ArticleBiochemical and biophysical research communications2012
Vα14iNKT cell deficiency prevents acetaminophen-induced acute liver failure by enhancing hepatic glutathione and altering APAP metabolism.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- The potential of curcumin in mitigating acetaminophen-induced liver damage.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Good Cells Go Bad: Immune Dysregulation in the Transition from Acute Liver Injury to Liver Failure After Acetaminophen Overdose.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- A dual role of inflammation in acetaminophen-induced liver injury.Liver research (Beijing, China) · 2023Review
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- Review
- Identification of key genes and infiltrating immune cells among acetaminophen-induced acute liver failure and HBV-associated acute liver failure.Annals of translational medicine · 2022Article
- Molecular pathogenesis of acetaminophen-induced liver injury and its treatment options.Journal of Zhejiang University. Science. B · 2022Review
- Immune-Mediated Drug-Induced Liver Injury: Immunogenetics and Experimental Models.International journal of molecular sciences · 2021Review
- Aedes aegypti mosquito saliva ameliorates acetaminophen-induced liver injury in mice.PloS one · 2021Article
- Natural Killer T Cells in Various Mouse Models of Hepatitis.BioMed research international · 2021Review
- Mechanisms and pathophysiological significance of sterile inflammation during acetaminophen hepatotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Review
- The Beneficial Roles of SIRT1 in Drug-Induced Liver Injury.Oxidative medicine and cellular longevity · 2019Review
- Loss of hypoxia inducible factor-1α aggravates γδ T-cell-mediated inflammation during acetaminophen-induced liver injury.Hepatology communications · 2018Article
- Role of the inflammasome in acetaminophen-induced liver injury and acute liver failure.Journal of hepatology · 2017Review
- The impact of sterile inflammation in acute liver injury.Journal of clinical and translational research · 2017Article
- Xenobiotic and Endobiotic Mediated Interactions Between the Cytochrome P450 System and the Inflammatory Response in the Liver.Advances in pharmacology (San Diego, Calif.) · 2015Review
- Interleukin-4 and acetaminophen hepatotoxicity: a story of conflicting results and conclusions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Metabolism and disposition of acetaminophen: recent advances in relation to hepatotoxicity and diagnosis.Pharmaceutical research · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Acetaminophen (APAP) overdose is widely regarded as a major cause of acute liver failure in the United States. Intentional or accidental overdose of APAP in man or rodent elicits direct hepatocellular injury that is accompanied by hepatic depletion of the antioxidant, glutathione (GSH). In recent years, the innate immune response has also been shown to promote the development of APAP hepatotoxicity via indirect liver damage. In the present study, we demonstrate that Jα18(-/-) mice, which are selectively deficient in the innate immune T cell, Vα14iNKT cells, were resistant to APAP hepatotoxicity relative to WT mice as reflected by biochemical and histological liver injury markers. In parallel, improvement in the biochemical and histological parameters of liver injury in Jα18(-/-) mice was associated with a significant increase in hepatic levels of GSH, which detoxified APAP metabolites to attenuate hepatic oxidative stress, liver injury and necrosis. Notably, the protective effect of hepatic GSH during Vα14iNKT cells deficiency was demonstrated by its depletion in Jα18(-/-) mice using dl-buthionine-[S,R]-sulfoximine which exacerbated hepatic oxidative and nitrosative stress as well as liver necrosis and caused mice mortality. Extraordinarily, APAP metabolism in Jα18(-/-) mice was altered in favor of hepatic GSH conjugates and decreased glucuronide conjugates. In summary, we reveal a novel finding establishing a unique association between hepatic innate immunity and GSH levels in altering APAP metabolism to suppress liver injury and necrosis during Vα14iNKT cells deficiency in Jα18(-/-) mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.