Accumulation of 8-hydroxydeoxyguanosine and its relationship with antioxidant parameters in patients with Eales'...

Eales' disease (ED) is an idiopathic retinal inflammatory disease, which affects the retina of young adult males. Oxidative stress has been associated with the development of various inflammatory diseases. Accumulation of DNA oxidation products has been considered as an early biomarker for assessing oxidative tissue damage. To our knowledge there are no human clinical reports available on the accumulation of DNA adducts in ocular inflammatory diseases. Hence the aim of the present study was to determine the levels of 8-hydroxy-2'deoxyguanosine (8-OHdG) and to correlate it with the antioxidant and oxidant parameters in patients with ED and healthy control subjects.

Twenty-two patients with ED [12 in active perivasculitis (AV) and 10 in healed vasculitis stages (HV)] were recruited for the study. 14 healthy volunteers were included as control. 8-OHdG was determined in their leukocytes by Gas chromatography-Mass Spectrometry (GC/MS) technique. Glutathione levels were determined in plasma, while Superoxide dismutase (SOD) activity and thiobarbituricacid reactive substances (TBARS) content were determined in their erythrocytes.

Our results indicated that 8-OHdG levels were elevated by 3 and 1.9 folds respectively in AV and HV stages of patients with ED, when compared with healthy control subjects. Increased 8-OHdG levels correlated with diminished SOD activity and decreased GSH content in patients with ED.

To our knowledge, this is the first report of DNA adduct accumulation in patients with ED. Increased DNA adduct accumulation correlated with the severity of the disease, and they lie in parallel with diminished antioxidant capacity observed in patients with ED. Based on the observations from our present work and our earlier studies, we reiterate that oxidative stress is involved in the disease process. Hence we believe antioxidant vitamin E and C supplementation might be beneficial to patients with ED.