The effect of aminoguanidine on diabetes-induced inactivation of kidney Na+,K+- ATPase in rats

Abstract

We studied the effect of aminoguanidine (AG), an inhibitor of advanced glycation product formation, on diabetes-induced oxidative damage. Renal cortex Na+,K+- ATPase was chosen for study as a potential cellular target of oxygen radicals. In this study, the enzyme activity was reduced while malondialdehyde (MDA) and carbonyl levels were enhanced but sulphydryl (SH) level remained unchanged in the renal cortex in diabetic animals. Treatment of diabetic rats with AG had no significant effect on diabetes-induced impairments of enzyme activity and MDA but the carbonyl level readjusted to control level in the kidney. These results show that AG treatment at that dose did not exhibit profound antioxidant properties even if carbonyl stress was ameliorated by this treatment.