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2014 Fiscal Year Final Research Report

Study on the exact mechanism for the polychlorinated biphenyl-induced decrease in the serum thyroxine level

Research Project

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Project/Area Number 23510083
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Risk sciences of radiation/Chemicals
Research InstitutionTokushima Bunri University

Principal Investigator

KATO Yoshihisa  徳島文理大学, 薬学部, 教授 (90161132)

Project Period (FY) 2011-04-28 – 2015-03-31
KeywordsPCB / 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
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.

Free Research Field

薬物の体内動態と薬効・毒性発現メカニズム

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Published: 2016-06-03  

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