Effect of ozone treatment on reactive oxygen species and adenosine production during hepatic ischemia-reperfusion

This study investigates whether ozone could confer protection from hepatic ischemia reperfusion by modifying the accumulation of adenosine and xanthin e during ischemia. A significant increase in both adenosine and xanthine ac cumulation was observed as a consequence of ATP degradation during hepatic ischemia. Adenosine exerts a protective effect on hepatic ischemia reperfus ion injury since the elimination of endogenous adenosine accumulation with adenosine deaminase increased the hepatic injury associated with this proce ss. On the other hand, the high xanthine levels observed after ischemia cou ld exert deleterious effects during reperfusion due to reactive oxygen spec ies generation from xanthine oxidase. The administration of allopurinol, an inhibitor of xanthine oxidase, attenuated the increase in reactive oxygen species and transaminase levels observed after hepatic reperfusion. Ozone t reatment in liver maintained adenosine levels similar to those found after ischemia but led to a marked reduction in xanthine accumulation. in order t o evaluate the role of both adenosine and xanthine, we tried to modify the protection confered by ozone, by modifying the concentrations of adenosine and xanthine. The metabolization of endogenous adenosine after ischemia abo lished the protective effect conferred by ozone. When xanthine was administ ered previous to ozone treatment, the protection conferred by adenosine dis appeared, showing both postischemic reactive oxygen species and transaminas e levels similar to those found after hepatic ischemia reperfusion. Ozone w ould confer protection against the hepatic ischemia reperfusion injury by t he accumulation of adenosine that in turns benefits the liver and by blocki ng the xanthine/xanthine oxidase pathway for reactive oxygen species genera tion.