Arif M, Islam MR, Waise TM, Hassan F, Mondal SI, Kabir Y.
Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh. This e-mail address is being protected from spambots. You need JavaScript enabled to view it
BACKGROUND AND AIM: Diabetes mellitus is a complex metabolic disorder characterized by a disturbance in glucose metabolism. Recent evidence suggests that increased oxidative stress as well as alteration of antioxidant capacity may be related to the complications seen in patients with type 2 diabetes. The aim of this study was to measure serum antioxidant status in type 2 diabetic patients and to assess its relationship with oxidative DNA damage. METHODS: A total of 57 subjects were included in this study. Of these, 32 were type 2 diabetic patients and 25 were non-diabetic subjects. Comet assay was used to quantify the level of DNA damage in lymphocytes. Spectrophotometric methods were used to assess serum levels of malondialdehyde (MDA) and protein carbonyl, and serum activity of superoxide dismutase (SOD) and the protein thiol (P-SH) group. RESULTS: A significant increase in mean comet tail DNA, indicating DNA damage, was observed in diabetic patients compared with controls. Diabetic patients had significantly higher levels of MDA and protein carbonyl in parallel with significant decreases in levels of SOD and the P-SH group compared with controls. Serum SOD was also inversely correlated with the increase in comet tail DNA. CONCLUSION: These results indicate the presence of significant lipid peroxidation, protein oxidation and oxidative DNA damage in patients with diabetes. Perturbation of glucose homoeostasis was associated with an increase in oxidants and a concomitant decrease of antioxidant enzymes in the type 2 diabetic patients' blood. The present study suggests that the status of oxidant-antioxidant imbalance may be one of the mechanisms leading to the DNA damage detected in the lymphocytes of type 2 diabetic patients. Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
PMID: 20036596
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