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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 2352361, 6 pages
Research Article

Markers of Antioxidant Defense in Patients with Type 2 Diabetes

1Department of Diagnostics, Chair of Clinical Biochemistry, Jagiellonian University Medical College, 31-501 Krakow, Poland
2Department of Medical Diagnostics, Jagiellonian University Medical College, 30-688 Krakow, Poland
3Chair of Metabolic Diseases, Jagiellonian University Medical College, 31-501 Krakow, Poland

Received 28 April 2015; Accepted 14 June 2015

Academic Editor: Umesh Yadav

Copyright © 2016 K. Gawlik et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aims. Diabetes is considered a state of increased oxidative stress. This study evaluates blood concentrations of selected markers of antioxidant defense in patients with type 2 diabetes. Methods. The study included 80 type 2 diabetes patients and 79 apparently healthy controls. Measured markers included ferric reducing ability of plasma (FRAP), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), γ-glutamyltransferase (GGT) and uric acid serum, and plasma and/or hemolysate levels. Results. FRAP, uric acid, CRP, and GGT levels were significantly higher in patients with diabetes. Plasma and hemolysate GR was significantly higher whereas GPx activity was significantly lower in patients with diabetes. There were no significant differences in antioxidant defense markers between patients with and without chronic diabetes complications. Fasting serum glucose correlated with plasma GPx, plasma and hemolysate GR, FRAP, and serum GGT, and HbA1c correlated with serum GGT. Only FRAP and serum uric acid were significantly higher in obese ( kg/m2) patients with diabetes than in nonobese patients. Conclusions. Some components of antioxidant defense such as GR, uric acid, and GGT are increased in patients with type 2 diabetes. However, the whole system cannot compensate for an enhanced production of ROS as reflected by the trend toward decreased erythrocytes GSH.