Journal
SCIENCE OF THE TOTAL ENVIRONMENT
Volume 790, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.scitotenv.2021.148160
Keywords
PFHxA; Liver injury; Multi-omics; Fatty acid metabolism; Oxidative stress
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Funding
- National Natural Science Foundation of China [21806136, 21707112, 21806134]
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PFHxA is considered as a substitute for PFOS, and its toxicity mainly targets the liver, involving fatty acid biosynthesis and degradation pathways, oxidative stress, and abnormal purine metabolism. This multi-omics study provides new insights into the mechanisms of PFHxA-induced liver injury.
Perfluorohexanoic acid (PFHxA), one of the short-chain perfluoroalkyl acids (PFAAs), is considered as a substitute of perfluorooctane sulfonate (PFOS). This emerging organic pollutant is persistent and highly bioavailable to humans, raising concerns about its potential health risks. There are currently few researches on the toxicity of PFHxA. Liver has been suggested to be the main target of PFHxA toxicity, and the mechanism remains unclear. Herein, we investigated the transcriptomic, proteomic, and metabolomic landscape in PFHxA-exposed mice. Using these approaches, we identified several valuable biological processes involved in the process of liver injury, comprising fatty acid biosynthesis and degradation pathways, which might be induced by peroxisome proliferator-activated receptor (PPAR) signaling pathway. These processes further promoted oxidative stress and induced liver injury. Meanwhile, abnormalities in purine metabolism and glutathione metabolism were observed during the liver injury induced by PFHxA, indicating the production of oxidative stress. Finally, our present multi-omics studies provided new insights into the mechanisms involved in PFHxA-induced liver injury.& nbsp; (c) 2021 Elsevier B.V. All rights reserved.
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