| Project/Area Number |
23510083
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | PCB / 甲状腺ホルモン撹乱 / サイロキシン / UDP-グルクロン酸転移酵素 / トランスサイレチン / 肝臓 / グルクロン酸抱合酵素 / ラット / マウス / 3,3',4,4'-テトラクロロビフェニル / 2,3',4,4',5-ペンクロロビフェニル / 2,2',4,5,5'-ペンクロロビフェニル / TTRノックアウトマウス |
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| Outline of Final Research Achievements |
We have demonstrated that polychlorinated biphenyl(PCB)-mediated decrease in serum thyroxine (T4) level in rats and mice occurred mainly through increased accumulation of T4 in the liver and partially through increased excretion of biliary T4 metabolite(s), development of liver hypertrophy and/or the inhibition of a T4-transthyretin complex formation. Since the several transporters, including apical and basolateral T4-transporters, are reported to exist in the liver cells, further studies on PCB-mediated changes in the expression and activity of hepatic T4 transporter(s) are necessary to understand the liver-selective accumulation of T4.
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