Chronic perfluorooctane sulfonate (PFOS) exposure induces hepatic steatosis in zebrafish
- Cheng, J., Lv, S., Nie, S., Liu, J., Tong, S., Kang, N., Xiao, Y., Dong, Q., Huang, C., Yang, D.
- Aquatic toxicology (Amsterdam, Netherlands) 176: 45-52 (Journal)
- Registered Authors
- Liu, Jing
- Chronic exposure, Lipid metabolism, PFOS, Zebrafish
- MeSH Terms
- Alkanesulfonic Acids/toxicity*
- Fatty Acids/chemistry
- Fatty Liver/etiology*
- Fatty Liver/metabolism
- Fatty Liver/veterinary
- Lipid Metabolism/drug effects*
- Lipoproteins, HDL/blood
- Lipoproteins, LDL/blood
- Real-Time Polymerase Chain Reaction
- Receptors, Cytoplasmic and Nuclear/genetics
- Receptors, Cytoplasmic and Nuclear/metabolism
- Water Pollutants, Chemical/toxicity*
- Zebrafish/growth & development
- 27108203 Full text @ Aquat. Toxicol.
Cheng, J., Lv, S., Nie, S., Liu, J., Tong, S., Kang, N., Xiao, Y., Dong, Q., Huang, C., Yang, D. (2016) Chronic perfluorooctane sulfonate (PFOS) exposure induces hepatic steatosis in zebrafish. Aquatic toxicology (Amsterdam, Netherlands). 176:45-52.
Perfluorooctane sulfonate (PFOS), one persistent organic pollutant, has been widely detected in the environment, wildlife and human. Currently few studies have documented the effects of chronic PFOS exposure on lipid metabolism, especially in aquatic organisms. The underlying mechanisms of hepatotoxicity induced by chronic PFOS exposure are still largely unknown. The present study defined the effects of chronic exposure to low level of PFOS on lipid metabolism using zebrafish as a model system. Our findings revealed a severe hepatic steatosis in the liver of males treated with 0.5μM PFOS as evidenced by hepatosomatic index, histological assessment and liver lipid profiles. Quantitative PCR assay further indicated that PFOS significantly increase the transcriptional expression of nuclear receptors (nr1h3, rara, rxrgb, nr1l2) and the genes associated with fatty acid oxidation (acox1, acadm, cpt1a). In addition, chronic PFOS exposure significantly decreased liver ATP content and serum level of VLDL/LDL lipoprotein in males. Taken together, these findings suggest that chronic PFOS exposure induces hepatic steatosis in zebrafish via disturbing lipid biosynthesis, fatty acid β-oxidation and excretion of VLDL/LDL lipoprotein, and also demonstrate the validity of using zebrafish as an alternative model for PFOS chronic toxicity screening.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes