We found that (1) after DFO treatment, the XOD concentration decreased dramatically, suggesting that DFO alleviated the hyperoxia-induced lung injury by inhibiting XOD activity; (2) a significant increase in GR concentration after DFO treatment indicated that DFO might exert a protective effect for the lungs by enhancing GR activity and increasing the content of reduced GSH; (3) given a generally low ROS level, the injury to AECII was mild, and the reduction in the concentrations of SP-C and SP-D was redressed significantly by DFO, which finally alleviated pulmonary edema. This evidence concerns the gene GSR and pulmonary edema.