Ischemia-induced oxidative damage to the reperfused kidney was examined. A modified
chemiluminescence method, an in situ nitro blue tetrazolium perfusion technique, and a
DNA fragmentation/apoptosis-related protein assay were adapted for demonstration de
novo and co-localization of reactive oxygen species (ROS) production and apoptosis
formation in rat kidneys subjected to ischemia/reperfusion injury. The results showed that
prolonged ischemia potentiated proapoptotic mechanisms, including increases in the …