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Cited by 532

The DOI matches its Crossref record.

Acetaminophen‐induced hepatic injury: Protective role of glutathione in man and rationale for therapy

Mitchell, Jerry R., Thorgeirsson, Snorri S., Potter, William Z., Jollow, David J., Keiser, Harry·1974·Clinical Pharmacology & Therapeutics
DOI 10.1002/cpt1974164676
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Abstract

Recent studies of acetaminophen‐induced liver damage in animals indicate that acetaminophen is converted in the liver to a chemically reactive arylating agent that normally is detoxified by conjugation with glutathione. When the dose of acetaminophen is large enough to deplete hepatic glutathione, however, there is extensive arylation of hepatic macromolecules and cell death. This paper presents evidence that administration of glutathione‐like nucleophiles, such as cysteamine, protects mice from arylation of hepatic macromolecules, hepatic necrosis, and death caused by the reactive acetaminophen metabolite. Additional studies indicate that glutathione may serve a similar protective function in man as in other animals. Thus, logical treatment of patients overdosed with acetaminophen might be based on cysteamine or other nucleophiles.

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Metadata

Authors
Mitchell, J. R., Thorgeirsson, S. S., Potter, W. Z., Jollow, D. J., & Keiser, H.
Venue
Clinical Pharmacology & Therapeutics
Publisher
Wiley
Published
1974-10
Volume
16
Issue
4
Pages
676-684
ISSN
  • 0009-9236 (ISSN-L)
  • 1532-6535
DOI
10.1002/cpt1974164676
OpenAlex
W2424133290
Cited by
532
References
0
FWCI
20.73
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.