Tuma D J, Sorrell M F
Recent Dev Alcohol. 1984;2:159-80. doi: 10.1007/978-1-4684-4661-6_10.
Both acute and chronic ethanol administration inhibit the secretion of albumin and glycoproteins from the liver. Impairment of posttranslational steps of the secretory process are mainly involved in this secretory defect, although in some instances altered synthesis of the protein moiety may be a factor. Decreased secretion following ethanol administration results in the intrahepatic retention of export proteins. The secretory defect is a consequence of the metabolism of ethanol and is likely mediated via acetaldehyde, although more conclusive proof is still required. The manner by which acetaldehyde impairs the secretory process is unknown, but may be related to its high reactivity with hepatocellular proteins. The specific posttranslational steps or processes involved in the secretory defect are still unclear; however, it appears that the final steps of secretion (post-Golgi events) may be the primary site of impairment. Impaired secretion of proteins from the liver could contribute to altered levels of plasma proteins and hepatomegaly as well as to the liver injury observed in the alcoholic.
急性和慢性乙醇摄入均会抑制肝脏白蛋白和糖蛋白的分泌。尽管在某些情况下蛋白质部分合成的改变可能是一个因素,但分泌过程中翻译后步骤的损伤主要参与了这种分泌缺陷。乙醇摄入后分泌减少导致输出蛋白在肝内潴留。分泌缺陷是乙醇代谢的结果,尽管仍需要更确凿的证据,但可能是通过乙醛介导的。乙醛损害分泌过程的方式尚不清楚,但可能与其与肝细胞蛋白的高反应性有关。分泌缺陷所涉及的具体翻译后步骤或过程仍不清楚;然而,似乎分泌的最后步骤(高尔基体后事件)可能是损伤的主要部位。肝脏蛋白质分泌受损可能导致血浆蛋白水平改变、肝肿大以及在酗酒者中观察到的肝损伤。