Aminoguanidine is an inhibitor of
nitric oxide synthase (NOS), with high selectivity for the inducible
isoform (iNOS). In addition to being an inhibitor of NOS,
aminoguanidine also exhibits
antioxidant activity. Recent studies suggest that
aminoguanidine reduces ischaemia-reperfusion (I/R)-induced damage. However, the role of
aminoguanidine, in renal injury associated with I/R remains unknown. This study was designed to investigate the effects of
aminoguanidine on renal I/R injury. There were three groups of eight rats each. I/R was induced by occlusion of the left renal vessels for 60 min, followed by 24 h reperfusion in rats.
Malondialdehyde (MDA) levels, a stable metabolite of the
free radical-mediated lipid peroxidation cascade, were found to be significantly higher in the I/R group (30.3 +/- 0.1 nmol g(-1) tissue) than in the control group (10 +/- 0.05 nmol g(-1)).
Aminoguanidine (100 mg kg(-1)) administration to rats significantly reduced the MDA values. We also demonstrated that I/R leads to structural change but
aminoguanidine did not reverse this change.
Aminoguanidine, according to the biochemical finding is protective but histopathological findings did not reveal protection against I/R injury in kidney. The effects of
aminoguanidine on I/R-induced damage remain a subject for future investigations.