The effect of ethanol or hepatotoxin exposure on rat transferrin desialylation

Serum carbohydrate-deficient transferrin (CDT) is being increasingly used as a biological indicator for excessive alcohol consumption. However, the mechanisms behind the changes in the carbohydrate moiety of transferrin are unclear, although they have been suggested to be mediated by acetaldehyde or liver damage. To study this, an animal model involving alterations in serum isotransferrin concentrations would be needed. The present work examined the changes in the carbohydrate moiety of transferrin in rats after different degrees of ethanol exposure, the effects of chronically elevated acetaldehyde levels, and also the changes, produced with liver toxins (galactosamine) and carbon tetrachloride). Ethanol was administered both in the drinking fluid and by intubation, 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 weeks by intragastric infusion were also analysed. Some rats simultaneously had cyanamide administered to elevate acetaldehyde levels. However, neither ethanol nor acetaldehyde had any effect on transferrin. Intraperitoneal galactosamine, but not carbon tetrachloride, induced transferrin desialylation. Thus, in the rat, neither chronic ethanol consumption nor elevated acetaldehyde induces changes in transferrin microheterogeneity.