Abstract:
Abstract: Alcoholic liver disease (ALD) is a worldwide health problem
that may lead to development of fatty liver steatosis, hepatitis and
cirrhosis. Alcohol is known to exert a harmful effect on a variety of
human tissues. In particular, the liver is the major site of alcohol-induced
damage because it is the direct recipient of the blood that contains
elevated levels of alcohol, and it is the major organ responsible for alcohol
metabolism. The damage caused by ethanol is mainly attributed to its
metabolic process that results in production of acetaldehyde and reactive
oxygen species (ROS) such as hydrogen peroxide, superoxide and free
hydroxyl radical. These metabolites cause depletion of reduced
glutathione (GSH), peroxidation of cellular membranes, oxidation of
macro-molecules such as proteins and nucleic acids, and eventually lead
to progressive injury of hepatocytes. Additionally, ethanol and its
metabolic products enhance the production of pro-inflammatory cytokines
such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The
enhanced production of those inflammation factors; stimulated partially
by oxidative stress; results in cytokine imbalance and immune disorders,
leading to further hepatic damage. Thus, agents with anti-inflammatory
and anti-oxidative properties might be potential candidates for protection
against alcohol-induced liver disease. The metabolic functions of the
alcoholic liver are seriously affected. Disorders in iron metabolism are
characteristic of ALD. Abnormal levels of iron, ferritin, and transferrin
were reported in ALD. Hepcidin, the principle hepatic regulator of the
metabolism of iron, is decreased in ALD.
