Protective effect of recombinant protein SOD-TAT on radiation-induced lung injury in mice

AimsRadiation-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 methodsSOD-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 findingsSOD-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.SignificanceCompared with amifostine, SOD-TAT treatment more effectively enhanced pulmonary antioxidant ability, reduced radiation-induced pulmonary fibrosis and improved the living quality of irradiated mice.