Alcoholic liver disease accounts for 12,000 deaths per year in the United States and is the second leading indication for liver transplantation. It covers a spectrum of disease conditions ranging from steatosis and cirrhosis to hepatic malignancies. Epidemiological data clearly show a strong correlation between alcohol consumption and liver diseases. A large body of evidence has accumulated over the years in determining the molecular mediators of alcohol-induced liver injury. In this review, we provide an overview of such mediators, which include alcohol metabolites and reactive oxygen/nitrogen species, endotoxin via bacterial translocation from the gut and TNF-α, and highlight the role of the sympathetic nervous stimuli, norepinephrine and the α2A-adrenergic receptors in contributing to the deleterious effect observed in alcohol-induced hepatic dysfunction.