ArticleToxicology and applied pharmacology2013
Acetaminophen-induced acute liver injury in HCV transgenic mice.
Article in Toxicology and applied pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Antimicrobial potentials and challenges of paracetamol: A comprehensive reassessment based on database reports.Pharmaceutical science advances · 2025Review
- International outbreak of acute pediatric hepatitis: Was acetaminophen the missing link?Pediatric investigation · 2024Article
- Review
- Article
- Hepatitis C virus structural proteins can exacerbate or ameliorate acetaminophen-induced liver injury in mice.Archives of toxicology · 2015Article
- Acute and chronic effects of IL-22 on acetaminophen-induced liver injury.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Role of the ¹³C-methacetin breath test in the assessment of acute liver injury in a rat model.World journal of gastroenterology · 2014Article
- Mechanisms of HCV-induced liver cancer: what did we learn from in vitro and animal studies?Cancer letters · 2014Review
- Fatal fulminant hepatitis E associated with autoimmune hepatitis and excessive paracetamol intake in Southeastern France.Journal of clinical microbiology · 2014Article
- Fluxomics of the eastern oyster for environmental stress studies.Metabolites · 2014Article
- Early Risk Factors of Moderate/Severe Hepatotoxicity After Suicide Attempts With Acetaminophen in 11- to 15-Year-Old Children.Global pediatric health · 2014Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
The exact etiology of clinical cases of acute liver failure is difficult to ascertain and it is likely that various co-morbidity factors play a role. For example, epidemiological evidence suggests that coexistent hepatitis C virus (HCV) infection increased the risk of acetaminophen-induced acute liver injury, and was associated with an increased risk of progression to acute liver failure. However, little is known about possible mechanisms of enhanced acetaminophen hepatotoxicity in HCV-infected subjects. In this study, we tested a hypothesis that HCV-Tg mice may be more susceptible to acetaminophen hepatotoxicity, and also evaluated the mechanisms of acetaminophen-induced liver damage in wild type and HCV-Tg mice expressing core, E1 and E2 proteins. Male mice were treated with a single dose of acetaminophen (300 or 500 mg/kg in fed animals; or 200 mg/kg in fasted animals; i.g.) and liver and serum endpoints were evaluated at 4 and 24h after dosing. Our results suggest that in fed mice, liver toxicity in HCV-Tg mice is not markedly exaggerated as compared to the wild-type mice. In fasted mice, greater liver injury was observed in HCV-Tg mice. In fed mice dosed with 300 mg/kg acetaminophen, we observed that liver mitochondria in HCV-Tg mice exhibited signs of dysfunction showing the potential mechanism for increased susceptibility.
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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.