that transport of amino acids and glucose by the human placenta is relatively resistant to the inhibitory effects of brief ethanol.
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