BACKGROUND: Since apoptosis of renal tubular cells is the basis of thedamage caused by ischaemia-reperfusion, the antiapoptotic effect on kidney tubular epithelial cells ofthe monoamino oxidase-B (MAO-B) inhibitor (-) deprenyl (selegiline), known neuroprotective agent, withantiapoptotic properties, was studied in a rat model. MATERIAL/METHODS: Warm renal ischaemia was causedby clamping the left renal artery of rats for 30 minutes. With the start of reperfusion 0.015 mg/kg,0.15 mg/kg and 1.5 mg/kg of (-)-deprenyl was injected simultaneously into the carotid artery of the animals,respectively. Five rats served as control, in which renal artery clamping was performed, but the ratswere only treated with the solvent (physiological saline). After 6 hours of reperfusion the rats wereexsanguinated and the kidneys were histologically examined. RESULTS: Severe tubular damage characterisedby apoptosis was found in the kidneys of the untreated rats. Apoptosis was verified on the basis of morphologicalfeatures, methylgreen-pyronin staining and TUNEL reaction. (-)-Deprenyl diminished dose-dependently theapoptotic damage, 0.15 mg/kg being the most effective dose. The same dose of (-)-Deprenyl is used inthe therapy of human Parkinson's disease. CONCLUSIONS: Our findings suggest, that (-)-deprenyl mighthave an impact on decreasing renal injury also in case of human cadaveric renal transplantation.

Keywords: In Situ Nick-End Labeling, Kidney, Monoamine Oxidase Inhibitors, Rats, Wistar, Research Support, Non-U.S. Gov, selegiline