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Toxic Liver Injury: Molecular, Mechanistic, and Medical Challenges 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 834

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Guest Editor
Department of Internal Medicine II, Division of Gastroenterology and Hepatology, Klinikum Hanau, Teaching Hospital of the Goethe University, 999035 Frankfurt, Germany
Interests: Heavy metals; Heavy metal uptake; Heavy metal disposition, Heavy metal homeostasis; Haber Weiss reaction; Fenton reaction; Benefits and risks for human health; Environmental pollution
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Special Issue Information

Dear Colleagues, 

Liver injury by potentially toxic exogenous and endogenous compounds represents major molecular, mechanistic, and medical challenges. Among the hepatotoxic exogenous compounds are conventional drugs, herbal drugs including various traditional herbal products and so-called herbal supplements lacking supplementary features in patients with a normal balanced diet, alcoholic beverages, industrial chemicals such as aliphatic halogenated hydrocarbons like carbon tetrachloride, environmental chemicals such as heavy metals, nature-based products, and compounds ingested with some fungi. Endogenous hepatotoxic compounds are found in individuals suffering from hereditary diseases such as hemochromatosis caused by iron overload, Wilson disease due to copper overload, Gaucher disease caused by accumulation of glucocerebroside, hepatic porphyria due to metabolic problems of hem synthesis, and a vast range of other hereditary diseases. Finally, much interest has focused more recently on molecular, mechanistic, and clinical aspects on overweight patients with nonalcoholic fatty liver disease and progression to nonalcoholic steatonecrosis (NASH) and nonalcoholic liver cirrhosis, including rare hepatocellular carcinoma. Submissions to the International Journal of Molecular Sciences with a current IF of 4.5 are welcome with focus on molecular, mechanistic, and medical challenges; discouraged are purely clinical papers. 

Prof. Dr. Rolf Teschke
Guest Editor

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Keywords

  • liver injury

  • nonalcoholic fatty liver disease
  • nonalcoholic steatonecrosis
  • nonalcoholic liver cirrhosis
  • hepatocellular carcinoma

Published Papers (1 paper)

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Research

13 pages, 2341 KiB  
Article
Application of TSPO-Specific Positron Emission Tomography Radiotracer as an Early Indicator of Acute Liver Failure Induced by Propacetamol, a Prodrug of Paracetamol
by Daehee Kim, Hye Won Lee, Sun Mi Park, Ji Eun Lee, Sang Ju Lee, Bom Sahn Kim, Seung Jun Oh, Byung Seok Moon and Hai-Jeon Yoon
Int. J. Mol. Sci. 2024, 25(11), 5942; https://doi.org/10.3390/ijms25115942 - 29 May 2024
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Abstract
Acetaminophen overdose is a leading cause of acute liver failure (ALF), and effective treatment depends on early prediction of disease progression. ALF diagnosis currently requires blood collection 24–72 h after APAP ingestion, necessitating repeated tests and hospitalization. Here, we assessed earlier ALF diagnosis [...] Read more.
Acetaminophen overdose is a leading cause of acute liver failure (ALF), and effective treatment depends on early prediction of disease progression. ALF diagnosis currently requires blood collection 24–72 h after APAP ingestion, necessitating repeated tests and hospitalization. Here, we assessed earlier ALF diagnosis using positron emission tomography (PET) imaging of translocator proteins (TSPOs), which are involved in molecular transport, oxidative stress, apoptosis, and energy metabolism, with the radiotracer [18F]GE180. We intraperitoneally administered propacetamol hydrochloride to male C57BL/6 mice to induce ALF. We performed in vivo PET/CT imaging 3 h later using the TSPO-specific radiotracer [18F]GE180 and quantitatively analyzed the PET images by determining the averaged standardized uptake value (SUVav) in the liver parenchyma. We assessed liver TSPO expression levels via real-time polymerase chain reaction, Western blotting, and immunohistochemistry. [18F]GE180 PET imaging 3 h after propacetamol administration (1500 mg/kg) significantly increased liver SUVav compared to controls (p = 0.001). Analyses showed a 10-fold and 4-fold increase in TSPO gene and protein expression, respectively, in the liver, 3 h after propacetamol induction compared to controls. [18F]GE180 PET visualized and quantified propacetamol-induced ALF through TSPO overexpression. These findings highlight TSPO PET’s potential as a non-invasive imaging biomarker for early-stage ALF. Full article
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