Reperfusion of ischemic tissues produces injury. Reperfusion injury may be mediated, at least in part, through the formation of reactive oxygen metabolites. These metabolites cause damage to proteins, lipids and nucleic acids.

The aim of this paper was to analyze the effect of ischemia-reperfusion after thoracic aortic ligation on various membrane enzymes and on the cellular redox status in rat liver.

The activity of alkaline phosphatase (ALP), 5’nucleotidase (5’NT), γ-glutamyl transferase (γ-GT), glucose-6-phosphatase (G-6-Pase), succinate cytochrome c reductase (SuccR), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were assayed in three experimental groups. Glutathione (GSH) and thiobarbituric acid reactive species (TBARS) were also analyzed. The experimental groups were: control rats (C), rats with acute ischemia for 50 min (I), rats with acute ischemia for 50 minutes and a posterior reflow of blood for 100 minutes (R).

ALP, γ-GT, G-6-Pase and CAT were not modified. TBARS increased in I group and then returned to control values. 5’NT diminished significantly after ischemia and increased drastically after reperfusion. SuccR activity decreased after reperfusion. On the contrary, SOD and GSH-Px increased after reperfusion.

A different susceptibility to ischemia-reperfusion was observed in liver membrane enzymes as well as varying changes in the antioxidant defense systems were detected. These changes didn`t were so drastic nor caused an appreciable modification in plasma aspartate aminotransferase (AST, a marker of global liver injury). This suggests that 50 minutes of aortic ligation followed by reperfusion is not extensively deleterious for the biochemist and function of the liver.