Abstract
Zinc is an essential trace element involved in various biological functions. It serves as a catalytic cofactor for hundreds of enzymes. Zinc is also required for stabilizing the zinc figure motif of a large number of zinc proteins, including critical transcription factors. Zinc deficiency is one of the most consistent nutritional/biochemical observations in alcoholic liver disease. Several mechanisms underlying alcohol-induced zinc deficiency have been suggested, including reduced dietary zinc intake and intestinal absorption, disturbed hepatic zinc metabolism, and increased urinary zinc excretion. Generation of reactive oxygen species in association with alcohol metabolism not only alters the expression of zinc transporters, but also releases zinc from zinc proteins. Dietary zinc supplementation has been shown to prevent/reverse alcohol-induced liver injury in animal models and clinical studies. The beneficial effects of zinc are achieved by both hepatic actions and extrahepatic actions. Inhibition of oxidative stress and restoration of alcohol-inactivated zinc finger transcription factors, hepatocyte nuclear factor 4α and peroxisome proliferation activator α, represent important molecular mechanisms of zinc actions.
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