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Ramachandran A, Jaeschke H. Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology. J Clin Transl Res. 2017;3:157-169doi: 10.18053/jctres.03.2017S1.002.
Ramachandran, A., & Jaeschke, H. (2017). Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology. Journal of clinical and translational research, 3157-169. https://doi.org/10.18053/jctres.03.2017S1.002
Ramachandran, Anup, and Jaeschke, Hartmut. "Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology." Journal of clinical and translational research vol. 3 (2017): 157-169. doi: https://doi.org/10.18053/jctres.03.2017S1.002
Ramachandran A, Jaeschke H. Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology. J Clin Transl Res. 2017 Feb;3:157-169. doi: 10.18053/jctres.03.2017S1.002. Epub 2017 Feb 12. PMID: 28670625; PMCID: PMC5489132.
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J Clin Transl Res. 2017 Feb;3:157-169. doi: 10.18053/jctres.03.2017S1.002. Epub 2017 Feb 12.

Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.

Journal of clinical and translational research

Anup Ramachandran, Hartmut Jaeschke

Affiliations

  1. Department of Pharmacology, Toxicology & Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.

PMID: 28670625 PMCID: PMC5489132 DOI: 10.18053/jctres.03.2017S1.002

Abstract

Acetaminophen (APAP) overdose is the most common cause of acute liver failure in the United States and mechanisms of liver injury induced by APAP overdose have been the focus of extensive investigation. Studies in the mouse model, which closely reproduces the human condition, have shown that hepatotoxicity is initiated by formation of a reactive metabolite

Keywords: DNA fragmentation; acetaminophen; biomarkers; hepatotoxicity; mitochondria; mitochondrial dynamics; nitric oxide; oxidative stress; protein adducts; regulated necrosis

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