کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2584518 | 1130746 | 2007 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Thyroid hormone receptor isoform selectivity of thyroid hormone disrupting compounds quantified with an in vitro reporter gene assay Thyroid hormone receptor isoform selectivity of thyroid hormone disrupting compounds quantified with an in vitro reporter gene assay](/preview/png/2584518.png)
Some compounds, including brominated diphenyl ethers (BDEs), can interfere with thyroid hormone (TH) receptor (TR)-mediated TH-signalling. In this study, the TR isoform selectivity of some TH disrupting compounds was investigated with TRα/β specific reporter gene assays. For this purpose, the effects of compounds on 3,3′,5-triiodothyronine (T3)-induced TRα- or TRβ-activation were tested in green monkey kidney fibroblast (CV-1) cells transiently transfected with Xenopus TRs and a luciferase reporter gene. The T3-like BDE-OH and diiodobiphenyl (DIB) increased T3-induced TRα-activation, but not T3-induced TRβ-activation. BDE28 (100 nM) did not act via TRα, but almost tripled T3-induced TRβ-activation relative to T3 at its EC50. BDE206 (100 nM) was antagonistic on both TRs with a maximum repression −54% relative to T3 at its EC50. Contrary to previous results obtained with the T-screen, HBCD was inactive. The present study illustrates the importance of testing potential TH disrupting compounds in model systems that enable independent characterization of effects on both T3-induced TRs.
Journal: Environmental Toxicology and Pharmacology - Volume 23, Issue 3, May 2007, Pages 302–307