Weesner R E, Mendenhall C L, Morgan D D, Kessler V, Kromme C
J Lab Clin Med. 1980 May;95(5):725-36.
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.
研究了急性和慢性乙醇摄入对成年雄性大鼠静息肝脏和再生肝脏血清甲胎蛋白的影响。与许多肝毒素不同，长期和短期摄入乙醇均会抑制血清甲胎蛋白浓度（p<0.05）。这种抑制并非由于降解增加，因为慢性乙醇处理并未显著改变甲胎蛋白的半衰期。然而，乙醇摄入后肝细胞溶质中的甲胎蛋白显著增加，提示存在肝细胞分泌或转运受损。在部分肝切除术后的肝脏再生过程中，对照组（390 ng·hr/ml）和乙醇处理组动物（288 ng·hr/ml）的甲胎蛋白均增加。乙醇处理组动物的值在任何时候都未达到对照组水平。血清甲胎蛋白的变化与肝切除时切除的肝脏量呈反指数相关，与处死时存在的核DNA量呈正相关。然而，在乙醇处理组动物中，需要切除1.9倍于对照组的肝脏才能刺激相同程度的肝脏再生（p<0.001）。在对照组中，观察到3H-胸腺嘧啶摄取与甲胎蛋白时间曲线下面积之间存在显著的负相关（p<0.001）。在乙醇组中，这种相关性无统计学意义（p<0.2）。结论是，虽然血清甲胎蛋白的变化可能与肝损伤和再生有关，但它们并非再生过程的直接结果。与可用核DNA的直接相关性表明，现有细胞需要肥大并产生甲胎蛋白。与急性和慢性乙醇摄入相关的抑制似乎反映了乙醇对蛋白质合成和/或释放的直接作用。
