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Cited by 38Liver Disease and TransplantationAlcohol Consumption and Health EffectsLiver physiology and pathology

Advanced oxidation protein products and inflammatory markers in liver cirrhosis: a comparison between alcohol-related and HCV-related cirrhosis.

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Zuwała-Jagiełło, Jolanta, Pazgan-Simon, Monika, Simon, Krzysztof, Warwas, Maria·2011·Acta Biochimica Polonica
DOI 10.18388/abp.2011_2286
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Abstract

Advanced oxidation protein products (AOPPs) are protein markers of oxidative stress with pro-inflammatory properties that accumulated in liver cirrhosis. In the present study, we investigated the association between chronic inflammatory response triggered by AOPPs and the severity of liver disease as assessed by the Child-Pugh score. Plasma concentrations of AOPPs and inflammatory markers such as C-reactive protein, tumor necrosis factor-α, and interleukin-6 were measured in 41 patients with HCV-related cirrhosis, 43 patients with alcohol-related liver cirrhosis (ALC), and in 30 age and sex matched controls. In comparison with controls, AOPPs were increased in HCV-related compensated (Child-Pugh A) and decompensated (Child-Pugh B-C) cirrhosis and in alcohol-related compensated cirrhosis. AOPPs level positively correlated with Child-Pugh score in alcohol-related cirrhosis but not in HCV-related cirrhosis and the correlation with the indices of chronic inflammation was stronger in ALC. In turn, AOPPs in HCV-related cirrhosis was related to inflammation to a lesser extent, but a significant correlation with antioxidant defense could be noted. In summary, liver cirrhosis was associated with increased formation of AOPPs, which differed between alcohol-related and HCV-related cirrhosis with respect to the relationship between AOPPs and antioxidant defense, stage of liver cirrhosis, and inflammatory response. The significant correlation between AOPPs accumulation and indices of chronic inflammation, more specifically TNF-α, suggests that oxidative stress may be a mediator of chronic inflammatory state in the early stage of alcohol-related cirrhosis.

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  • AP-1 and NF-kappaB-dependent gene products modulate hepatocyte death induced by oxidative stress.

    “In addition, AP-1 and NF-κB-dependent gene products modulate hepatocyte death induced by oxidative stress (Zuwała-Jagiełło et al., 2011).”

    From Iron, Oxidative Stress and Health (2012) · cites this paper as Zuwała-Jagiełło et al., 2011

    The Introduction (page not available) links oxidative-stress products to NF-κB activation and an inflammatory response. It does not say that AP-1 or NF-κB-dependent gene products modulate oxidative-stress-induced hepatocyte death; searches for those terms and hepatocyte death found no supporting passage. (LLM, conf=0.76)

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  • Iron catalyzes the formation of NO from peroxynitrite and can modulate gene expression in cells leading to altered cell functions.

    “Further iron catalyzes the formation of NO from peroxynitrite and can modulate gene expression in cells leading to altered cell functions (Zuwała-Jagiełło et al., 2011).”

    From Iron, Oxidative Stress and Health (2012) · cites this paper as Zuwała-Jagiełło et al., 2011

    The Introduction discusses gene transcription induced by advanced glycation end products, and the Discussion mentions gene expression associated with TNF-α; neither attributes these effects to iron. A search of our copy for iron, peroxynitrite, and nitric oxide found no passage addressing the claimed iron-catalyzed reaction or iron-mediated changes in cell function. The cited paper's References list a study of iron storage, but that title does not establish the claim. (LLM, conf=0.74)

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  • MDA-acetaldehyde adducts may play a role in the development and progression of liver fibrosis as they stimulate the secretion of several cytokines and chemokines by liver endothelial cells.

    “These adducts may play a role in the development and progression of liver fibrosis as they have been shown to stimulate the secretion of several cytokines and chemokines by liver endothelial cells (Zuwała-Jagiełło et al., 2011).”

    From Iron, Oxidative Stress and Health (2012) · cites this paper as Zuwała-Jagiełło et al., 2011

    The Introduction discusses advanced glycation end products and advanced oxidation protein products in inflammatory signaling, but not MDA-acetaldehyde adducts. Searches for those adducts, liver endothelial cells, and cytokine or chemokine secretion found no passage addressing the claimed mechanism. Page numbers were unavailable in our copy. (LLM, conf=0.76)

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Authors
Zuwała-Jagiełło, J., Pazgan-Simon, M., Simon, K., & Warwas, M.
Affiliations
Wroclaw Medical University (PL)
ORCID
Simon, Krzysztof
Venue
Acta Biochimica Polonica
Publisher
Frontiers Media SA
Published
2011-03-14
Volume
58
Issue
1
Pages
59-65
ISSN
  • 0001-527X (ISSN-L)
  • 1734-154X
DOI
10.18388/abp.2011_2286
OpenAlex
W2018667252
Cited by
38
References
54
Citations by year
2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 4 · 2016: 2 · 2015: 6 · 2014: 8 · 2013: 1 · 2012: 6
FWCI
3.46
Type
journal article
Language
en
Open access
Licence
cc-by-sa
Locations
  • Acta Biochimica Polonica (publishedVersion, cc-by-sa)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
advanced oxidation protein products, liver cirrhosis, alcoholic cirrhosis, oxidative stress, chronic inflammation, inflammatory markers, C-reactive protein, TNF-α, interleukin-6, Child-Pugh score, antioxidant defense, decompensated cirrhosis
MeSH terms
Adult, Aged, Antioxidants, C-Reactive Protein, Female, Humans, Liver Cirrhosis, Liver Cirrhosis, Alcoholic, Male, Middle Aged, Tumor Necrosis Factor-alpha, Interleukin-6, Hepacivirus, Reactive Oxygen Species

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