| Functional and ultrastructural features of ethanol/bile salts interaction in the isolated perfused rat liver. | |
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MedLine Citation:
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PMID: 7705787 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We investigated whether bile salts (BS) with different hydrophobic-hydrophilic properties interact with ethanol on bile secretion, enzyme (aspartate transaminase [AST], lactate dehydrogenase [LDH]) release in the perfusate, liver ultrastructure, and vesicular exocytosis in the isolated perfused rat liver. Ethanol (0.1 or 1%) promoted a rapid decrease of bile flow and BS secretion in livers perfused with taurocholate (TCA), the physiologic BS in the rat (-28% decrease of baseline values with 0.1% and -34% with 1% ethanol). The inhibitory effect of ethanol on bile flow and BS secretion was significantly (P < .02) attenuated by perfusing liver with the hydrophilic BS, tauroursodeoxycholate (TUDCA), and it was exacerbated (P < .02) by perfusion with the hydrophobic BS, taurodeoxycholate (TDCA). The release of AST and LDH in the perfusate was unaffected by 0.1% ethanol, but increased threefold to fivefold by 1% ethanol in TCA-perfused livers. This cytolitic effect of ethanol was not observed in TUDCA-perfused livers, but it was enhanced (P < .03) by perfusion with TDCA. No ultrastructural abnormalities were found in either TCA- or TUDCA-perfused livers, with or without 1% ethanol. Only minimal changes were found in livers perfused with TDCA alone, but, in the presence of TDCA, 1% ethanol induces marked mitochondrial damage. The biliary excretion of the fluid phase marker horseradish peroxidase was inhibited by ethanol, an effect reversed by TUDCA (P < .02) and exacerbated by TDCA (P < .04). In conclusion, this study demonstrates that hydrophilic BS such as TUDCA counteract the inhibitory effect of ethanol on bile secretion and vesicular exocytosis as well as the ethanol-induced cytolitic effect in the isolated perfused rat liver. In the presence of hydrophobic BS such as TDCA, the exposure to ethanol promotes a marked inhibition of bile secretion and vesicular exocytosis as well as prominent mitochondrial damage. |
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Authors:
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D Alvaro; A Benedetti; A Gigliozzi; A Bini; P Della Guardia; T La Rosa; A M Jezequel; L Capocaccia |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Hepatology (Baltimore, Md.) Volume: 21 ISSN: 0270-9139 ISO Abbreviation: Hepatology Publication Date: 1995 Apr |
Date Detail:
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Created Date: 1995-05-09 Completed Date: 1995-05-09 Revised Date: 2003-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8302946 Medline TA: Hepatology Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1120-9 Citation Subset: IM |
Affiliation:
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II Department of Gastroenterology, University of Rome La Sapienza, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aspartate Aminotransferases / secretion Bile / drug effects, secretion Bile Acids and Salts / pharmacology*, secretion Ethanol / toxicity* L-Lactate Dehydrogenase / secretion Liver / drug effects*, physiology, ultrastructure Male Perfusion Rats Rats, Wistar Taurochenodeoxycholic Acid / pharmacology Taurocholic Acid / pharmacology Taurodeoxycholic Acid / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Bile Acids and Salts; 14605-22-2/tauroursodeoxycholic acid; 516-35-8/Taurochenodeoxycholic Acid; 516-50-7/Taurodeoxycholic Acid; 64-17-5/Ethanol; 81-24-3/Taurocholic Acid; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.6.1.1/Aspartate Aminotransferases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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