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Hepatocellular injury that results from chronic alcohol abuse may be a consequence
of (1) augmented viremia in hepatitis C virus; (2) the carcinogenic effect of DNA,
which results from the combination of alcohol-induced CYP2E1 and ingestion of low
levels of carcinogenic compounds or choline deficiency; (3) differential proliferation
of hepatocytes versus nonparenchymal cells during injury, regeneration, and repair;
(4) alteration of the regenerative response of hepatocytes in response to agonists,
which stimulate the cell cycle through membrane signal transduction-nuclear pathways;
(5) Kupffer cell activation by endotoxin, which generates cytokines that signal hepatocellular
programmed cell death (apoptosis) through signal transduction mechanisms; or (6) dietary
and immune mechanisms (i.e., formation of neoantigens).
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© 1996 Elsevier Inc. Published by Elsevier Inc. All rights reserved.