J 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. SCHIRMER

Basic 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

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.