ABSTRACT
beta-Hexosaminidase (Hex) activity was previously found to be increased in the sera of patients with liver cirrhosis, cholestasis and acute alcohol intoxication, as well as in rats with CCl4-induced liver cirrhosis. We studied this enzymatic activity in the sera and liver tissue of rats with alcoholic fatty liver due to prolonged alcohol intake and CCl4-induced liver fibrosis in association with moderate alterations in liver function tests. Serum and liver Hex activity did not show any significant change in both experimental models. These data suggest that Hex is not an alcohol-induced enzyme, and that severe, but not moderate, liver damage can determine the increase in this lysosomal enzymatic activity.
Subject(s)
Carbon Tetrachloride Poisoning/enzymology , Fatty Liver, Alcoholic/enzymology , Liver/enzymology , beta-N-Acetylhexosaminidases/metabolism , Alanine Transaminase/metabolism , Alkaline Phosphatase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Biomarkers/blood , Carbon Tetrachloride Poisoning/pathology , Fatty Liver, Alcoholic/pathology , Fibrosis , Liver/pathology , Male , Rats , Rats, Inbred Strains , Reference Values , beta-N-Acetylhexosaminidases/blood , gamma-Glutamyltransferase/metabolismABSTRACT
Angiotensin-converting enzyme (ACE) activity was found increased in serum of patients with chronic alcoholism. We studied this enzymatic activity in serum and liver tissue of rats with alcoholic fatty liver due to prolonged intake of ethanol with a liquid diet, according to De Carli and Lieber. Serum and liver ACE activity did not show any significant increase in rats with alcoholic fatty liver when compared with controls, whereas gamma-glutamyltransferase activity exhibited a striking enhancement in serum and liver. Our data suggest that ACE is not an alcohol-induced enzyme in the experimental rat model.
