Advertisement

Environmental Science and Pollution Research

, Volume 26, Issue 18, pp 18240–18246 | Cite as

Effect of prenatal PFOS exposure on liver cell function in neonatal mice

  • Xiaoliu Liang
  • Guojie Xie
  • Xinmou Wu
  • Min SuEmail author
  • Bin YangEmail author
Research Article
  • 68 Downloads

Abstract

Perfluorooctane sulfonate (PFOS), a hepatotoxic pollutant, is detected in the human cord blood, and it may induce health risk to an embryo. In this study, we established intrauterine exposure to PFOS in mice to evaluate potential impacts of PFOS on postnatal day 1 (PND1) offspring through conducting biochemical tests, quantitative PCR, and immunostaining. As results, PFOS-exposed maternal mice showed marked hepatomegaly and induced liver steatosis in a high dose of 5 mg PFOS/kg. In PND1 mice, intrahepatic contents of triglyceride, total cholesterol, and LDL were elevated by high-dose PFOS exposure, while intracellular HDL content was decreased. As shown in quantitative PCR, functional messenger RNAs of cytochrome P4A14 (CYP4A14) for fatty acid oxidation, CD36 for hepatic fatty acid uptake, and apolipoprotein B100 (APOB) and fibroblast growth factor 21 (FGF21) for hepatic export of lipids in PND1 livers were changed when compared to those in PFOS-free controls. In further validations, immunofluorescence stains showed that hepatic CYP4A14 and CD36 immunoreactive cells were increased in PFOS-exposed PND1 mice. In addition, reduced immunofluorescence-positive cells of APOB and FGF21 were observed in PND1 livers. Collectively, these preliminary findings demonstrate that prenatal exposure to PFOS may affect lipid metabolism in liver cells of PND1 mice.

Keywords

Perfluorooctane sulfonate Prenatal exposure Lipid Liver cells 

Notes

Funding

Our study is granted in part by the National Natural Science Foundation of China (No. 81660091) and the National Natural Science Foundation of Guangxi (Nos. 2016GXNSFBA380055 and 2018GXNSFAA281242).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

