| Project/Area Number |
10671234
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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 |
Digestive surgery
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
KORENAGA Daisuke Fukuoka Dental College, Dentistry, Professor, 歯学部, 教授 (90170414)
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| Co-Investigator(Kenkyū-buntansha) |
TAKESUE Fumio Fukuoka Dental College, Dentistry, Assistant, 歯学部, 助手 (30299599)
YASUDA Mitsuhiro Fukuoka Dental College, Dentistry, Assistant, 歯学部, 助手 (90269043)
INUTSUKA Sadaaki Fukuoka Dental College, Dentistry, Lecturer, 歯学部, 講師 (40258596)
HONDA Masayuki Fukuoka Dental College, Dentistry, Assistant, 歯学部, 助手 (40330972)
長濱 俊一 福岡歯科大学, 歯学部, 助手 (70279321)
楠本 宏記 福岡歯科大学, 歯学部, 助教授 (00195447)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | ulcerative colitis / colon cancer / carcinogenesis / DSS / free radical / SOD / superoxide / antioxidants |
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| Research Abstract |
Purpose : The mechanisms underlying the frequent development of carcinomas associated with ulcerative colitis (UC) is not understood. The cellular antioxidants play a crucial role in protection against neoplastic disease. The purpose of this study is to investigate a critical balance between free radical activity and antioxidant defense system on carcinogenesis associated with UC, using a model of experimental colitis induced in mice by dextran sulfate sodium (DSS) treatment. Methods : Chronic colitis was induced by feeding the mice for 7 days with 4% DSS, followed by drinking water alone for the subsequent 14 days. Animals were sacrificed after one, two, three and four cycles of DSS administration, respectively. Developments of dysplastic epithelium and invasive carcinoma were histologically examined. Alternations of malondialdehyde (MDA) and superoxide dismutase (SOD) activities in colonic tissues together with production of serum tumor necrosis factor (TNF)-α were determined. We investigated whether treatments with SOD or Vit-C would block cancer development. Results : Colonic neoplasms including dysplastic epithelium and invasive carcinoma developed in 28.6% and 25.0% at the end of the third and fourth cycles, respectively. In accordance with elevation of serum TNF-α, there was a substantial increase in tissue MDA content, while SOD activity tended to be suppressed during the treatment periods. Neoplasms revealed significantly lower SOD levels compared with chronic colitis, although MDA levels were not statistically different among these diseases. Treatments with SOD or Vit-C increased tissue SOD activity, but were not effective in preventing cancer development. Conclusions : These findings suggested that impaired antioxidant defense system might be critical for cancer development associated with UC.
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