Paracetamol metabolism, hepatotoxicity, biomarkers and therapeutic interventions: a perspective (2024)

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Volume 7 Issue 3 May 2018
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Toby J. Athersuch

Division of Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, South Kensington, London SW7 2AZ, UK

toby.athersuch@imperial.ac.uk

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Daniel J. Antoine

MRC Centre for Inflammation Research, The University of Edinburgh, Edinburgh, EH16 4TJ, UK

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Alan R. Boobis

Department of Medicine, Imperial College London, London W12 0NN, UK

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Muireann Coen

Division of Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, South Kensington, London SW7 2AZ, UK

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Ann K. Daly

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK

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Department of Hepatology, St Mary's Hospital, Imperial College London, London W2 1NY, UK

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Jeremy K. Nicholson

Division of Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, South Kensington, London SW7 2AZ, UK

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Ian D. Wilson

Division of Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, South Kensington, London SW7 2AZ, UK

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Toxicology Research, Volume 7, Issue 3, May 2018, Pages 347–357, https://doi.org/10.1039/c7tx00340d

Published:

06 March 2018

Article history

Received:

21 December 2017

Accepted:

07 February 2018

Published:

06 March 2018

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    Toby J. Athersuch, Daniel J. Antoine, Alan R. Boobis, Muireann Coen, Ann K. Daly, Lucia Possamai, Jeremy K. Nicholson, Ian D. Wilson, Paracetamol metabolism, hepatotoxicity, biomarkers and therapeutic interventions: a perspective, Toxicology Research, Volume 7, Issue 3, May 2018, Pages 347–357, https://doi.org/10.1039/c7tx00340d

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Abstract

After over 60 years of therapeutic use in the UK, paracetamol (acetaminophen, N-acetyl-p-aminophenol, APAP) remains the subject of considerable research into both its mode of action and toxicity. The pharmacological properties of APAP are the focus of some activity, with the role of the metabolite N-arachidonoylaminophenol (AM404) still a topic of debate. However, that the hepatotoxicity of APAP results from the production of the reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI/NABQI) that can deplete glutathione, react with cellular macromolecules, and initiate cell death, is now beyond dispute. The disruption of cellular pathways that results from the production of NAPQI provides a source of potential biomarkers of the severity of the damage. Research in this area has provided new diagnostic markers such as the microRNA miR-122 as well as mechanistic biomarkers associated with apoptosis, mitochondrial dysfunction, inflammation and tissue regeneration. Additionally, biomarkers of, and systems biology models for, glutathione depletion have been developed. Furthermore, there have been significant advances in determining the role of both the innate immune system and genetic factors that might predispose individuals to APAP-mediated toxicity. This perspective highlights some of the progress in current APAP-related research.

Paracetamol metabolism, hepatotoxicity, biomarkers and therapeutic interventions: a perspective (11)

Graphical Abstract

After over 60 years of therapeutic use in the UK, paracetamol (acetaminophen, N-acetyl-p-aminophenol, APAP) remains the subject of considerable research into both its mode of action and toxicity.

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