THE EFFECT OF ETHANOL OR HEPATOTOXIN EXPOSURE ON RAT TRANSFERRIN DESIALYLATION

Serum carbohydrate-deficient transferrin (CDT) is being increasingly u sed as a biological indicator for excessive alcohol consumption. Howev er, the mechanisms behind the changes in the carbohydrate moiety of tr ansferrin are unclear, although they have been suggested to be mediate d by acetaldehyde or liver damage. To study this, an animal model invo lving alterations in serum isotransferrin concentrations would be need ed. The present work examined the changes in the carbohydrate moiety o f transferrin in rats after different degrees of ethanol exposure, the effects of chronically elevated acetaldehyde levels, and also the cha nges produced with liver toxins (galactosamine and carbon tetrachlorid e). Ethanol was administered both in the drinking fluid and, by intuba tion, reaching a dose of 11 g/kg/day over 7 weeks, or 16 g/kg/day over 4 weeks. Serum samples from rats maintained on high ethanol for 10 we eks by intragastric infusion were also analysed. Some rats simultaneou sly had cyanamide administered to elevate acetaldehyde levels. However , neither ethanol nor acetaldehyde had any effect on transferrin. Intr aperitoneal galactosamine, but not carbon tetrachloride, induced trans ferrin desialylation. Thus, in the rat, neither chronic ethanol consum ption nor elevated acetaldehyde induces changes in transferrin microhe terogeneity.