Patients with breast and lung cancer and with various lymphomas constitute a large demographic receiving radiotherapy that is affected by lung complications. The ability to deliver tumoricidal doses while preserving the integrity of surrounding normal tissue is critical to successful treatment with ionizing radiation. Developing an understanding of the mechanisms associated with radiation-induced normal lung damage is imperative. In this thesis a superoxide dismutase-catalase mimetic and a kinase inhibitor were studied for their effects on the expression of DNA and functional damage post irradiation. We hypothesized that chronic oxidative stress and inflammation generated post irradiation contribute to the progression of clinically evident tissue damage. The data suggest that chronic DNA damage is generated secondarily to the initial insult of radiation and is exacerbated by the chronic inflammatory response. Future strategies for reducing radiation-induced lung damage should focus on the development of chronic oxidative damage and the dysregulation of inflammation.