| Project/Area Number |
11470038
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Tetsuo University of Tsukuba, Institute of Basic Medical Sciences, Associate Prof., 基礎医学系, 助教授 (20111370)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Masayuki University of Tsukuba, Institute of Basic Medical Sciences, Associate Prof., 基礎医学系, 教授 (50166823)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2001: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2000: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1999: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Nrf2 / HO-1 / Prx I / A170 / LDL / Prx I / MSP23 |
|---|
| Research Abstract |
We found that transcription factor Nrf2, known to interact with electrophile response elements or antioxidant responsive elements, regulates expression of detoxifying enzymes and antioxidant proteins such as HO-1, Prx I, A170 and the cystine transporter in murine peritoneal macrophages. Nrf2 was activated by various types of oxidative stress-causing agents : low levels of H_2O_2 that is added to the medium or produced by glucose oxidase in the culture medium, paraquat that produces superoxide, arsenite, cadmium, and electrophilic agents such as diethylmaleate and catechol. Nrf2 also controlled expression of genes encoding detoxifying enzymes such as GSTs and NQO1 in small intestine and liver by dietary 2(3)-t-butyl-4-hydroxyanisole (BHA). We found that dietary BHA induced intestinal and hepatic Prx I in a manner similar to the induction of GSTs. Thus, Nrf2 plays important roles in defense against various types of cytotoxic agents.
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