The effect of aminoguanidine on the kidney of diabetic albino Balb/c mice

Abstract

The aim of this study is to find out how activated inducible nitric oxide synthase (iNOS) and nitric oxide (NO) affect kidney tissue in streptozotocin (STZ)-induced diabetic mice and whether its influence can be prevented by aminoguanidine (AG), a specific iNOS inhibitor. Twenty-four male mice were divided into four study groups (n=6) receiving a daily dose of 100 mg.kg-1 AG for 90 days (Group AG), a single dose of 150 mg.kg-1 STZ (Group STZ), a single dose of 150 mg.kg-1 STZ followed by daily administration of 100 mg.kg-1 AG for 90 days (Group STZ-AG), and intraperitoneally injections of saline only (Group Control) for 90 days. Dispersion of NADPH-diaphorase (NADPH-d) was stronger in the kidney sections of STZ-treated animals compared with the controls. STZ treatment caused disruption of continuity of the brush borders in proximal tubules, glomerular endothelial damage, and considerable renin granules in the juxtaglomerular cells. AG administration following STZ treatment partly prevented histological and cytological changes in kidney cortex, and renin dispersion was similar to that in control animals. We found that increased inducible nitric oxide (iNO) caused kidney tissue degeneration that could be prevented to some extent by AG treatment. There is a possible relationship between increased iNOS and dispersion of renin granules in juxtaglomerular cells in diabetes.