SERUM ALPHA-FETOPROTEIN - CHANGES ASSOCIATED WITH ACUTE AND CHRONIC ETHANOL INGESTION IN THE RESTING AND REGENERATING RAT-LIVER

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  • 1 January 1980
    • journal article
    • research article
    • Vol. 95  (5) , 725-736
Abstract
The effect of acute and chronic ethanol consumption on serum .alpha.-fetoprotein was studied in adult male rats with resting and regenerating livers. Unlike many hepatotoxins, ethanol consumed over both the long and short term suppressed serum .alpha.-fetoprotein concentrations (P < 0.05). This suppression was not due to increased degradation, since the half-life of .alpha.-fetoprotein was not significantly altered by chronic ethanol treatment. Liver cytosolic .alpha.-fetoprotein was markedly increased after ethanol consumption, suggesting the presence of impaired secretion or mobilization from the liver cells. During liver regeneration following partial hepatectomy, .alpha.-fetoprotein increased in both the control (390 ng-h/ml) and ethanol-treated animals (288 ng-h/ml). At no time did the ethanol animal values equal the control levels. The change in serum .alpha.-fetoprotein showed an inverse exponential correlation with the amount of liver removed at hepatectomy and a positive correlation with the amount of nuclear DNA present at sacrifice. In the ethanol-treated animals it required the removal of 1.9 times as much liver to stimulate the same degree of liver regeneration as in the controls (P < 0.001). A significant inverse correlation was observed between [3H]-thymidine uptake and the areas under the .alpha.-fetoprotein time curves in the controls (P < 0.001). In the ethanol groups the correlation was not statistically significant (P < 0.2). Although changes in serum .alpha.-fetoprotein may be associated with liver injury and regeneration, they are probably not a direct result of the regenerative process. The direct correlation with available nuclear DNA indicates the need for existing cells to hypertrophy and produce the .alpha.-fetoprotein. The depression associated with acute and chronic ethanol ingestion appears to reflect a direct effect of ethanol on protein synthesis and/or release.