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Prolonged ischemia potentiates apoptosis formation during reperfusion by increase of caspase 3 activity and free radical generation

2000; Elsevier BV; Volume: 32; Issue: 7 Linguagem: Inglês

10.1016/s0041-1345(00)01560-8

1873-2623

Chiang‐Ting Chien, S M Hsu, C.F Chen, Po–Huang Lee, Ming‐Chih Lai,

Electron Spin Resonance Studies

ISCHEMIC injury to the kidney or renal allograft before implantation is an important cause of renal dysfunction and delayed graft function. In the setting of prolonged ischemia, a major source of primary renal dysfunction comes from the generation of reactive oxygen species (ROS) during the reperfusion phase. The overproduction of ROS after reoxygenation of the kidney may initiate the cascade of renal tubular injury and necrosis/apoptosis and can lead to oxidative damage of DNA, proteins, and lipids. It has been implicated that the prolonged ischemic interval during renal surgery potentiates damage to the kidneys. However, it is uncertain whether the kidney damage elicited by the prolonged ischemic interval is directly related to the overproduction of ROS. Lucigenin luminescence can be used as the basis for assaying superoxide dismutase activity, but should not be used for measuring, or even detecting O2 . In this investigation, by using MCLA-amplified ultrasensitive chemiluminescence (CL), we studied the production of reactive oxygen species (ROS) in rat kidneys after ischemia-reperfusion (I/R) injury in vivo and the relationship of ROS production to the duration of the ischemic interval.