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. SCHIRMERZákladní 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
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.