Detailed Information on Publication Record
2014
Effects of clofibric acid alone and in combination with 17 beta-estradiol on mRNA abundance in primary hepatocytes isolated from rainbow trout
SOVADINOVÁ, Iva, A. LIEDTKE and K. SCHIRMERBasic information
Original name
Effects of clofibric acid alone and in combination with 17 beta-estradiol on mRNA abundance in primary hepatocytes isolated from rainbow trout
Authors
SOVADINOVÁ, Iva (203 Czech Republic, guarantor, belonging to the institution), A. LIEDTKE (276 Germany) and K. SCHIRMER (276 Germany)
Edition
Toxicology in vitro, OXFORD, PERGAMON-ELSEVIER SCIENCE LTD, 2014, 0887-2333
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30304 Public and environmental health
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 2.903
RIV identification code
RIV/00216224:14310/14:00079361
Organization unit
Faculty of Science
UT WoS
000339599300003
Keywords in English
Clofibric acid; Primary fish hepatocytes; Rainbow trout; Vitellogenin; Endocrine disruption
Tags
International impact, Reviewed
Změněno: 4/3/2015 10:52, Ing. Filip Vaculovič
Abstract
V originále
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, 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.