Helicobacter pylori infection affects mitochondrial function and DNA repair, thus, mediating genetic instability in gastric cells

摘要: Helicobacter pylori infection is an important factor for the development of atrophic gastritis and gastric carcinogenesis. However, mechanisms explaining effects H. are not fully elucidated. known to induce genetic instability in both nuclear mitochondrial DNA epithelial cells. The mutagenic effect on be a consequence, part, down-regulation expression activity major repair pathways. In this study, we demonstrate that adenocarcinoma cells causes mtDNA mutations decrease content. Consequently, show respiration coupled ATP turnover respiratory capacity accordingly lower level complex I electron transport chain. We wanted investigate if increased mutational load genome was caused by lowered APE-1 YB-1, which believed involved base excision mismatch repair. Our results suggest YB-1 during infection, furthermore, multiple activities protecting infection.