Effect of perfluorooctanesulfonic acid (PFOS) on the liver lipid metabolism of the developing chicken embryo.
Alkanesulfonic Acids
/ toxicity
Animals
Ceramides
/ metabolism
Chick Embryo
Chickens
Diglycerides
/ metabolism
Fatty Acids
/ metabolism
Female
Fluorocarbons
/ toxicity
Lipid Metabolism
/ drug effects
Lipid Peroxidation
/ drug effects
Liver
/ drug effects
Male
Mitochondria
/ metabolism
Phosphatidylethanolamine N-Methyltransferase
/ metabolism
Phospholipids
/ metabolism
Triglycerides
/ metabolism
Avian model
Lipidomics
Liver metabolism
Mass spectrometry
Perfluorooctanesulfonate
Journal
Ecotoxicology and environmental safety
ISSN: 1090-2414
Titre abrégé: Ecotoxicol Environ Saf
Pays: Netherlands
ID NLM: 7805381
Informations de publication
Date de publication:
15 Apr 2019
15 Apr 2019
Historique:
received:
02
10
2018
revised:
11
12
2018
accepted:
13
12
2018
pubmed:
24
12
2018
medline:
16
2
2019
entrez:
24
12
2018
Statut:
ppublish
Résumé
Perfluorooctanesulfonate (PFOS) is a well-known contaminant in the environment and it has shown to disrupt multiple biological pathways, particularly those related with lipid metabolism. In this study, we have studied the impact of in ovo exposure to PFOS on lipid metabolism in livers in developing chicken embryos using lipidomics for detailed characterization of the liver lipidome. We used an avian model (Gallus gallus domesticus) for in ovo treatment at two levels of PFOS. The lipid profile of the liver of the embryo was investigated by ultra-high performance liquid chromatography combined with quadrupole-time-of-flight mass spectrometry and by gas chromatography mass spectrometry. Over 170 lipids were identified, covering phospholipids, ceramides, di- and triacylglycerols, cholesterol esters and fatty acid composition of the lipids. The PFOS exposure caused dose dependent changes in the lipid levels, which included upregulation of specific phospholipids associated with the phosphatidylethanolamine N-methyltransferase (PEMT) pathway, triacylglycerols with low carbon number and double bond count as well as of lipotoxic ceramides and diacylglycerols. Our data suggest that at lower levels of exposure, mitochondrial fatty acid β-oxidation is suppressed while the peroxisomal fatty acid β -oxidation is increased. At higher doses, however, both β -oxidation pathways are upregulated.
Identifiants
pubmed: 30580163
pii: S0147-6513(18)31327-7
doi: 10.1016/j.ecoenv.2018.12.040
pii:
doi:
Substances chimiques
Alkanesulfonic Acids
0
Ceramides
0
Diglycerides
0
Fatty Acids
0
Fluorocarbons
0
Phospholipids
0
Triglycerides
0
perfluorooctane sulfonic acid
9H2MAI21CL
Phosphatidylethanolamine N-Methyltransferase
EC 2.1.1.17
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
691-698Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.