Circulating acylcarnitines as biomarkers of mitochondrial dysfunction after acetaminophen overdose in mice and humans
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Title
Circulating acylcarnitines as biomarkers of mitochondrial dysfunction after acetaminophen overdose in mice and humans
Authors
Keywords
Acetaminophen toxicity, Biomarkers, Mitochondria, Acylcarnitines
Journal
ARCHIVES OF TOXICOLOGY
Volume 88, Issue 2, Pages 391-401
Publisher
Springer Nature
Online
2013-08-24
DOI
10.1007/s00204-013-1118-1
References
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- The mechanism underlying acetaminophen-induced hepatotoxicity in humans and mice involves mitochondrial damage and nuclear DNA fragmentation
- (2012) Mitchell R. McGill et al. JOURNAL OF CLINICAL INVESTIGATION
- c-Jun N-terminal Kinase (JNK)-dependent Acute Liver Injury from Acetaminophen or Tumor Necrosis Factor (TNF) Requires Mitochondrial Sab Protein Expression in Mice
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- HepaRG cells: A human model to study mechanisms of acetaminophen hepatotoxicity
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- c-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity
- (2010) Chieko Saito et al. TOXICOLOGY AND APPLIED PHARMACOLOGY
- Serum Metabolomics Reveals Irreversible Inhibition of Fatty Acid β-Oxidation through the Suppression of PPARα Activation as a Contributing Mechanism of Acetaminophen-Induced Hepatotoxicity
- (2009) Chi Chen et al. CHEMICAL RESEARCH IN TOXICOLOGY
- Novel mechanisms of protection against acetaminophen hepatotoxicity in mice by glutathione and N-acetylcysteine
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- Deletion of Apoptosis Signal-Regulating Kinase 1 Attenuates Acetaminophen-Induced Liver Injury by Inhibiting c-Jun N-Terminal Kinase Activation
- (2008) Hayato Nakagawa et al. GASTROENTEROLOGY
- Role of JNK Translocation to Mitochondria Leading to Inhibition of Mitochondria Bioenergetics in Acetaminophen-induced Liver Injury
- (2008) Naoko Hanawa et al. JOURNAL OF BIOLOGICAL CHEMISTRY
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