AB0002 INCREASED SENSITIVITY TO DNA DAMAGING AGENTS IN HUMAN PERIPHERAL BLOOD MONONUCLEAR CELLS FROM PATIENTS WITH RHEUMATOID ARTHRITIS

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disorder with not fully elucidate pathogenesis. Rheumatoid arthritis patients have increased risk of developing lymphomas. One of the possible mechanisms of this predisposition is increased genomic instability and impaired DNA repair. It is unclear how this genomic instability contributes to diseases pathogenesis. Objectives: The aim of this study was to analyze the sensitivity and repair efficiency of mononuclear cells isolated from RA patients to DNA damaging agents. Methods: The study group consisted of 22 patients with RA (age years - 60,77±13,00 women-17, men - 5) hospitalized in the Department of Rheumatology between 2017 and 2018 and 10 healthy controls without autoimmune and oncological diseases in clinical history (age 44,09±16,56; women-5, men-6). The peripheral blood mononuclear cells (PBMC) from all subjects were isolated. Using comet assay the degree of intracellular DNA damage as a result of exposure to standard damage factors: tert-butyl hydroperoxide (TBH), bleomycin, methyl methanesulfonate (MMS) and UV radiation was assessed. Results: RA patients show a statistically significant higher level of endogenous damage in PBMC DNA than controls (mean RA- 8,64% vs 4,68% in control; p Conclusion: DNA of people with rheumatoid arthritis is significantly more susceptible to damage in baseline and induced. The kinetics of DNA repair from RA patients after the introduction (TBH and bleomycin) was statistically less effective as compared to healthy control. Understanding the ethology of this phenomenon in RA may provide insight into disease pathogenesis and explain the increased susceptibility of patients to malignancies. Acknowledgement: The project is financed under the funds of the National Science Center (2017/25/B/NZ6/01358) Disclosure of Interests: None declared