Effects of Aminoguanidine on Lipid and Protein Oxidation in Diabetic Rat Kidneys

Nonenzymatic glycation of tissue and plasmaproteins may stimulate the production of oxidantand carbonyl stress in diabetes. The aimof this study was to evaluate the effects ofaminoguanidine (AG) on lipid peroxidation,protein oxidation and nitric oxide (NO) releasein diabetic rat kidneys. After induction of diabeteswith streptozotocin, female Wistar ratswere divided into 2 groups. Group DAG (n=9)rats were given AG hydrogen carbonate (1 g/L)in drinking water and group D (n=8) was diabeticcontrol rats given only tap water. GroupH (n=8) was followed as healthy controls. Atthe end of an 8 week period, NO release, lipidand protein oxidation were determined in kidneytissues. NO release was significantly lowerin diabetic rats compared with healthy controls(p<0.05). Lipid peroxidation was significantlyhigh in group D (3.9 ± 0.3 nmol MDA/g tissue)compared with the group DAG (2.6 ± 0.1 nmolMDA/g tissue, p<0.01) and group H (2.4 ± 0.2nmol MDA/g tissue). Protein oxidation wassignificantly higher in diabetics than healthycontrols (563.8 ± 23.9, 655.8 ± 7.2 , 431.5 ±8.8 mmol carbonyl / g tissue for group DAG, Dand H, respectively, p< 0.05). A positive correlationbetween albuminuria and thiobarbituricacid reactive substance (TBARS) levels (r= 0.54,p<0.005) and carbonyl content (r=0.70,p<0.0005) in kidney homogenate wereobserved.Although AG treatment had no effect on NOrelease, it significantly decreased lipid peroxidationin diabetic rat cortices. Consequentlyincreased lipid peroxidation -as well as- proteinoxidation could be involved in the pathogenesisof diabetic albuminuria.