Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (19)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bykov, I.
Right arrow Articles by Lindros, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bykov, I.
Right arrow Articles by Lindros, K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Alcohol and Alcoholism Vol. 38, No. 5, pp. 400-406, 2003
© 2003 Medical Council on Alcohol

L-CARNITINE ALLEVIATES ALCOHOL-INDUCED LIVER DAMAGE IN RATS: ROLE OF TUMOUR NECROSIS FACTOR-ALPHA

I. Bykov, H. Järveläinen and K. Lindros*

National Public Health Institute, Department of Mental Health and Alcohol Research, Helsinki, Finland

(Received 21 February 2003; first review notified 11 April 2003; in revised form 12 May 2003; accepted 2 June 2003)

Aims: Excessive alcohol intake induces hepatic fatty infiltration, which has been suggested to sensitize the liver to further damage. To test this hypothesis, L-carnitine, a constitutional lipotropic compound, was administered to rats chronically treated with ethanol by liquid diet feeding for 10 weeks. Results: Ethanol administration caused marked steatosis, mild inflammation and elevated plasma alanine aminotransferase and tumour necrosis factor alpha (TNF-{alpha}) concentrations. Dietary supplementation with L-carnitine significantly reduced all these parameters as well as the hepatic concentration of thiobarbituric acid reactive substances, an indicator of lipid peroxidation products. Pretreatment with L-carnitine also significantly blunted ethanol-induced stimulation of TNF-{alpha} release by isolated Kupffer cells. Conclusions: This study provides direct support for the notion that steatosis sensitizes the liver to further damage and suggests an involvement of TNF-{alpha} in this process.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Clin. Pathol.Home page
P Riley, J O'Donohue, and M Crook
A growing burden: the pathogenesis, investigation and management of non-alcoholic fatty liver disease
J. Clin. Pathol., December 1, 2007; 60(12): 1384 - 1391.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
X. Wang and A. A. Abdel-Rahman
Effect of chronic ethanol administration on hepatic eNOS activity and its association with caveolin-1 and calmodulin in female rats
Am J Physiol Gastrointest Liver Physiol, September 1, 2005; 289(3): G579 - G585.
[Abstract] [Full Text] [PDF]


Home page
Toxicol PatholHome page
U. M. Apte, R. Mcree, and S. K. Ramaiah
Hepatocyte Proliferation is the Possible Mechanism for the Transient Decrease in Liver Injury During Steatosis Stage of Alcoholic Liver Disease
Toxicol Pathol, August 1, 2004; 32(5): 567 - 576.
[Abstract] [PDF]


Home page
International Journal of ToxicologyHome page
S. K. Ramaiah, C. Rivera, and G. E. Arteel
Early-Phase Alcoholic Liver Disease: An Update on Animal Models, Pathology, and Pathogenesis
International Journal of Toxicology, July 1, 2004; 23(4): 217 - 231.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.