ACETAMINOPHEN-INDUCED HEPATIC NECROSIS. IV. PROTECTIVE ROLE OF GLUTATHIONE
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When glutathione stores fall below about 30% of normal, free NAPQI rapidly binds and arylates critical cell proteins, triggering events that can lead to cell death.
“When glutathione stores are depleted below a critical value (about 30% of normal stores) free NAPQI rapidly and covalently binds and arylates critical cell proteins, inducing a series of events that may result in cell death (143).”
From Paracetamol: New Vistas of an Old Drug (2006) · cites this paper as [143]
Key, possibly irreversible, events in cell death include enzyme oxidation, DNA fragmentation, and mitochondrial injury.
“Critical, possibly irreversible, events in cell death include oxidation of enzymes, DNA fragmentation, and mitochondrial injury (Fig. 3).”
From Paracetamol: New Vistas of an Old Drug (2006) · cites this paper as [143]
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- Authors
- Mitchell, J. R., Jollow, D. J., Potter, W. Z., Gillette, J. R., & Brodie, B. B.
- Affiliations
- National Institutes of Health (US)
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1973-10
- Volume
- 187
- Issue
- 1
- Pages
- 211-217
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2222772859
- Cited by
- 1,737
- References
- 0
- Citations by year
- 2026: 12 · 2025: 19 · 2024: 26 · 2023: 31 · 2022: 20 · 2021: 32 · 2020: 44 · 2019: 35 · 2018: 33 · 2017: 43 · 2016: 46 · 2015: 62 · 2014: 46 · 2013: 49 · 2012: 54
- FWCI
- 24.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Topics
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Keywords
- paracetamol, liver necrosis, glutathione, drug-induced liver injury, diethyl maleate, cysteine, glutathione depletion, covalent binding, acetaminophen metabolites, hepatoprotection, alkylating agents
- MeSH terms
- Acetaminophen, Animals, Autoradiography, Cysteine, Glutathione, Liver, Male, Maleates, Mice, Inbred Strains, Necrosis, Time Factors, Tritium, Mice, Chemical and Drug Induced Liver Injury
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