Abstract
Purpose: :
Glaucoma is a heterogeneous group of ocular disorder, which is characterized by progressive degeneration of optic nerve axon. Oxidative stress may play important role in glaucoma development, what suggests an important role of base excision repair (BER) pathway responsible for removing of oxidative DNA lesions. The aim of study was to evaluate the level of oxidative DNA lesions and its repair in peripheral lymphocytes of glaucoma patients.
Methods: :
The study was performed on group of 10 patients with primary open-angle glaucoma (POAG) and 10 healthy subjects. An alkaline comet assay was used to measure DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pirmidines as endonuclease III (Nth) sites. We measured endogenous as well as exogenous DNA damage after 10 μM hydrogen peroxide treatment (H2O2). The efficiency of DNA repair was measured within 120 min of post treatment incubation with hydrogen peroxide.
Results: :
Endogenous level of oxidative DNA damage in POAG patients was found to be statistically higher than the controls (P<0.001). Moreover, lymphocytes isolated from POAG patients with were more susceptible for oxidative DNA lesions induced by hydrogen peroxide than control subjects (P<0.001). Finally, we found an impaired repair of oxidative DNA lesions in POAG patients as compared to healthy controls (P<0.05).
Conclusions: :
In conclusion our data revealed that oxidative stress might play an important role in POAG development and an impaired BER repair may be critical factor in glaucoma pathogenesis. Therefore, we suggested that the modulation of a pro-oxidant/antioxidant status might be a relevant target for prevention and therapy of glaucoma patients.This work was supported by grants N N402 375838 and N N402 248936 from Polish Ministry of Science and Higher Education.
Keywords: genetics • optic nerve • neuroprotection