Ethanol-dependent induction of bilirubin UDP-glucuronosyl-transferase in rat liver is mediated by Kupffer cells

Recently we have reported that bilirubin UDP-glucuronosyltransferase (UGT1A1) is induced in rat liver by chronic ethanol treatment. Several studies have shown that Kupffer cells play a central role in the mediation of various hepatic effects of chronic alcohol consumption. In the present work, the p...

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Published in:Life sciences (1973) 2002-01, Vol.70 (10), p.1205-1212
Main Authors: Kardon, Tamás, Mile, Valéria, Bánhegyi, Gábor, Csala, Miklós, Burchell, Brian, Mandl, József, Braun, László
Format: Article
Language:English
Subjects:
Animals
Bilirubin
Bilirubin - metabolism
Enzyme Induction - drug effects
Ethanol
Ethanol - pharmacology
Gadolinium - pharmacology
Gadolinium chloride
Glucuronidation
Glucuronosyltransferase - biosynthesis
Glucuronosyltransferase - genetics
Kupffer cell
Kupffer Cells - physiology
Liver
Male
Microsomes, Liver - enzymology
Rats
Rats, Wistar
RNA, Messenger - analysis
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Summary:Recently we have reported that bilirubin UDP-glucuronosyltransferase (UGT1A1) is induced in rat liver by chronic ethanol treatment. Several studies have shown that Kupffer cells play a central role in the mediation of various hepatic effects of chronic alcohol consumption. In the present work, the participation of Kupffer cells in the ethanol dependent induction of UGT1A1 was investigated. A group of rats was pretreated with gadolinium chloride, a known Kupffer-cell-depleting agent. We compared the effect of chronic ethanol ingestion on UGT1A1 expression in the liver of normal and gadolinium chloride treated rats. The effect of ethanol on bilirubin glucuronidation was completely prevented in Kupffer cell deficient rats. The western and northern blot analyses showed that the increase of both the protein and mRNA of UGT1A1 was prevented in these animals. These results suggest that Kupffer cells play a major role in the mediation of ethanol-stimulated induction of UGT1A1 in liver parenchymal cells.
ISSN:0024-3205
1879-0631
DOI:10.1016/S0024-3205(01)01492-8