Circulating glycolaldehyde induces oxidative damage in the kidney of rats.

Abstract Renal failure is a key pathological issue in diabetic patients. Increased levels of advanced glycation end-products (AGEs) have been associated to diabetic complications, including diabetic nephropathy. Models of AGE-treated animals have been applied to evaluate the effect of such molecules on oxidative parameters involved in the pathogenesis and evolution of diabetes disease. However, little is known about the effect of glycating agents other than glucose. Here we investigate the effect of intravenously administrated glycolaldehyde (GA) on oxidative stress parameters of the kidney. Male Wistar rats received a single injection of GA in different doses (10, 50 or 100 mg/kg) and were sacrificed after 6, 12 or 24 h. Activities of antioxidant enzymes catalase, superoxide dismutase and glyoxalase I were assayed. Damage to proteins and lipids were also assayed. The content of N ɛ -(carboxymethyl)lysine (CML) was quantified. Glycolaldehyde induced a decrease in the activity of all enzymes studied. Lipoperoxidation and protein carbonylation raised, accompanied by a decrease in sulfhydryl groups. Despite the oxidative stress generated by GA, no change was found in the content of CML, suggesting that accumulation of AGEs in the kidney might occur at later steps in the development of diabetic nephropathy.