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Am J Physiol Gastrointest Liver Physiol 275: G387-G392, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 3, G387-G392, September 1998

THEMES
Mechanisms of Hepatic Toxicity
I. TNF-induced liver injury*

Cynthia A. Bradham1, Jörg Plümpe2, Michael P. Manns2, David A. Brenner1, and Christian Trautwein2

1 Departments of Medicine and Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599-7080; and 2 Department of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, 30625 Hannover, Germany

Tumor necrosis factor-alpha (TNF-alpha ) functions as a two-edged sword in the liver. TNF-alpha is required for normal hepatocyte proliferation during liver regeneration. It functions both as a comitogen and to induce the transcription factor nuclear factor-kappa B, which has antiapoptotic effects. On the other hand, TNF-alpha is the mediator of hepatotoxicity in many animal models, including those involving the toxins concanavalin A and lipopolysaccharide. TNF-alpha has also been implicated as an important pathogenic mediator in patients with alcoholic liver disease and viral hepatitis.

tumor necrosis factor receptor; concanavalin A; lipopolysaccharide; liver regeneration; viral hepatitis; alcoholic liver disease; fulminant hepatic failure

* First in a series of invited articles on Mechanisms of Hepatic Toxicity.




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