|ISSN No. 1606-7754 Vol.13 No.2 August 2005|
Malondialdehyde and carbonyl contents in the erythrocytes of streptozotocin-induced diabetic rats
Durdi Qujeq, Masomeh Habibinudeh, Hamideh Daylmkatoli, Timur Rezvani
Department of Biochemistry and Biophysics, Faculty of Medicine, Babol University of Medical Sciences, Babol, IRAN
Oxidative stress is involved in degenerative disease, including atherosclerosis and diabetes mellitus. Impaired antioxidant defense mechanism may be an important factor in the pathogenesis of diabetes. Oxidative stress can be measured by monitoring the changes in blood malondialdehyde and carbonyl content. Determination of carbonyl level is used as an index of the extent of the oxidative damage of protein. Moreover, malondialdehyde level is a marker of lipid oxidation. We investigated the status of lipid peroxidation and protein oxidative damage in erythrocytes of streptozotocin (STZ) induced diabetic rats by measuring erythrocyte malondialdehyde and carbonyl levels using a spectrophotometer. We found that carbonyl and malondialdehyde levels were significantly increased in the erythrocytes of STZ-induced diabetic rats. This observation indirectly suggests an increase in free radical-mediated damage of the cell membrane.
Key words: Malondialdehyde, carbonyl, diabetes, antioxidant
Antioxidants work together in human blood cells against toxic reactive oxygen species.1,2 Reactive oxygen species (ROS) cause lipid peroxidation and oxidation of some specific proteins, thus affecting many intra- and intercellular systems.3,4 Total superoxide dismutase, catalase, and glutathione peroxidase activities are higher in the liver of STZ-treated rats.5 The levels of malondialdehyde and protein carbonyl, as markers of lipid and protein oxidation do not increase in aminoguanidine-treated rats.6 The antioxidant enzyme superoxide dismutase activity is significantly higher in the erythrocytes of diabetic patients independently of the presence of microvascular complications.7 The levels of malondialdehyde and carbonyls in the liver, kidney and pancreas mitochondria are significantly increased in STZ-treated rats.8 Significant increases in lipid peroxidation, as measured by thiobarbituric acid, and protein oxidation, as measured by protein carbonyl content, were observed 6 weeks after the occurrence of diabetes.9 A broad derangement in nonenzymatic biochemistry involving both lipids and carbohydrates exists in diabetic glomerular lesions.10 Protein oxidation may, therefore, represent an important factor in the development of symptoms in diabetic patients.11 Higher concentrations of malondialdehyde and carbonyl proteins were found in ocular tissues of diabetic compared to nondiabetic patients.12 The aim of the present study was to investigate the status of lipid peroxidation.