| Project/Area Number |
06454638
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
環境影響評価(含放射線生物学)
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
YONEI Shuji Kyoto Univ., Graduate School of Science, Associate Professor, 大学院・理学研究科, 助教授 (60093340)
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| Co-Investigator(Kenkyū-buntansha) |
ZHANG Qiu-mei Kyoto Univ., Graduate School of Science, Instructor, 大学院・理学研究科, 助手 (00260604)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 1995: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1994: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Redox / SoxRS / Thioredoxin / Active oxygen species / DNA repair / Signal transfer / Oxidative stress / Gene expression / soi遺伝子 / 活性酵素 / mutM遺伝子 / soxRSレギュロン / スーパーオキサイド |
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| Research Abstract |
The ability of Escherichia coli thioredoxin and thioredoxin reductase was examined with respect to protect the cells against hydrogen peroxide (H_2O_2) and super-oxide-generating agents. In late stationary phase, thioredoxin-and thioredoxin reductase-deficient mutant, trxA and trxB,respectively, exhibited increased sensitivity to these oxidizing agents compared with wild-type strain. Exponentially growing cells of trxA mutant was also more sensitive to H_2O_2 than wild-type strain. On the other hand, trxB mutant in exponentially growing phase acquired resistance to H_2O_2 over the level of wild-type strain. Catalase-hydroperoxidase I (HPI), encoded by the katG,is known to be the major defense enzyme against peroxides and inducible by H_2O_2. We examined the level of HPI expression in trxA and trxB mutants after treatment with H_2O_2. Interestingly, the trxB mutation stimulated the expression of katG : : lacZ fusion gene, while the trxA reduced. These results suggested that thioredoxin protects E.coli cells against H_2O_2 by at least two different mechanisms, by serving as a radical scavenger in its reduced form and by stimulating the induction of HPI in its oxidized form.
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