Under conditions of oxidative stress damage can occur to all cellular biomolecules, including lipids, proteins, carbohydrates and DNA. Such damage has been implicated in the pathogenesis and long-term complications of Type I diabetes mellitus. Levels of oxidative DNA damage in eight well controlled Type I diabetic subjects (mean HbA1c 7.03 0.10) and eight age and sex matched control’s (mean HbA1c 4.58 0.06) were compared using the modified comet assay. DNA strand breaks, oxidised pyrimidines (endonuclease III sensitive-sites) and ring-opened purines as well as 8-oxo-guanine (formamidopyrimidine glycosylase sensitive-sites) were measured. The results failed to demonstrate a statistically significant difference in the mean levels of oxidative DNA damage in Type I diabetic subjects (mean endonuclease III 9.77 2.6; mean formamidopyrimidine glycosylase 13.08 2.3) compared to control subjects (mean endonuclease III 12.19 2.2; mean formamidopyrimidine glycosylase 12.48 1.4). However linear regression analysis revealed a statistically significant (p = 0.024) positive correlation between the number of formamidopyrimidine glycosylase sensitive-sites and duration of Type I diabetes mellitus. In addition a positive correlation was observed between the number of endonuclease III sensitive-sites and duration of Type I diabetes mellitus, though this was not significant (p = 0.078). These results indicate that even with good glycaemic control there was a positive correlation between levels of oxidative DNA damage and duration of Type I diabetes in vivo. The physiological effect(s) of this DNA damage remain to be elucidated.
|Publication status||Published (in print/issue) - 2009|