000201121 001__ 201121
000201121 005__ 20181203023557.0
000201121 0247_ $$2doi$$a10.1016/j.tiv.2014.05.002
000201121 022__ $$a0887-2333
000201121 02470 $$2ISI$$a000339599300003
000201121 037__ $$aARTICLE
000201121 245__ $$aEffects of clofibric acid alone and in combination with 17 beta-estradiol on mRNA abundance in primary hepatocytes isolated from rainbow trout
000201121 260__ $$bPergamon-Elsevier Science Ltd$$c2014$$aOxford
000201121 269__ $$a2014
000201121 300__ $$a11
000201121 336__ $$aJournal Articles
000201121 520__ $$aClofibric acid (CA) is the active substance of lipid lowering drugs. It is resistant to degradation, polar in nature, and has been found ubiquitously in the aquatic environment. Though CA is classified as a peroxisomal proliferator in rodents and is considered as a potential endocrine disruptor, little information exists on the effects of CA in aquatic organisms, such as fish. In the present study, we examined the mRNA levels of peroxisome proliferator- and estrogen-sensitive genes on the exposure of primary rainbow trout (Oncorhynchus mykiss) hepatocytes to CA alone and in combination with the natural female sex hormone, 17 beta-estradiol (E2). Our results demonstrate that rainbow trout hepatocytes are relatively refractory to the effects of CA on the PPAR signaling pathway and lipid metabolism. Moreover, CA did not show recognizable estrogenic activity, but after the induction of vitellogenesis by E2, CA significantly reduced vitellogenin (VTG) mRNA abundance. Apparently, the indirect repression of VTG transcription, independent of estrogen receptors, occurred. The mechanism is not yet clearly understood but may involve disruption of the stabilization of VTG mRNA known to be induced by E2. (C) 2014 Elsevier Ltd. All rights reserved.
000201121 6531_ $$aClofibric acid
000201121 6531_ $$aPrimary fish hepatocytes
000201121 6531_ $$aRainbow trout
000201121 6531_ $$aVitellogenin
000201121 6531_ $$aEndocrine disruption
000201121 700__ $$uEnvironm Res Ctr, UFZ, Dept Cell Toxicol, D-04318 Leipzig, Germany$$aSovadinova, I.
000201121 700__ $$uEnvironm Res Ctr, UFZ, Dept Cell Toxicol, D-04318 Leipzig, Germany$$aLiedtke, A.
000201121 700__ $$g205918$$uEnvironm Res Ctr, UFZ, Dept Cell Toxicol, D-04318 Leipzig, Germany$$aSchirmer, K.$$0245915
000201121 773__ $$j28$$tToxicology In Vitro$$k6$$q1106-1116
000201121 909C0 $$xU12482$$0252401$$pTOX
000201121 909CO $$particle$$pENAC$$ooai:infoscience.tind.io:201121
000201121 937__ $$aEPFL-ARTICLE-201121
000201121 973__ $$rREVIEWED$$sPUBLISHED$$aEPFL
000201121 980__ $$aARTICLE