Ethanol is directly and indirectly hepatotoxic. The toxicity of alcohol is influenced by genetic factors (including gender differences) on the one hand and environmental variables (including nutrition, intestinal microflora, interactions with xenobiotics, and so on) on the other. In the past year, research on the pathogenesis of alcohol-induced liver injury has emphasized the importance of CYP2E1 in producing reactive oxygen species and oxidative stress, and the role of acetaldehyde and hydroxyethyl radicals in producing protein adducts. Research has further implicated a complex cascade of autocrine and paracrine pathways that involves endotoxemia, oxidative stress and activation of Kupffer cells, proliferation and transformation of hepatic stellate cells, and stimulation of sinusoidal endothelial cells.
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