| Project/Area Number |
14572070
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
KIKUGAWA Kiyomi Tokyo University of Pharmacy and Life Science, School of Pharmacy, Prof., 薬学部, 教授 (90120146)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | oxidized protein / oxidized protein hydrolase (OPH) / COS-7 cell / oxidative stress / proteasome / OPH |
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| Research Abstract |
Functions and behavior of newly found oxidized protein hydrolase (OPH) in cells were investigated. It was found that the enzyme acted as a secondary antioxidant system in cells by prevention of the accumulation of oxidized proteins in cells.
COS-7 cells overexpressing OPH (COS-7-OPH) were established. While protein carbonyls were accumulated in pareteral COS-7 cells depending on the degree of oxidative stress induced by hydrogen peroxide and paraquat, protein carbonyls were not accumulated in COS-7-OPH cells. While COS-7 cells were dead depending on the degree of oxidative stress, the cell death of COS-7-OPH cells induced by the oxidative stress was inhibited. When COS-7-OPH cells were treated with an inhibitor of OPH, paraquat-induced accumulation of protein carbonyls and the degree of cell death were increased. In contrast, when COS-7-OPH cells were treated with an inhibitor of proteasome, paraquat-induced accumulation of protein carbonyls and the degree of cell death were not increased. These findings demonstrated that OPH protected cell death of COS-7-OPH cells from oxidative stress.
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