Studies on the possible role of oxygen-derived free radicals for impairment of protein and energy metabolism in liver ischemia.

The role of oxygen-derived free radicals for impaired protein and energy metabolism in ischemia and reperfusion injury to the liver is not known. In the present study, groups of rats received either catalase (20 mg/kg body weight), superoxide dismutase (SOD; 4 mg/kg body weight), or catalase + SOD i.v. 10 min before induction of ischemia in the left and median liver lobes. Control animals received corresponding volumes of solvent. The length of the ischemic period was 60 or 90 min. Protein synthesis was measured in incubated liver slices before induction of ischemia, at the end of the ischemia period, and during 2 h of reperfusion. Tissue concentrations of ATP, ADP, AMP, and hepatic tissue water were determined at the same time points. Protein synthesis and energy level were markedly reduced at the end of ischemia and were restituted during the 2-h reperfusion when the ischemic period was 60 min; they remained depressed during reperfusion when the ischemic period was 90 min. Hepatic tissue water was increased at the end of the ischemic period and remained elevated during reperfusion. There were no significant differences in protein synthesis, energy level or tissue water between catalase- or SOD-treated animals and controls either at the end of a 60- or 90-min ischemic period or during the 2-h reperfusion. The results suggest that oxygen-derived free radicals do not play a major role for impaired protein and energy metabolism in liver ischemia and following reperfusion.