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


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 4.5h after injection. C57BL/6 mice were randomly divided into four groups: a control group, an irradiation group, an irradiation group treated with amifostine 0.5h before the irradiation and an irradiation group treated with SOD-TAT 4.5h 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.


RESULTS
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.


CONCLUSIONS
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.
College of Bioscience and Biotechnology, Fuzhou University, Fuzhou 350002, China.
Jianru
J
Pan
Ying
Y
Su
Xiaojun
X
Hou
Huocong
H
He
Shutao
S
Liu
Junxin
J
Wu
Pingfan
P
Rao
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight; D004195:Disease Models, Animal; D006801:Humans; D006909:Hydroxyproline / Q000737:chemistry / Q000378:metabolism; D055370:Lung Injury / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D010843:Pichia / Q000378:metabolism; D017434:Protein Structure, Tertiary; D011832:Radiation Injuries / Q000517:prevention & control; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism*; D054322:tat Gene Products, Human Immunodeficiency Virus / Q000378:metabolism*
D000975:Antioxidants; D011993:Recombinant Fusion Proteins; D011994:Recombinant Proteins; D054322:tat Gene Products, Human Immunodeficiency Virus; D013482:Superoxide Dismutase; D006909:Hydroxyproline