| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2146490 | Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis | 2012 | 5 Pages |
Evidence has been presented recently that type 2 diabetes patients have an increased level of DNA damage. This DNA damage could be associated with oxidative, inflammatory, and endothelial biomarkers and could represent a possible indication of injury in the endothelium and induction of inflammation in type 2 diabetes. To confirm this possible association, DNA strand breakage was evaluated by use of the comet assay and its association with oxidative, inflammatory, and endothelial biomarkers in type 2 diabetes patients. A case–control study (30 healthy controls and 32 subjects with type 2 diabetes) was performed to evaluate the association between DNA damage and NOx (nitrate/nitrite), interleukin-6 (IL-6), urinary albumin, fasting glucose, and glycated hemoglobin (HbA1c) levels. Type 2 diabetes patients presented higher DNA damage than control subjects, higher levels of IL-6 and urinary albumin, and lower NOx. Significant correlations between DNA damage and NOx (r = −0.303, p = 0.016), IL-6 (r = 0.845, p < 0.001), urinary albumin (r = 0.496, p < 0.001), fasting glucose (r = 0.449, p < 0.001), and HbA1c (r = 0.575, p < 0.001) were reported. Our findings showed an increase of DNA damage in type 2 diabetes especially in those patients with poor glycemic control and associations among NOx, IL-6 and urinary albumin levels with DNA damage.
► We performed the comet assay to verify the occurrence of DNA damage in patients with type 2 diabetes. ► We observed an increase of DNA damage in type 2 diabetes, especially in those patients with poor glycemic control. ► We reported associations among NOx, IL-6 and urinary albumin levels with DNA damage.
