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Metabolomics-based investigation of PFOS-induced molecular perturbations across multiple rat organs.

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Title: Metabolomics-based investigation of PFOS-induced molecular perturbations across multiple rat organs.
Authors: Yen, Tzu-Hsin1 (AUTHOR), Lee, Sheng-Han2,3 (AUTHOR), Liang, Hao-Jan1 (AUTHOR), Huang, Zou-Xiao1 (AUTHOR), Chen, Chi-Tsung1,4 (AUTHOR), Li, Christopher5 (AUTHOR), Lin, Ching-Yu1,6 (AUTHOR) chingyulin@ntu.edu.tw
Source: Environmental Toxicology & Pharmacology. Mar2026, Vol. 122, pN.PAG-N.PAG. 1p.
Subject Terms: Perfluorooctane sulfonate, Metabolomics, Energy metabolism, Succinates, Inflammation, Mitochondrial pathology, Oxidative stress, Organs (Anatomy)
Abstract: This study aimed to investigate the perfluorooctane sulfonic acid (PFOS)-induced metabolic alterations in several organs and establish the potential mechanisms underlying the organ toxicity. A nuclear magnetic resonance-based metabolomics approach was employed to analyze metabolic alterations in multiple organs and serum of male rats exposed to varying doses of PFOS. We observed significant alterations in metabolites associated with inflammation (e.g., uridine diphosphate glucose), energy metabolism (e.g., adenosine monophosphate and adenosine triphosphate), amino acid (e.g., branched-chain amino acids), carbohydrate metabolism, and oxidative stress modulation (e.g., glutathione and taurine) in several organs. These alterations could be linked to inflammation, fibrosis, mitochondrial dysfunction, insulin resistance, and oxidative stress. Succinate accumulation was observed in the heart and liver, suggesting the susceptibility of these organs to mitochondrial dysfunction. Overall, our findings revealed potential key molecular events triggered by PFOS exposure, contributing to a deeper understanding of the possible adverse effects on multiple organs. • Metabolomics revealed PFOS-induced metabolic disruptions in multiple organs. • Metabolic changes reflect inflammation, energy disruption, and oxidative stress. • UDP-glucose upregulation may be a key event of PFOS-induced inflammation. • Increased accumulation of succinate may be a liver- and heart-specific response. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Metabolomics-based investigation of PFOS-induced molecular perturbations across multiple rat organs.
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  Data: <searchLink fieldCode="AR" term="%22Yen%2C+Tzu-Hsin%22">Yen, Tzu-Hsin</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Lee%2C+Sheng-Han%22">Lee, Sheng-Han</searchLink><relatesTo>2,3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Liang%2C+Hao-Jan%22">Liang, Hao-Jan</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Huang%2C+Zou-Xiao%22">Huang, Zou-Xiao</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Chen%2C+Chi-Tsung%22">Chen, Chi-Tsung</searchLink><relatesTo>1,4</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Li%2C+Christopher%22">Li, Christopher</searchLink><relatesTo>5</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Lin%2C+Ching-Yu%22">Lin, Ching-Yu</searchLink><relatesTo>1,6</relatesTo> (AUTHOR)<i> chingyulin@ntu.edu.tw</i>
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  Data: <searchLink fieldCode="JN" term="%22Environmental+Toxicology+%26+Pharmacology%22">Environmental Toxicology & Pharmacology</searchLink>. Mar2026, Vol. 122, pN.PAG-N.PAG. 1p.
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  Data: <searchLink fieldCode="DE" term="%22Perfluorooctane+sulfonate%22">Perfluorooctane sulfonate</searchLink><br /><searchLink fieldCode="DE" term="%22Metabolomics%22">Metabolomics</searchLink><br /><searchLink fieldCode="DE" term="%22Energy+metabolism%22">Energy metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22Succinates%22">Succinates</searchLink><br /><searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink><br /><searchLink fieldCode="DE" term="%22Mitochondrial+pathology%22">Mitochondrial pathology</searchLink><br /><searchLink fieldCode="DE" term="%22Oxidative+stress%22">Oxidative stress</searchLink><br /><searchLink fieldCode="DE" term="%22Organs+%28Anatomy%29%22">Organs (Anatomy)</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: This study aimed to investigate the perfluorooctane sulfonic acid (PFOS)-induced metabolic alterations in several organs and establish the potential mechanisms underlying the organ toxicity. A nuclear magnetic resonance-based metabolomics approach was employed to analyze metabolic alterations in multiple organs and serum of male rats exposed to varying doses of PFOS. We observed significant alterations in metabolites associated with inflammation (e.g., uridine diphosphate glucose), energy metabolism (e.g., adenosine monophosphate and adenosine triphosphate), amino acid (e.g., branched-chain amino acids), carbohydrate metabolism, and oxidative stress modulation (e.g., glutathione and taurine) in several organs. These alterations could be linked to inflammation, fibrosis, mitochondrial dysfunction, insulin resistance, and oxidative stress. Succinate accumulation was observed in the heart and liver, suggesting the susceptibility of these organs to mitochondrial dysfunction. Overall, our findings revealed potential key molecular events triggered by PFOS exposure, contributing to a deeper understanding of the possible adverse effects on multiple organs. • Metabolomics revealed PFOS-induced metabolic disruptions in multiple organs. • Metabolic changes reflect inflammation, energy disruption, and oxidative stress. • UDP-glucose upregulation may be a key event of PFOS-induced inflammation. • Increased accumulation of succinate may be a liver- and heart-specific response. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1016/j.etap.2026.104957
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      – Code: eng
        Text: English
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      – SubjectFull: Metabolomics
        Type: general
      – SubjectFull: Energy metabolism
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      – SubjectFull: Succinates
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      – SubjectFull: Inflammation
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      – SubjectFull: Mitochondrial pathology
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      – SubjectFull: Oxidative stress
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      – SubjectFull: Organs (Anatomy)
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      – TitleFull: Metabolomics-based investigation of PFOS-induced molecular perturbations across multiple rat organs.
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            NameFull: Yen, Tzu-Hsin
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            – D: 01
              M: 03
              Text: Mar2026
              Type: published
              Y: 2026
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              Value: 122
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