Matsuda Y, Takada A, Takase S, Yasuhara M
Department of Internal Medicine, Kanazawa Medical University Uchinada, Ishikawa, Japan.
Alcohol. 1991 Nov-Dec;8(6):433-7. doi: 10.1016/s0741-8329(91)90051-w.
It has been pointed out that one of the pathogenetic causes of alcoholic liver injury is the hepatocytic accumulation of exportable proteins due to a decrease in hepatic microtubules caused by acetaldehyde. To confirm and extend this secretory protein accumulation in the hepatocytes, the effects of alcohol treatment on the intracellular transport of secretory protein in the hepatocyte was studied using radioisotope-labeled leucine and fucose. Acute ethanol administration to rats did not show any effects on intrahepatocytic transport and secretion of transferrin. In alcohol pyrazole hepatitis rats, the secretion of transferrin labeled with both radioactive leucine and fucose into the serum was significantly delayed. Delaying in the secretion of fucose-labeled transferrin was more prominent than in leucine-labeled transferrin. This secretory inhibition was accompanied by a corresponding increase in the hepatic retention of both leucine- and fucose-labeled transferrin. At the time of the maximum inhibition of secretion, radioisotope labeled transferrin mainly retained in the Golgi apparatus. These results indicated that movement of secretory proteins along the secretory pathway impaired in alcoholic liver injury and that accumulation of the secretory proteins might play an important role in the development of alcoholic liver injury.
