Effects of chronic ethanol administration on total asialoglycoprotein receptor content in isolated rat hepatocytes

Conference · Fri May 01 00:00:00 EDT 1987 · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)

OSTI ID:6366332

Casey, C A; Kragskow, S L; Sorrell, M F; Tuma, D J

The authors have previously shown that chronic ethanol administration impairs receptor-mediated endocytosis of asialoorosomucoid (ASOR) in hepatocytes. Decreased surface binding, degradation, and internalization of /sup 125/I-ASOR, along with decreased receptor recycling, was shown in hepatocytes isolated from rats fed a liquid ethanol diet for 5-7 weeks as compared to values obtained from hepatocytes isolated from chow-fed and pair-fed control rats. The present study was undertaken to determine the effect of chronic ethanol feeding on total asialoglycoprotein receptor number and on the distribution of intracellular versus surface membrane receptor content of the hepatocytes. Chronic ethanol administration produced a significant decrease (30-50%, p<.01) in the total number of binding sites/10/sup 6/ cells, as determined by /sup 125/I-ASOR binding to cells which has been permeabilized with .055% digitonin, when compared to controls. The distribution of surface membrane/intracellular binding site number was, however, unchanged by chronic ethanol feeding. The decrease in both total and surface binding of /sup 125/I-ASOR to cells from ethanol-fed rats was confirmed using anti-rat antibody binding to intact and permeabilized cells. These results indicate that both surface and total asialoglycoprotein receptor content is decreased by chronic ethanol feeding.

• Research Organization: Univ. of Nebraska, Omaha
• OSTI ID: 6366332
• Report Number(s): CONF-870644-; TRN: 87-034176
• Journal Information: Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Vol. 46:6; Conference: 78. annual meeting of the American Society of Biological Chemists conference, Philadelphia, PA, USA, 7 Jun 1987
• Country of Publication: United States
• Language: English

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