Effect of acute and chronic ethanol administration on rat liver alpha 2,6-sialyltransferase activity responsible for sialylation of serum transferrin.

Abstract

The effect of a single administration and a 6-week treatment with ethanol on rat liver sialyltransferase activity towards asialoglycoproteins and N-acetyllactosamine (Gal beta 1,4GlcNAc) was studied. Since only the alpha 2,6-sialyltransferase is involved in the in vivo sialylation of transferrin, Gal beta 1,4GlcNAc was chosen as an acceptor and alpha 2,6-sialyl-N-acetyllactosamine was separated from the corresponding alpha 2,3-sialyl isomer present in the sialyltransferase reaction mixture by high-performance liquid chromatography. After a single ethanol administration there was a low (about 20%) but significant (p less than 0.005) reduction of sialyltransferase activity towards asialotransferrin as well as a reduced alpha 2,6-sialyltransferase activity towards N-acetyllactosamine. An opposite result was found in the chronically ethanol-treated rats: in these animals either the total or alpha 2,6-sialyltransferase activity was slightly higher than in control animals. Blood ethanol concentration was significantly high (3.3 +/- 1.2 mg/ml) only in the acute-treated animals, suggesting that the accumulation in the body of ethanol and/or its metabolites induces a reduction of liver alpha 2,6-sialyltransferase activity responsible for the transferrin sialylation. Current results are consistent with the finding (Stibler H, Hultcrantz R: Alcohol Clin Exp Res 11:468-473, 1987) that an enhanced level of hyposialylated transferrin isoforms is a marker of present but not previous alcohol abuse.