References

  1. Bjork JA, Butenhoff JL, Wallace KB (2011) Multiplicity of nuclear receptor activation by PFOA and PFOS in primary human and rodent hepatocytes. Toxicology 288:8–17CrossRefGoogle Scholar
  2. Clarke DB, Bailey VA, Routledge A, Lloyd AS, Hird S, Mortimer DN, Gem M (2010) Dietary intake estimate for perfluorooctanesulphonic acid (PFOS) and other perfluorocompounds (PFCs) in UK retail foods following determination using standard addition LC-MS/MS. Food Addit Contam Part A Chem Anal Control Expo Risk Assess 27:530–545CrossRefGoogle Scholar
  3. Das KP, Wood CR, Lin MT, Starkov AA, Lau C, Wallace KB, Corton JC, Abbott BD (2017) Perfluoroalkyl acids-induced liver steatosis: effects on genes controlling lipid homeostasis. Toxicology 378:37–52CrossRefGoogle Scholar
  4. Fàbrega F, Kumar V, Schuhmacher M, Domingo JL, Nadal M (2014) PBPK modeling for PFOS and PFOA: validation with human experimental data. Toxicol Lett 230:244–251CrossRefGoogle Scholar
  5. Fai Tse WK, Li JW, Kwan Tse AC, Chan TF, Hin Ho JC, Sun Wu RS, Chu Wong CK, Lai KP (2016) Fatty liver disease induced by perfluorooctane sulfonate: novel insight from transcriptome analysis. Chemosphere 159:166–177CrossRefGoogle Scholar
  6. Glatz JF, Luiken JJ (2017) From fat to FAT (CD36/SR-B2): Understanding the regulation of cellular fatty acid uptake. Biochimie 136:21–26CrossRefGoogle Scholar
  7. Itoh N (2014) FGF21 as a hepatokine, adipokine, and myokine in metabolism and diseases. Front Endocrinol (Lausanne) 5:107CrossRefGoogle Scholar
  8. Jiang W, Zhang Y, Yang L, Chu X, Zhu L (2015) Perfluoroalkyl acids (PFAAs) with isomer analysis in the commercial PFOS and PFOA products in China. Chemosphere 127:180–187CrossRefGoogle Scholar
  9. Kim HS, Jun Kwack S, Sik Han E, Seok Kang T, Hee Kim S, Young Han S (2011) Induction of apoptosis and CYP4A1 expression in Sprague-Dawley rats exposed to low doses of perfluorooctane sulfonate. J Toxicol Sci 36:201–210CrossRefGoogle Scholar
  10. Kishi R, Nakajima T, Goudarzi H, Kobayashi S, Sasaki S, Okada E, Miyashita C, Itoh S, Araki A, Ikeno T, Iwasaki Y, Nakazawa H (2015) The association of prenatal exposure to perfluorinated chemicals with maternal essential and long-chain polyunsaturated fatty acids during pregnancy and the birth weight of their offspring: the Hokkaido Study. Environ Health Perspect 123:1038–1045CrossRefGoogle Scholar
  11. Lai KP, Li JW, Cheung A, Li R, Billah MB, Chan TF, Wong CKC (2017) Transcriptome sequencing reveals prenatal PFOS exposure on liver disorders. Environ Pollut 223:416–425CrossRefGoogle Scholar
  12. Lee YY, Wong CK, Oger C, Durand T, Galano JM, Lee JC (2015) Prenatal exposure to the contaminant perfluorooctane sulfonate elevates lipid peroxidation during mouse fetal development but not in the pregnant dam. Free Radic Res 49:1015–1025CrossRefGoogle Scholar
  13. Li R, Song J, Wu W, Wu X, Su M (2016) Puerarin exerts the protective effect against chemical induced dysmetabolism in rats. Gene 595:168–174CrossRefGoogle Scholar
  14. Lien GW, Huang CC, Wu KY, Chen MH, Lin CY, Chen CY, Hsieh WS, Chen PC (2013) Neonatal-maternal factors and perfluoroalkyl substances in cord blood. Chemosphere 92:843–850CrossRefGoogle Scholar
  15. Maratos-Flier E (2017) Fatty liver and FGF21 physiology. Exp Cell Res 360:2–5CrossRefGoogle Scholar
  16. Persson S, Magnusson U (2015) Environmental pollutants and alterations in the reproductive system in wild male mink (Neovison vison) from Sweden. Chemosphere 120:237–245CrossRefGoogle Scholar
  17. Rutledge AC, Su Q, Adeli K (2010) Apolipoprotein B100 biogenesis: a complex array of intracellular mechanisms regulating folding, stability, and lipoprotein assembly. Biochem Cell Biol 88:251–267CrossRefGoogle Scholar
  18. Saikat S, Kreis I, Davies B, Bridgman S, Kamanyire R (2013) The impact of PFOS on health in the general population: a review. Environ Sci Process Impacts 15:329–335CrossRefGoogle Scholar
  19. Starling AP, Engel SM, Whitworth KW, Richardson DB, Stuebe AM, Daniels JL, Haug LS, Eggesbø M, Becher G, Sabaredzovic A, Thomsen C, Wilson RE, Travlos GS, Hoppin JA, Baird DD, Longnecker MP (2014) Perfluoroalkyl substances and lipid concentrations in plasma during pregnancy among women in the Norwegian Mother and Child Cohort Study. Environ Int 62:104–112CrossRefGoogle Scholar
  20. Su M, Liang X, Xu X, Wu X, Yang B (2019) Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice through suppressing inflammatory reaction and ER stress. Environ Toxicol Pharmacol 65:60–65CrossRefGoogle Scholar
  21. Wan HT, Zhao YG, Leung PY, Wong CK (2014) Perinatal exposure to perfluorooctane sulfonate affects glucose metabolism in adult offspring. PLoS One 9:e87137CrossRefGoogle Scholar
  22. Wang T, Wang P, Meng J, Liu S, Lu Y, Khim JS, Giesy JP (2015) A review of sources, multimedia distribution and health risks of perfluoroalkyl acids (PFAAs) in China. Chemosphere 129:87–99CrossRefGoogle Scholar
  23. Wei C, Pan Q, Wu K, Li R (2015) Clinical characterization for proliferation and metastasis in advanced hepatocellular carcinoma patients. Int J Clin Exp Pathol 8:13429–13431Google Scholar
  24. Wu K, Fan J, Huang X, Wu X, Guo C (2018a) Hepatoprotective effects exerted by Poria cocos polysaccharides against acetaminophen-induced liver injury in mice. Int J Biol Macromol 114:137–142CrossRefGoogle Scholar
  25. Wu X, Xie G, Xu X, Wu W, Yang B (2018b) Adverse bioeffect of perfluorooctanoic acid on liver metabolic function in mice. Environ Sci Pollut Res Int 25:4787–4793CrossRefGoogle Scholar
  26. Xu C, Jiang ZY, Liu Q, Liu H, Gu A (2017) Estrogen receptor beta mediates hepatotoxicity induced by perfluorooctane sulfonate in mouse. Environ Sci Pollut Res Int 24:13414–13423CrossRefGoogle Scholar
  27. Yao L, Wang C, Zhang X, Peng L, Liu W, Zhang X, Liu Y, He J, Jiang C, Ai D, Zhu Y (2016) Hyperhomocysteinemia activates the aryl hydrocarbon receptor/CD36 pathway to promote hepatic steatosis in mice. Hepatology 64:92–105CrossRefGoogle Scholar
  28. Zhang X, Li S, Zhou Y, Su W, Ruan X, Wang B, Zheng F, Warner M, Gustafsson JÅ, Guan Y (2017) Ablation of cytochrome P450 omega-hydroxylase 4A14 gene attenuates hepatic steatosis and fibrosis. Proc Natl Acad Sci U S A 114:3181–3185CrossRefGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  1. 1.College of PharmacyGuangxi Medical UniversityNanningChina
  2. 2.Department of Gynecology, Guigang City People’s HospitalThe Eighth Affiliated Hospital of Guangxi Medical UniversityGuigangPeople’s Republic of China
  3. 3.Key Laboratory of Tumor Immunology and Microenvironmental RegulationGuilin Medical UniversityGuilinPeople’s Republic of China

Personalised recommendations