| Project/Area Number |
18591399
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
MAKOTO Akashi National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Director (10222514)
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| Co-Investigator(Kenkyū-buntansha) |
HACHIYA Misao National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Senior Researcher (00198756)
NAKAYAMA Fumiaki National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Senior Researcher (50277323)
TOMINAGA Takako National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Researcher (50415436)
YASUDDA Takeshi National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Senior Researcher (60332269)
SUDO Makoto National Institute of Radiological Sciences, The Department of Radiation Emergency Medicine, Researcher (40415427)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,890,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | radiation / TNF_α / R / O mouse / survival |
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| Research Abstract |
Exposure to high dose radiation results in radiation injury that is a serious problem in accidental exposure and also in radiation therapy. Radiation activates the production of tumor necrosis factor α (TNF α) in various cells. However, the role (s) of TNF α was not fully understood. In this study, we investigated the roles of TNF α in mice exposed to radiation. We compared the wild-type (wt) and the TNF α knock-out (k/o) BALB/c mice. Both groups of mice were subjected to γ-ray radiation. The survival durations in the wt were significantly longer than those in the k/o. Furthermore, administration of TNF α before or after radiation increased a survival rate in both mice. We also compared numbers of blood cells, numbers of surviving intestinal crypts, apoptosis in crypt cells and activity of an antioxidant enzyme manganese superoxide dismutase (MnSOD) following radiation in these mice. There was no significant difference in numbers of white blood cells after exposure. On day 15 after exposure, however, numbers of red blood cells in the wt was higher than those in the k/o. Moreover, there was also no significant difference in surviving intestinal crypts and apoptosis in crypt cells after exposure between the wt and k/o. Administration of TNF α before radiation increased apoptosis in the k/o intestine. Activities of MnSOD were lower in liver of the k/o than that of the wt. Moreover, we studied the expression of apoptosis-related proteins in intestinal epithelial cells along the crypt-villus axis after radiation. The Bc12 protein was constitutively expressed and its level was reduced by radiation in the wt. In contrast, Bc12 was not expressed in the k/o and radiation did not induce its expression. Our results suggest that TNF α endogenously-produced may play important roles in the radiation-induced injuries.
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