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 a K. SCHIRMER

Základní údaje

Originální název

Effects of clofibric acid alone and in combination with 17 beta-estradiol on mRNA abundance in primary hepatocytes isolated from rainbow trout

Autoři

SOVADINOVÁ, Iva (203 Česká republika, garant, domácí), A. LIEDTKE (276 Německo) a K. SCHIRMER (276 Německo)

Vydání

Toxicology in vitro, OXFORD, PERGAMON-ELSEVIER SCIENCE LTD, 2014, 0887-2333

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30304 Public and environmental health

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 2.903

Kód RIV

RIV/00216224:14310/14:00079361

Organizační jednotka

Přírodovědecká fakulta

UT WoS

000339599300003

Klíčová slova anglicky

Clofibric acid; Primary fish hepatocytes; Rainbow trout; Vitellogenin; Endocrine disruption

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 4. 3. 2015 10:52, Ing. Filip Vaculovič

Anotace

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.