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Background  Oxygen toxicity is a major cause of lung injury. The base excision repair pathway is one of the most important cellular protection mechanisms that responds to oxidative DNA damage. Lesion-specific DNA repair enzymes include  hOgg1 ,  hMYH ,  hNTH  and  hMTH.Methods  The above lesion-specific DNA repair enzymes were expressed in human alveolar epithelial cells (A549) using the pSF91.1 retroviral vector. Cells were exposed to a 95% oxygen environment, ionizing radiation (IR), or H 2 O 2 . Cell growth analysis was performed under non-toxic conditions. Western blot analysis was performed to verify over-expression and assess endogenous expression under toxic and non-toxic conditions. Statistical analysis was performed using the paired Student's  t  test with significance being accepted for p < 0.05.    Results  Cell killing assays demonstrated cells over-expressing  hMYH  had improved survival to both increased oxygen and IR. Cell growth analysis of A549 cells under non-toxic conditions revealed cells over-expressing  hMYH  also grow at a slower rate. Western blot analysis demonstrated over-expression of each individual gene and did not result in altered endogenous expression of the others. However, it was observed that O 2  toxicity did lead to a reduced endogenous expression of  hNTH  in A549 cells.    Conclusion  Increased expression of the DNA glycosylase repair enzyme  hMYH  in A549 cells exposed to O 2  and IR leads to improvements in cell survival. DNA repair through the base excision repair pathway may provide an alternative way to offset the damaging effects of O 2  and its metabolites.

Protection of pulmonary epithelial cells from oxidative stress by hMYH adenine glycosylase