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Effects of clofibric acid alone and in combination with 17β-estradiol on mRNA abundance in primary hepatocytes isolated from rainbow trout
I. Sovadinová, A. Liedtke, K. Schirmer,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Apolipoprotein C-II genetics MeSH
- Water Pollutants, Chemical toxicity MeSH
- Cytochrome P-450 CYP3A genetics MeSH
- Estradiol toxicity MeSH
- Glutathione Transferase genetics MeSH
- Hepatocytes drug effects metabolism MeSH
- Hypolipidemic Agents toxicity MeSH
- Cells, Cultured MeSH
- Clofibric Acid toxicity MeSH
- RNA, Messenger metabolism MeSH
- Estrogen Receptor Modulators toxicity MeSH
- Oncorhynchus mykiss * MeSH
- Fish Proteins genetics MeSH
- Cytochrome P-450 Enzyme System genetics MeSH
- Vitellogenins genetics MeSH
- Animals MeSH
- Check Tag
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Clofibric 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, 17β-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.
Harlan Laboratories Ltd Zelgliweg 1 CH 4452 Itingen Switzerland
School of Architecture Civil and Environmental Engineering Station 18 CH 1015 Lausanne Switzerland
References provided by Crossref.org
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- $a Clofibric 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, 17β-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.
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