The attractive potential of natural superoxide dismutase (SOD) in the fields of medicine and functional food is limited by its short half-life in circulation and poor permeability across the cell membrane. The nanoparticle form of SOD might overcome these limitations. However, most preparative methods have disadvantages, such as complicated operation, a variety of reagents—some of them even highly toxic—and low encapsulation efficiency or low release rate. The aim of this study is to present a simple and green approach for the preparation of SOD nanoparticles (NPs) by means of co-incubation of Cu/Zn SOD with glucose. This method was designed to prepare nanoscale aggregates based on the possible inhibitory effect of Maillard reaction on heating-induced aggregation during the co-incubation. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) results indicated that the Maillard reaction occurred during the co-incubation process. It was found that enzymatically active NPs of Cu/Zn SOD were simultaneously generated during the reaction, with an average particle size of 175.86 ± 0.71 nm, and a Zeta potential of −17.27 ± 0.59 mV, as established by the measurement of enzymatic activity, observations using field emission scanning electron microscope, and analysis of dynamic light scattering, respectively. The preparative conditions for the SOD NPs were optimized by response surface design to increase SOD activity 20.43 fold. These SOD NPs showed storage stability for 25 days and better cell uptake efficacy than natural SOD. Therefore, these NPs of SOD are expected to be a potential drug candidate or functional food factor. To our knowledge, this is the first report on the preparation of nanoparticles possessing the bioactivity of the graft component protein, using the simple and green approach of co-incubation with glucose, which occurs frequently in the food industry during thermal processing.

Superoxide dismutase (SOD) fusion of TAT was proved to be radioprotective in our previous work. On that basis, a bifunctional recombinant protein which was the fusion of glutathione S‐transferase (GST), SOD, and TAT was constructed and named GST‐TAT‐SOD. Herein we report the investigation of the cytotoxicity, cell‐penetrating activity, and in vitro radioprotective effect of GST‐TAT‐SOD compared with wild SOD, single‐function recombinant protein SOD‐TAT, and amifostine. We demonstrated that wild SOD had little radioprotective effect on irradiated L‐02 and Hep G2 cells while amifostine was protective to both cell lines. SOD‐TAT or GST‐TAT‐SOD pretreatment 3 h prior to radiation protects irradiated normal liver cells against radiation damage by eliminating intracellular excrescent superoxide, reducing cellular MDA level, enhancing cellular antioxidant ability and colony formation ability, and reducing apoptosis rate. Compared with SOD‐TAT, GST‐TAT‐SOD was proved to have better protective effect on irradiated normal liver cells and minimal effect on irradiated hepatoma cells. Besides, GST‐TAT‐SOD was safe for normal cells and effectively transduced into different organs in mice, including the brain. The characteristics of this protein suggest that it may be a potential radioprotective agent in cancer therapy better than amifostine. Fusion of two antioxidant enzymes and cell‐penetrating peptides is potentially valuable in the development of radioprotective agent.

Background: Paraspeckle component 1 (PSPC1) is overexpressed in various cancer and correlated with poor survival in the patients. However, little is known about its expression and role in the progression of nasopharyngeal carcinomas (NPC). The purpose of this study is to examine PSPC1 expression in NPC and explore its role in clinical prognosis of radiation therapy. Methods: The association of PSPC1 expression with clinicopathological features of 109 NPC patients was examined using partial correlation analysis. Cancer tissues were obtained prior to clinical treatment. All cases were diagnosed and pathologically confirmed to be poorly differentiated or undifferentiated NPC without distant metastasis. The patients were then treated with radiation and followed-up. Survival analysis was performed. Results: Partial correlation analysis revealed that the PSPC1 expression in NPC was correlated with N classification, recurrence, prognosis and radiosensitivity in NPC patients, but not with the gender, age, pathohistological pattern, clinical stage, and T classification. The overexpression of PSPC1 was detected in 64 samples (58.72%). Kaplan–Meier survival analysis revealed that the overall survival (OS) was longer in NPC patients with PSPC1 low expression than that in those with PSPC1 high expression. Moreover, patients with the overexpression of PSPC1 had a low progression-free survival and distant metastasis-free survival rate, compared to those who had a low expression of PSPC1. Although not statistically significant, patients with high expression of PSPC1 had a lower locoregional recurrence-free survival rate than those with low expression, and the curves between the two groups was well separated. Conclusion: PSPC1 overexpression was associated with poor prognosis for NPC, which might be a novel useful biomarker to predict the response of NPC to radiation therapy and its clinical outcome.

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.

GST‐TAT‐SOD, a cell‐permeable bifunctional antioxidant enzyme, is a potential selective radioprotector. This study aimed to investigate the cytoprotective activity of GST‐TAT‐SOD against cisplatin‐induced damage. The current study showed that cisplatin induced the formation of reactive oxygen species in normal L‐02 cells. GST‐TAT‐SOD (2000 U/mL) executed its antioxidant role by directly scavenging excess intracellular free radicals and augmenting cellular antioxidant defense such as reducing MDA level, enhancing the SOD activity, GST activity, and T‐AOC. Thus, it suppressed the growth inhibition and apoptosis of cisplatin‐treated normal cells. Meanwhile, the growth inhibition of tumor cells (SMMC‐7721) caused by cisplatin was unaffected by GST‐TAT‐SOD pretreatment. GST‐SOD, as a comparison, seemed to be powerless for related indicators as it could not enter into cells without cell‐permeating peptide. These results suggest that GST‐TAT‐SOD might be a potential cytoprotective agent for cisplatin‐induced side effects.