ABSTRACT
An alternate and/or complementary hypothesis to explain the selective perivenular hepatotoxicity of ethanol postulates that the low oxygen tensions normally prevailing in perivenular zones could exaggerate the redox shift produced by ethanol. The hypoxia hypothesis originated from the observation that liver slices from rats fed alcohol chronically consume more oxygen than those of controls. Two of the earliest and most conspicuous features of the hepatic damage produced by alcohol are the deposition of fat and the enlargement of the liver. This hepatomegaly was traditionally attributed to the accumulation of lipids. Free-radical generation by neutrophils may provide a potential mechanism of cellular injury in acute alcoholic liver disease. Alcoholism and viral hepatitis can occur in the same patients, but in many patients with alcoholic cirrhosis there is no evidence for antecedent viral hepatitis; similarly, in the baboons that developed alcoholic cirrhosis, no concomitant virus infection was detectable.
