Abstract
The activities of hepatic alcohol (ADH), aldehyde (ALDH), and lactate dehydrogenases were measured in 69 patients with various liver diseases (15 controls, 20 with alcoholic and 8 with non-alcoholic fatty liver, 13 with alcoholic cirrhosis, 2 with alcoholic hepatitis, 3 with cryptogenic and 3 with primary biliary cirrhosis, and 5 with acute or chronic hepatitis). The specific activities of all these enzymes were decreased in both alcoholic and non-alcoholic liver diseases. The activities of ADH and low-Km ALDH were significantly decreased both in alcoholic (ADH, 7.22 mU/mg protein, p < 0.001; low-Km ALDH, 5.00 mU/mg protein, p 0.001) and in other liver diseases (ADH, 10.70 mU/mg protein, p < 0.001; low-Km ALDH, 6.80mU/mg protein, p < 0.005) when compared with controls (ADH, 20.87 mU/mg protein; low-Km ALDH, 14.41 mU/mg protein). The hepatic protein content was significantly (p < 0.001) increased in alcoholic fatty degeneration but not in alcoholic cirrhosis or other liver diseases. The results suggest that in man alcohol- and acetaldehyde-metabolizing enzymes are not induced by chronic alcohol consumption. On the contrary, the hepatic activities of these enzymes appeared to be lower in alcoholic than in non-alcoholic liver diseases. Consequently, in addition to liver injury alcohol may also directly affect the synthesis or breakdown of alcohol-metabolizing enzymes.