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  • Title: Serum alpha-fetoprotein: changes associated with acute and chronic ethanol ingestion in the resting and regenerating rat liver.
    Author: Weesner RE, Mendenhall CL, Morgan DD, Kessler V, Kromme C.
    Journal: J Lab Clin Med; 1980 May; 95(5):725-36. PubMed ID: 6154115.
    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 less than 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. However, 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-hr/ml) and ethanol-treated animals (288 ng-hr/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. However, 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 less than 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 less than 0.001). In the ethanol groups the correlation was not statistically significant (p less than 0.2). It is concluded that although changes in serum alpha-fetoprotein may be associated with liver injury and regeneration, they are 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.
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