Abstract
GST-TAT-SOD was the fusion of superoxide dismutase (SOD), cell-permeable peptide TAT, and glutathione-S-transferase (GST). It was proved to be a potential selective radioprotector in vitro in our previous work. This study evaluated the in vivo radioprotective activity of GST-TAT-SOD against whole-body irradiation. We demonstrated that intraperitoneal injection of 0.5 ml GST-TAT-SOD (2 kU/ml) 2 h before the 6 Gy whole-body irradiation in mice almost completely prevented the splenic damage. It could significantly enhance the splenic antioxidant activity which kept the number of splenic white pulp and consequently resisted the shrinkage of the spleen. Moreover, the thymus index, hepatic antioxidant activity, and white blood cell (WBC) count of peripheral blood in irradiated mice pretreated with GST-TAT-SOD also remarkably increased. Although the treated and untreated irradiated mice showed no significant difference in the growth rate of animal body weight at 7 days postirradiation, the highest growth rate of body weight was observed in the GST-TAT-SOD-pretreated group. Furthermore, GST-TAT-SOD pretreatment increased resistance against 8 Gy whole-body irradiation and enhanced 30 d survival. The overall effect of GST-TAT-SOD seemed to be a bit more powerful than that of amifostine. In conclusion, GST-TAT-SOD would be a safe and potentially promising radioprotector.
Highlights
50% of all cancer patients received radiation therapy during their course of illness
Radiation therapy side effects are mainly induced by the reactive oxygen species (ROS) such as superoxide, hydroxyl radicals, and hydrogen peroxide produced through the radiolysis of the water [1]
In addition to the loss from tile circulation, morphological changes rapidly appear in the lymphoid tissues, such as those in the spleen and thymus, which quickly decrease in size
Summary
50% of all cancer patients received radiation therapy during their course of illness. Radiation therapy side effects are mainly induced by the reactive oxygen species (ROS) such as superoxide, hydroxyl radicals, and hydrogen peroxide produced through the radiolysis of the water [1]. These free radicals react with critical cellular macromolecules resulting in cell dysfunction and death, depletion of stem cell pools, and organ system dysfunction [2]. Amifostine, a radioprotector in use clinically, can freely diffuse into cells and can act as a free radical scavenger through dephosphorylation [4] It is the only cytoprotective agent approved by the FDA as a radioprotector. There is a continued need for the development of a nontoxic and efficient radioprotector
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