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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 Search for other works by this author on: Oxford Academic Daniel J. Antoine MRC Centre for Inflammation Research, The University of Edinburgh, Edinburgh, EH16 4TJ, UK Search for other works by this author on: Oxford Academic Alan R. Boobis Department of Medicine, Imperial College London, London W12 0NN, UK Search for other works by this author on: Oxford Academic 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 Search for other works by this author on: Oxford Academic Ann K. Daly Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK Search for other works by this author on: Oxford Academic Lucia Possamai Department of Hepatology, St Mary's Hospital, Imperial College London, London W2 1NY, UK Search for other works by this author on: Oxford Academic 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 Search for other works by this author on: Oxford Academic 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 Search for other works by this author on: Oxford Academic
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.
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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