| Project/Area Number |
15K08294
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Yamagata University |
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Principal Investigator |
Fujii Junichi 山形大学, 大学院医学系研究科, 教授 (00222258)
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| Co-Investigator(Kenkyū-buntansha) |
倉橋 敏裕 京都府立医科大学, 医学(系)研究科(研究院), 講師 (00596570)
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| Co-Investigator(Renkei-kenkyūsha) |
SATO Hideyo 新潟大学, 医歯学系研究科, 教授 (60235380)
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| Research Collaborator |
HOMMA Takujiro 山形大学, 大学院医学系研究科, 助教 (70743566)
KOBAYASHI Sho 山形大学, 大学院医学系研究科, 助教 (10779490)
LEE Jaeyong 山形大学, 大学院医学系研究科, 大学院生
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | グルタチオン / システイン / 肝障害 / トランススルフィレーション経路 |
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| Outline of Final Research Achievements |
xCT, a cystine transporter, was not expressed in liver of wild-type mice but induced by acetaminophen overdose or under cultivation conditions. Acetaminophen overdose aggravated the xCT-deficient mouse more strongly than the wild-type mouse. While xCT-deficient hepatocytes showed normal phenotype regarding the cysteine-glutathione system, ophthalmic acid accumulated more in the xCT-deficient hepatocytes. These results implied that the transsulfuration pathway plays a central role in supplying cysteine in the liver. When glutathione levels decline, such as the case of elevated oxidative stress, xCT is induced and functions as a backup system to supply cysteine to maintain liver redox homeostasis.
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