The impact of chronic Trimethylamine N-oxide administration on liver oxidative stress, inflammation, and fibrosis.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 8207483 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-6351 (Electronic) Linking ISSN: 02786915 NLM ISO Abbreviation: Food Chem Toxicol Subsets: MEDLINE
    • Publication Information:
      Publication: Exeter : Elsevier Science Ltd
      Original Publication: Oxford ; New York : Pergamon Press, c1982-
    • Subject Terms:
      Interleukin-10*/metabolism ; Liver* ; Methylamines*; Rats ; Animals ; Cyclooxygenase 2/metabolism ; Glutathione Disulfide/metabolism ; Fibrosis ; Inflammation/chemically induced ; Inflammation/metabolism ; Oxidative Stress
    • Abstract:
      TMAO, a gut microbiota derived byproduct, has been associated with various cardiometabolic diseases by promoting oxidative stress and inflammation. The liver is the main organ for TMAO production and chronic exposure to high doses of TMAO could alter its function. In this study, we evaluated the effect of chronic exposure of high TMAO doses on liver oxidative stress, inflammation, and fibrosis. TMAO was administered daily via gastric gavage to laboratory rats for 3 months. Blood was drawn for the quantification of TMAO, and liver tissues were harvested for the assessment of oxidative stress (MDA, GSH, GSSG, GPx, CAT, and 8-oxo-dG) and inflammation by quantification of IL-1α, TNF-α, IL-10, TGF-β, NOS and COX-2 expression. The evaluation of fibrosis was made by Western blot analysis of α-SMA and Collagen-3 protein expression. Histological investigation and immunohistochemical staining of iNOS were performed in order to assess the liver damage. After 3 months of TMAO exposure, TMAO serum levels enhanced in parallel with increases in MDA and GSSG levels in liver tissue and lower values of GSH and GSH/GSSG ratio as well as a decrease in GPx and CAT activities. Inflammation was also highlighted, with enhanced iNOS, COX-2, and IL-10 expression, without structural changes and without induction of liver fibrosis.
      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.
      (Copyright © 2024 Elsevier Ltd. All rights reserved.)
    • Contributed Indexing:
      Keywords: Fibrosis; TMAO; inflammation; liver; oxidative stress
    • Accession Number:
      FLD0K1SJ1A (trimethyloxamine)
      130068-27-8 (Interleukin-10)
      EC 1.14.99.1 (Cyclooxygenase 2)
      ULW86O013H (Glutathione Disulfide)
      0 (Methylamines)
    • Publication Date:
      Date Created: 20240104 Date Completed: 20240129 Latest Revision: 20240129
    • Publication Date:
      20240129
    • Accession Number:
      10.1016/j.fct.2023.114429
    • Accession Number:
      38176578