Changes in hepatic TNF-α levels, antioxidant status, and oxidation products after renal ischemia/reperfusion injury in mice

Background. Ischemia/reperfusion (I/R) injury induces an inflammatory response and production of reactive oxygen species (ROS), which affects the organs remote to the sites of I/R. The aim was to assess the hepatic changes after renal I/R injury. Materials and methods. Twenty mice were subjected to either sham operation or varying degrees of renal I/R injury. Hepatic TNF-alpha levels, myeloperoxidase (MPO), superoxide dismutase (SOD), and catalase (CAT) activities and reduced glutathione (GSH) levels, thiobarbituric acid-reactive substances (TBARS), and protein carbonyl levels were evaluated to show hepatic response to renal I/R injury. Results. Hepatic tumor necrosis factor-alpha levels were found to be increased significantly after 30 min ischemia-1 h reperfusion and remained elevated through 60 min ischemia-1 h reperfusion. Supporting the neutrophil recruitment, about 10-fold increase in MPO activity was detected after 30 min ischemia-1 h reperfusion. Antioxidant enzymes were detected to be decreased after 30 min ischemia-1 h reperfusion and reached to the minimum levels after 60 min ischemia-1 h reperfusion. Decreased levels of GSH and increased levels of TBARS and protein carbonyls after 60 min ischemia-1 h reperfusion supported the ROS-mediated biomolecular alterations. Conclusions. A minumum of 30 min ischemia-1 h reperfusion is enough to elicit remote effects of renal I/R injury. Care should be taken to protect other organs remote from I/R sites especially during renal surgery. (C) 2002 Elsevier Science (USA).