Abstract
Results of this study indicate a radioprotective effect of peroxiredoxin‐I. Peroxiredoxin‐I is an antioxidant that scavenges hydroperoxides, whereas reactive oxygen species are the main mediators of ionizing radiation toxicity. We hypothesized that peroxiredoxin‐I might be induced by cellular exposure to radiation and act to protect them against its cytotoxic effects. Western blot and Northern blot analyses were used to assess peroxiredoxin‐I protein and mRNA expression. Rat C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin‐I using retroviral vectors. Clonogenic cell survival was used to assess radiosensitivities of the engineered cells. Ionizing radiation induced peroxiredoxin‐I protein and mRNA expression in human HT29 colon cancer and rat C6 glioma cells in a dose‐ and time‐dependent manner over a 24 hr period. To determine the effect of peroxiredoxin‐I on radiation responses, C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin‐I. In clonogenic assays, cells overexpressing peroxiredoxin‐I were more radioresistant. Cells transduced with antisense peroxiredoxin‐I were marginally more sensitive to radiation toxicity. Irradiation can induce peroxiredoxin‐I expression, and the increased peroxiredoxin‐I may protect cells from further radiation damage. These results suggest that protection by peroxiredoxin‐I may play an important role in the survival of glioma and colon cancer cells in patients undergoing radiation therapy. © 2002 Wiley‐Liss, Inc.