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Effect of Acute and Chronic Ethanol Administration on Rat Liver α 2,6‐Sialyltransferase Activity Responsible for Sialylation of Serum Transferrin
Author(s) -
Malagolini Nadia,
Dall'Olio Fabio,
SerafiniCessi Franca,
Cessi Carlo
Publication year - 1989
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1989.tb00398.x
Subject(s) - sialyltransferase , transferrin , ethanol , chemistry , alcohol , alpha (finance) , medicine , endocrinology , in vivo , biochemistry , sialic acid , biology , surgery , construct validity , microbiology and biotechnology , patient satisfaction
The effect of a single administration and a 6‐week treatment with ethanol on rat liver sialyltransferase activity towards asialoglycoproteins and N ‐acetyllactosamine (Galβ91,4GlcNAc) was studied. Since only the cα2,6‐sialyltransferase is involved in the in vivo sialylation of transferrin, GalβS1,4GlcNAc was chosen as an acceptor and α2,6‐sialyl‐N‐acetyllactosamine was separated from the corresponding α2,3‐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 < 0.005) reduction of sialyltransferase activity towards asialotransferrin as well as a reduced α2,6‐sialyltransferase activity towards N ‐acetyllactosamine. An opposite result was found in the chronically ethanol‐treated rats: in these animals either the total or α2,6‐sialyl‐transferase 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 α2,6‐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.