ETHANOL-ASSOCIATED PLACENTO-TOXICITY: Na, K-ATPase ACTIVITY

Abstract

Ethanol (E) abuse during pregnancy may be associated with intrauterine growth retardation (IUGR), due in part to E-induced interference with placental transport of amino acids. Since this placental transport is energy dependent, we measured the effect of acute and chronic E exposure upon rat placental Na,K-ATPase activity. Acutely, term pregnant rats (n=8) were gavaged with 4 gm E/kg body weight (2.5 hr before sacrifice). Control (C) animals (n=4) received sucrose. Chronic E animals (n=5) were fed a liquid diet containing 6% E (v/v) throughout pregnancy. Controls were isocalorically pairfed. All dams were sacrificed at 20 days gestation. A membrane fraction was prepared for each placenta and mean Na,K-ATPase activity was determined per litter. Maternal blood E levels were 319 ± 27.8 mg/dl (mean ± SE) for acute animals at sacrifice and 195 ± 26.0 mg/dl throughout pregnancy for chronic animals. RESULTS: There was a significant decrease in Na,K-ATPase activity for the chronically E treated animals (C=55.0 ± 7.4 vs. E=31.8 ± 6.0 pmoles P/min/mg protein; p=0.05; paired t-test). However, there was no difference between acutely treated E and C placentae. CONCLUSION: Chronic, but not acute ethanol exposure causes a reduction in rat placental Na,K-ATPase activity. This may help explain the etiology of IUGR association with maternal ethanol abuse.

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