作者: Dean J. Tuma , Michael F. Sorrell
DOI: 10.1007/978-1-4684-4661-6_10
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摘要: Both acute and chronic ethanol administration inhibit the secretion of albumin glycoproteins from liver. Impairment posttranslational steps secretory process are mainly involved in this defect, although some instances altered synthesis protein moiety may be a factor. Decreased following results intrahepatic retention export proteins. The defect is consequence metabolism likely mediated via acetaldehyde, more conclusive proof still required. manner by which acetaldehyde impairs unknown, but related to its high reactivity with hepatocellular specific or processes unclear; however, it appears that final (post-Golgi events) primary site impairment. Impaired proteins liver could contribute levels plasma hepatomegaly as well injury observed alcoholic.