| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
We strongly suggested that the decrease in serum thyroxine (T4) level caused by exposure to polychlorinated biphenyls (PCBs) occurs mainly through increased accumulation of T4 in the liver. We suggested that the PCB-mediated liver-selective accumulation of T4 might occur, at least in part, through the increased expression of T4 influx transporters, such as LAT1 and oatp2. We further suggested that the PCB-mediated decrease in serum T4 levels occurs through the enhanced hepatic accumulation of T4 and, at least in part, through increases in the Mrp3-mediated excretion of T4 conjugate(s), not only through the induction of T4- UDP-glucuronosyltransferase. Further studies on the effects of PCBs on hepatic T4-transporters would be necessary to understand the exact mechanism for the PCB-induced decrease in serum T4 level.
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