In response to the rising demand for renal transplantations, more and more marginal (e.g. older) organs are being transplanted with the result of decreasing graft survival rates. Ischemia-reperfusion injury via oxidative stress is thought to be the main pathogenetic factor for this phenomenon. The cytosolic antioxidative capacity (CAC; expressed as superoxide anion radical scavenging capacity and quantified as the amount of cytosol (=ID50), which scavenges 50% of superoxide anions generated by a defined xanthine oxidase activity in vitro) and the catalase activity were therefore quantified in renal tissues of young (10 weeks) and older (40 and 60 weeks) Wistar rats and compared to each other. CAC with an ID50 of 0.064 μl in 10-week-old rats was significantly higher than in older rats (0.152 μl in 40- and 0.100 μl in 60-week-old rats; p < 0.01). The catalase activity in 10-week-old rats was 18,200 ± 3,500 U/g w/w and 18,900 ± 850 U/g w/w in 40-week-old rats. In 60-week-old rats, however, catalase activity was found to be significantly less (7,500 ± 175 U/g w/w; p < 0.01). In conclusion, the aforementioned significant decrease of the cytosolic antioxidative capacity of kidneys in older rats should be the rationale for extensive cytoprotective, antioxidative treatment trials especially after renal transplantation from aged donors.

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