2002 Fiscal Year Final Research Report Summary
Reactive oxygen species are involved in p53 expression and apoptosis via p38MAPK activation in cisplatin-induced acute renal failure of rats
| Project/Area Number |
13671108
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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 |
Kidney internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
YONEMURA Katsuhiko Hamamatsu University School of Medicine, Hemodialysis Unit, Associate Professor, 医学部附属病院, 助教授 (40252176)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIGAKI Yoshihide Hamamatsu University School of Medicine, First Department of Medicine, Research Associate, 医学部, 助手 (20283351)
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| Project Period (FY) |
2001 – 2002
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| Keywords | acute renal failure / reactive oxygen species / cisplatin / apoptosis / p53 / p38 MAPK |
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| Research Abstract |
It is well known that reactive oxygen species have a pivotal role for the development of cisplatin-induced acute renal failure. However, the mechanism whether cisplatin induces apoptosis remains to be elucidated. The purpose of the present study was to examine that hydroxyl radical, a member of reactive oxygen radicals, influence p53 expression in the renal tubular cells in cisplatin-induced acute renal failure of rats. Pretreatment with dimethylthiourea (DMTU), a scavenger of hydroxyl radical, functionally and morphologically inhibited cisplatin-induced acute renal failure. In addition, DMTU suppressed the extent of p53 expression and the number of apoptotic tubular cells induced by cisplatin. The activity of p38 MAPK, an upstream effector of p53 expression, was also suppressed by DMTU. These findings indicate that reactive oxygen radicals are involved in apotosis of renal tubular cells associated with p53 expression via p38 MAPK activity in cisplatin-induced acute renal failure.
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