Apoptosis and alcoholic liver disease

Citation
Aa. Nanji et Frc. Path, Apoptosis and alcoholic liver disease, SEM LIV DIS, 18(2), 1998, pp. 187-190
Citations number
54
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
SEMINARS IN LIVER DISEASE
ISSN journal
02728087 → ACNP
Volume
18
Issue
2
Year of publication
1998
Pages
187 - 190
Database
ISI
SICI code
0272-8087(1998)18:2<187:AAALD>2.0.ZU;2-I
Abstract
Apoptosis occurs in both clinical and experimental alcoholic liver disease. The mechanisms involved in alcohol-induced apoptosis of liver cells are no t completely understood Induction of cytochrome P450 2E1, the alcohol-induc ible cytochrome P450, is one of the proposed mechanisms. Exposure of Hep G2 cells expressing cy cytochrome P450 2E1 to arachidonic acid leads to incre ased lipid peroxidation and apoptosis. Increased levels of iron in the live r also promote lipid peroxidation and are associated with increased numbers of apoptotic hepatocytes. Tumor necrosis factor (TNF) acting through its r eceptors can induce apoptosis in hepatocytes. Increased levels of tumor nec rosis factor and its receptors have been described in alcoholic liver disea se. The liver is also CD95 receptor positive and in liver tissue from patie nts with alcoholic hepatitis, the CD95 ligand is expressed at high levels i n hepatocytes. Cytotoxic T lymphocytes could, through the CD95 receptor-lig and interaction, promote apoptosis.