c-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity
Top Cited Papers
- 25 April 2010
- journal article
- Published by Elsevier in Toxicology and Applied Pharmacology
- Vol. 246 (1-2), 8-17
- https://doi.org/10.1016/j.taap.2010.04.015
Abstract
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This publication has 59 references indexed in Scilit:
- Acetaminophen‐induced acute liver failureHepatology, 2005
- Peroxynitrite-Induced Mitochondrial and Endonuclease-Mediated Nuclear DNA Damage in Acetaminophen HepatotoxicityJournal of Pharmacology and Experimental Therapeutics, 2005
- Inhibition of Fas Receptor (CD95)-Induced Hepatic Caspase Activation and Apoptosis by Acetaminophen in MiceToxicology and Applied Pharmacology, 1999
- Nitrotyrosine−Protein Adducts in Hepatic Centrilobular Areas following Toxic Doses of Acetaminophen in MiceChemical Research in Toxicology, 1998
- Role of nitric oxide in acetaminophen-induced hepatotoxicity in the ratHepatology, 1998
- Mitochondrial permeability transition in hepatocytes induced by t-BuOOH: NAD(P)H and reactive oxygen speciesAmerican Journal of Physiology-Cell Physiology, 1997
- Selective Protein Covalent Binding and Target Organ ToxicityToxicology and Applied Pharmacology, 1997
- Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.Genes & Development, 1993
- Glutathione disulfide formation and oxidant stress during acetaminophen-induced hepatotoxicity in mice in vivo: the protective effect of allopurinol.1990
- Molecular Mechanisms of the Hepatotoxicity Caused by AcetaminophenSeminars in Liver Disease, 1990