The association between inefficient repair of oxidative DNA lesions and common polymorphisms of the key base excision repair genes as well as their expression levels in patients with Rheumatoid Arthritis

Introduction RA is a common autoimmune heterogeneous joint disease of still unknown etiology. One the characteristic features oxidative stress, most probably induced and stimulated by inappropriate B T-cell activity. We have hypothesized, that stress together with impaired DNA damage response to lesions could be responsible for increased incidence in patients some diseases genetic instability background such as lymphoma. Material methods determined level kinetics removal TBH PBMCs 30 healthy individuals. The metrics from repair study were correlated genotypes polymorphisms key BER genes well their expression levels. evaluated comet assay, polymorphism Taqman Assay PrimeTime qPCR was used analyze profile related BER. Results observed an association between occurrences PBMCs. After dividing subjects controls’ quartiles efficiency, we found risk inefficient Repair. also identified interaction Repair UNG gene (rs246079), lower – MUTH, NEIL3 UNG. Conclusions Our result suggest variations within epigenetic factors may linked modulation cellular stress.