دورية أكاديمية
أعرض في EDS

Transcriptional pathways linked to fetal and maternal hepatic dysfunction caused by gestational exposure to perfluorooctanoic acid (PFOA) or hexafluoropropylene oxide-dimer acid (HFPO-DA or GenX) in CD-1 mice.

التفاصيل البيبلوغرافية
العنوان: Transcriptional pathways linked to fetal and maternal hepatic dysfunction caused by gestational exposure to perfluorooctanoic acid (PFOA) or hexafluoropropylene oxide-dimer acid (HFPO-DA or GenX) in CD-1 mice.
المؤلفون: Blake BE; Chemical and Pollutant Assessment Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC, USA; Mechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: blake.bevin@epa.gov., Miller CN; Cardiopulmonary Immunotoxicology Branch, Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC, USA., Nguyen H; Oak Ridge Institute for Science and Education, Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Research Triangle Park, NC, USA., Chappell VA; Mechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA., Phan TP; Mechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA., Phadke DP; Sciome LLC, Research Triangle Park, NC, USA., Balik-Meisner MR; Sciome LLC, Research Triangle Park, NC, USA., Mav D; Sciome LLC, Research Triangle Park, NC, USA., Shah RR; Sciome LLC, Research Triangle Park, NC, USA., Fenton SE; Mechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
المصدر: Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2022 Dec 15; Vol. 248, pp. 114314. Date of Electronic Publication: 2022 Nov 24.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 7805381 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2414 (Electronic) Linking ISSN: 01476513 NLM ISO Abbreviation: Ecotoxicol Environ Saf Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam, Netherlands : Elsevier
مواضيع طبية MeSH: Fluorocarbons*/toxicity, Adult ; Humans ; Female ; Pregnancy ; Mice ; Animals ; Oxides ; Caprylates/toxicity ; Fetus ; Polymers
مستخلص: Per- and polyfluoroalkyl substances (PFAS) comprise a diverse class of chemicals used in industrial processes, consumer products, and fire-fighting foams which have become environmental pollutants of concern due to their persistence, ubiquity, and associations with adverse human health outcomes, including in pregnant persons and their offspring. Multiple PFAS are associated with adverse liver outcomes in adult humans and toxicological models, but effects on the developing liver are not fully described. Here we performed transcriptomic analyses in the mouse to investigate the molecular mechanisms of hepatic toxicity in the dam and its fetus after exposure to two different PFAS, perfluorooctanoic acid (PFOA) and its replacement, hexafluoropropylene oxide-dimer acid (HFPO-DA, known as GenX). Pregnant CD-1 mice were exposed via oral gavage from embryonic day (E) 1.5-17.5 to PFOA (0, 1, or 5 mg/kg-d) or GenX (0, 2, or 10 mg/kg-d). Maternal and fetal liver RNA was isolated (N = 5 per dose/group) and the transcriptome analyzed by Affymetrix Array. Differentially expressed genes (DEG) and differentially enriched pathways (DEP) were obtained. DEG patterns were similar in maternal liver for 5 mg/kg PFOA, 2 mg/kg GenX, and 10 mg/kg GenX (R 2 : 0.46-0.66). DEG patterns were similar across all 4 dose groups in fetal liver (R 2 : 0.59-0.81). There were more DEGs in fetal liver compared to maternal liver at the low doses for both PFOA (fetal = 69, maternal = 8) and GenX (fetal = 154, maternal = 93). Upregulated DEPs identified across all groups included Fatty Acid Metabolism, Peroxisome, Oxidative Phosphorylation, Adipogenesis, and Bile Acid Metabolism. Transcriptome-phenotype correlation analyses demonstrated > 1000 maternal liver DEGs were significantly correlated with maternal relative liver weight (R 2 >0.92). These findings show shared biological pathways of liver toxicity for PFOA and GenX in maternal and fetal livers in CD-1 mice. The limited overlap in specific DEGs between the dam and fetus suggests the developing liver responds differently than the adult liver to these chemical stressors. This work helps define mechanisms of hepatic toxicity of two structurally unique PFAS and may help predict latent consequences of developmental exposure.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Published by Elsevier Inc.)
