4.5 Article

Oxidative Damage to DNA and lipids: Correlation With Protein Glycation in Patients With Type 1 Diabetes

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JOURNAL OF CLINICAL LABORATORY ANALYSIS
卷 24, 期 2, 页码 72-76

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WILEY
DOI: 10.1002/jcla.20328

关键词

oxidative damage to DNA; diabetes Type 1; 8-hydroxydeoxyguanosine; glycated hemoglobin

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Diabetic hyperglycemia is associated with increased production of reactive oxygen species (ROS) ROS reacts with DNA resulting in various products, such as 8-hydroxydeoxyguanosine (8-OHdG), that excrete in urine owing to DNA repair processes Urinary 8-OHdG has been proposed as an indicator of oxidative damage to DNA. This study aimed to evaluate relationship between oxidative damage to DNA and protein glycation in patients with Type 1 diabetes. We measured urinary 8-OHdG level in diabetic patients and healthy subjects and discussed its relationship to glycated hemoglobin (HbA(1c)) and glycated serum protein (GSP) levels Furthermore plasma malondialdehyde (MDA) level monitored as an important indicator of lipid peroxidation in diabetes We studied 32 patients with Type 1 diabetes mellitus and compared the measured factors with those of 48 age-matched nondiabetic controls GSP and MDA were measured bycolorimetric assay Urinary 8-OHdG measurement was carried out using ELISA In this study urinary 8-OHdG, HbA(1c), plasma MDA, and GSP levels were progressively higher in diabetics than in control subjects (P<0 05) Furthermore we found significant correlation between urinary 8-OHdG and HbA(1c) (P<0.05) in diabetic group Correlation between fasting blood sugar and GSP were significant. We also found significant correlation between fasting blood sugar and MDA This case control study in young diabetic patients showed increased blood glucose and related metabolic disorders result in oxidative stress and oxidative damage to DNA and lipids Furthermore oxidative damage to DNA is associated to glycemic control level, whereas lipid peroxidation level was not significantly correlated with glycemic control level J Clin Lab Anal. 24 72-76, 2010. (C) 2010 Wiley-Liss, Inc

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