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Time course of ethanol‐induced impairment in fluid‐phase endocytosis in isolated rat hepatocytes
Author(s) -
Camacho Kenneth B.,
Casey Carol A.,
Wiegert Robert L.,
Sorrell Michael F.,
Tuma Dean J.
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840170421
Subject(s) - lucifer yellow , endocytosis , internalization , intracellular , endocrinology , medicine , efflux , biology , ethanol , chemistry , biochemistry , cell , gap junction
The time‐course effects of long‐term ethanol administration on fluid‐phase endocytosis were studied in isolated rat hepatocytes. Rats were pair‐fed an ethanol‐supplemented liquid diet or an isocaloric control diet for 3 days, 1 wk, 2 wk or 5 wk. Hepatocytes were isolated and incubated at 37° C with various concentrations of the fluid‐phase marker Lucifer yellow.‐Net internalization of the marker dye was determined. After as little as 1 wk, ethanol‐fed rats demonstrated marked decreases in the net internalization of dye compared with pair‐fed controls; these changes persisted throughout 5 wk of feeding. Because net internalization is the balance between uptake into the cells vs. efflux from the cells, these components were examined individually. Early uptake was not significantly decreased by ethanol feeding; however, efflux of preloaded Lucifer yellow from cells from the ethanol‐fed animals was markedly faster than efflux from pair‐fed controls. This increased efflux was more prominent in the longer preload time (90 min) compared with a shorter preload time (15 min), indicating an alteration in dye distribution among various intracellular pools. These ethanol‐induced changes in fluid‐phase endocytosis were apparent for 1 wk through 5 wk of feeding and were similar for all Lucifer yellow concentrations examined. These results indicate that the decreased net internalization of Lucifer yellow through fluid‐phase endocytosis is mainly a result of an ethanol‐induced increase in efflux possibly caused by altered intracellular trafficking rather than by reduction in uptake. (H EPATOLOGY 1993;17:661–667.)