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Comet Assay as an Indirect Measure of Systemic Oxidative Stress
Published on: May 22, 2015
Relationship Between Zinc Status and DNA Oxidative Damage in Patients with Type 2 Diabetes Mellitus
Hivi M Mahmoud1, Ardawan F Ali2, Dhia J Al-Timimi3
1Department of Medical Chemistry, College of Medicine, University of Duhok, Duhok, Kurdistan Region, Iraq. jody79hivi@yahoo.com.
Abstract:
Although zinc deficiency increases the risk of oxidative DNA damage, data regarding the association between zinc and oxidative DNA damage in diabetes are controversial. In this article, we focus on serum zinc levels and its relation to an established biomarker of oxidative DNA damage (8-hydroxy-2-deoxyguanosine) in patients with type 2 diabetes, and to ascertain the beneficial effects of zinc supplementation on the level of oxidative DNA damage. The study consisted of 2 interrelated parts: The first part was a cross-sectional study conducted on patients with type 2 diabetes (n = 297) and healthy individuals (n = 188). The second part was an interventional study that enrolled 38 diabetic patients with low zinc status and high DNA damage. The demographic parameters including age, gender, and body mass index were recorded, and DNA damage marker through 8-hydroxy-2-deoxyguanosine levels, and zinc status of serum zinc, was measured. Significantly higher 8-hydroxy-2-deoxyguanosine levels (P < 0.00) together with lower zinc levels (P < 0.001) were found in the diabetics compared to healthy controls. Patients with low zinc status had higher levels of 8-hydroxy-2-deoxyguanosine compared to patients with normal zinc status. In diabetic patients, a negative correlation of 8-hydroxy-2-deoxyguanosine was observed with zinc (P = 0.070). Zinc supplementation showed a significant decrease in 8-hydroxy-2-deoxyguanosine by (26.0%) and increased in serum zinc by (42.0%). Elevated 8-hydroxy-2-deoxyguanosine levels in conjunction with low zinc status may indicate a high degree of oxidative DNA damage in diabetic patients. The results confirm that zinc supplementation in this group may help correct abnormal levels of 8-hydroxy-2-deoxyguanosine.
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