Evidence for only a moderate lipid peroxidation during ischemia-reperfusion of rat kidney due to its high antioxidative capacity

The extent of lipid peroxidation after ischemia-reperfusion (I-R) injury in rat kidney has been controversial. After I. xanthine oxidase (XO) is thoug ht to be the main oxygen radical-generating system and malondialdehyde (MDA ) is considered to be a marker of lipid peroxidation (LPO). In young rats ( 10 weeks old) a unilateral warm I of 40 and 60 min duration with subsequent R up to 1 h was conducted. Beside the "footprints" of oxidative stress, th e cytosolic antioxidative capacity, expressed as superoxide anion (SOA) sca venging capacity, and the renal catalase were also investigated. There was only a moderate and transient increase of renal MDA 5 and 10 min after the onset of reoxygenation (133.57/70.67 and 97.34/91.57 vs. 49.47 nmol/g ww in preischemic controls). ATP breakdown (to 83/65 from 2947 nmol/g ww) with c onsecutive accumulation of hypoxanthine (up to 1105 nmol/g ww) at the end o f ischemic period and the subsequent rapid decline of hypoxanthine by XO du ring reperfusion were used for an assessment of the SOA-generating capacity of these kidneys. Superoxide dismutase (SOD) activity, glutathione (GSH) a nd the high activity of catalase (18000 U/g ww) remained nearly unchanged d uring R. Only 1/25-1/50 of the kidney cytosol was able to scavenge the whol e amount of SOA generated by the total XO activity of rat kidney. Thus, it could be analytically and stoichiometrically shown that after IR there is o nly a moderate oxidative stress in kidneys of young rats; this is due to th eir high SOA-scavenging capacity compared with their SOA-generating ability .