References: Toxicology. 2007 Sep 24;239(1-2):15-33. (PMID: 17681415)
Kaohsiung J Med Sci. 2022 May;38(5):437-446. (PMID: 35080113)
Curr Environ Health Rep. 2019 Sep;6(3):95-104. (PMID: 31090041)
J Hepatol. 2016 Apr;64(4):933-45. (PMID: 26658682)
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50. (PMID: 16199517)
Sci Total Environ. 2017 Oct 15;596-597:97-105. (PMID: 28426990)
J Hepatol. 2022 Feb;76(2):283-293. (PMID: 34627976)
J Expo Sci Environ Epidemiol. 2019 Mar;29(2):131-147. (PMID: 30470793)
Aging (Albany NY). 2021 Mar 21;13(8):11096-11119. (PMID: 33744857)
Environ Int. 2021 Jan;146:106204. (PMID: 33126064)
Environ Health Perspect. 2022 Apr;130(4):46001. (PMID: 35475652)
Environ Health Perspect. 2019 Mar;127(3):37008. (PMID: 30920876)
J Pediatr. 2013 Mar;162(3):496-500.e1. (PMID: 23084707)
Environ Health Perspect. 2015 Aug;123(8):841-6. (PMID: 25809098)
Comput Biol Chem. 2004 Dec;28(5-6):367-74. (PMID: 15556477)
J Clin Endocrinol Metab. 2021 Aug 18;106(9):e3760-e3770. (PMID: 33740056)
Environ Health Perspect. 2017 Sep 20;125(9):097018. (PMID: 28934720)
Sci Total Environ. 2022 May 10;820:153281. (PMID: 35066053)
Environ Int. 2019 Mar;124:482-492. (PMID: 30684806)
Biochim Biophys Acta. 1975 Oct 20;405(2):442-51. (PMID: 1180967)
Environ Health. 2019 Jan 9;18(1):5. (PMID: 30626391)
Nat Rev Endocrinol. 2021 Nov;17(11):662-670. (PMID: 34417588)
Environ Int. 2020 Jan;134:105220. (PMID: 31744629)
Toxicol Pathol. 2015 Jun;43(4):558-68. (PMID: 25398757)
Environ Toxicol Chem. 2021 Mar;40(3):606-630. (PMID: 33017053)
Bioinformatics. 2014 Feb 15;30(4):523-30. (PMID: 24336805)
Sci Rep. 2019 Jun 24;9(1):9179. (PMID: 31235847)
Onco Targets Ther. 2019 Jul 02;12:5153-5162. (PMID: 31303768)
Sci Total Environ. 2021 Oct 10;790:148160. (PMID: 34380288)
Hepatology. 2007 Aug;46(2):504-13. (PMID: 17640041)
Metabolism. 2020 Oct;111S:154170. (PMID: 32006558)
Environ Health Perspect. 2014 Oct;122(10):1040-51. (PMID: 24968389)
Mol Cell Endocrinol. 2009 May 25;304(1-2):97-105. (PMID: 19433254)
Pediatr Res. 2014 Jan;75(1-2):140-7. (PMID: 24192698)
Environ Health Perspect. 2012 May;120(5):668-73. (PMID: 22306490)
Toxicol Environ Chem. 2020;102(1-4):1-36. (PMID: 33304027)
Obesity (Silver Spring). 2016 Jan;24(1):231-7. (PMID: 26554535)
J Hepatol. 2020 Jul;73(1):202-209. (PMID: 32278004)
Reprod Toxicol. 2009 Jun;27(3-4):278-288. (PMID: 19429403)
Transl Gastroenterol Hepatol. 2020 Apr 05;5:16. (PMID: 32258520)
Toxicol Sci. 2011 Jul;122(1):134-45. (PMID: 21482639)
Cell Syst. 2015 Dec 23;1(6):417-425. (PMID: 26771021)
Environ Sci Technol. 2021 Dec 7;55(23):15575-15578. (PMID: 34751569)
Onco Targets Ther. 2019 Sep 03;12:7175-7191. (PMID: 31564902)
Clin Gastroenterol Hepatol. 2022 Nov;20(11):2542-2550.e8. (PMID: 34798335)
J Dairy Sci. 1980 Sep;63(9):1514-29. (PMID: 7000867)
Toxicol Sci. 2006 Apr;90(2):510-8. (PMID: 16415327)
Cancer Biol Ther. 2020 Nov 1;21(11):1005-1013. (PMID: 33054568)
Environ Res. 2021 Sep;200:111400. (PMID: 34081971)
Arch Toxicol. 2016 Mar;90(3):701-15. (PMID: 25827101)
Environ Health Perspect. 2020 Feb;128(2):27006. (PMID: 32074459)
Emerg Contam. 2021;7:219-235. (PMID: 35097227)
Exp Ther Med. 2020 Nov;20(5):26. (PMID: 32934691)
Toxicology. 2017 Jul 15;387:95-107. (PMID: 28558994)
Hepatology. 2020 Nov;72(5):1758-1770. (PMID: 32738061)
Nat Rev Endocrinol. 2017 Aug;13(8):445-457. (PMID: 28524171)
Toxicology. 2020 Oct;443:152565. (PMID: 32861749)
Reprod Toxicol. 2012 Jul;33(4):491-505. (PMID: 22154759)
World J Gastroenterol. 2017 Dec 21;23(47):8263-8276. (PMID: 29307986)
Toxicol Sci. 2007 Mar;96(1):133-44. (PMID: 17132714)
Environ Int. 2021 Dec;157:106843. (PMID: 34479135)
Toxicol Pathol. 2015 Jun;43(4):546-57. (PMID: 25326589)
Environ Health Perspect. 2021 Oct;129(10):107004. (PMID: 34637358)
Environ Int. 2020 Apr;137:105583. (PMID: 32106048)
معلومات مُعتمدة: T32 ES007126 United States ES NIEHS NIH HHS; ZIA ES102785 United States ImNIH Intramural NIH HHS
فهرسة مساهمة: Keywords: Animal models; Developmental exposure; Emerging contaminants; Liver disease; PFAS
المشرفين على المادة: 947VD76D3L (perfluorooctanoic acid)
0 (Fluorocarbons)
0 (Oxides)
0 (Caprylates)
0 (Polymers)
تواريخ الأحداث: Date Created: 20221127 Date Completed: 20221206 Latest Revision: 20240216
رمز التحديث: 20240216
مُعرف محوري في PubMed: PMC9742811
DOI: 10.1016/j.ecoenv.2022.114314
PMID: 36436258
قاعدة البيانات: MEDLINE
الوصف
تدمد:1090-2414
DOI:10.1016/j.ecoenv.2022.114314