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.