Aims:　Radiation-induced　lung　injury　is　one　of　the　limiting　factors　for　radiation　therapy.　SOD-TAT,　a　fusion　protein　of　HIV-1　Tat　protein　transduction　domain　and　hCuZn-superoxide　dismutase　(SOD),　has　been　proved　to　be　effective　in　preventing　and　treating　the　damage　of　the　skin　of　guinea　pigs　by　UVB　radiation.　In　this　study,　we　demonstrated　SOD-TAT＇s　radioprotective　effects　on　lung　injury　in　irradiated　mice.　Main　methods:　SOD-TAT　was　purified　from　yeast　culture　with　ion　exchange　chromatography.　Kunming　mice　were　randomly　divided　into　three　groups:　a　control　group,　a　group　injected　with　wild　SOD　and　a　group　injected　with　SOD-TAT.　Pulmonary　SOD　activity　of　mice　was　determined　4.5　h　after　injection.　C57BL/6　mice　were　randomly　divided　into　four　groups:　a　control　group,　an　irradiation　group,　an　irradiation　group　treated　with　amifostine　0.5　h　before　the　irradiation　and　an　irradiation　group　treated　with　SOD-TAT　4.5　h　before　irradiation.　The　monthly　growth　rate　of　every　mouse＇s　weight　was　calculated　and　the　level　of　hydroxyproline　content　and　antioxidant　activity　in　lung　were　determined　5　months　after　irradiation.　Key　findings:　SOD-TAT　was　transduced　into　the　lung　in　vivo.　SOD-TAT　pretreatment　could　improve　the　growth　rate　of　irradiated　mice,　significantly　reduce　the　pulmonary　hydroxyproline　content,　and　maintain　the　SOD　activity,　glutathione　peroxidase　(GSH-Px)　activity　and　total　anti-oxidation　capacity　(T-AOC).　Compared　with　amifostine,　SOD-TAT　was　more　effective　in　increasing　the　activities　of　pulmonary　antioxidant　enzymes.　Significance:　Compared　with　amifostine,　SOD-TAT　treatment　more　effectively　enhanced　pulmonary　antioxidant　ability,　reduced　radiation-induced　pulmonary　fibrosis　and　improved　the　living　quality　of　irradiated　mice.　©　2012　Elsevier　Inc.