ArticleScientific reports2017
Immature mice are more susceptible than adult mice to acetaminophen-induced acute liver injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- New Insights into the Diurnal Rhythmicity of Gut Microbiota and Its Crosstalk with Host Circadian Rhythm.Animals : an open access journal from MDPI · 2022Review
- Genetic and pharmacological inhibition of XBP1 protects against APAP hepatotoxicity through the activation of autophagy.Cell death & disease · 2022Article
- Pulmonary implications of acetaminophen exposures independent of hepatic toxicity.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Roles ofOxidative medicine and cellular longevity · 2021Article
- Preliminary Study on Hepatoprotective Effect and Mechanism of (-)-Epigallocatechin-3-gallate against Acetaminophen-induced Liver Injury in Rats.Iranian journal of pharmaceutical research : IJPR · 2021Article
- Weaning Mice and Adult Mice Exhibit Differential Carbon Tetrachloride-Induced Acute Hepatotoxicity.Antioxidants (Basel, Switzerland) · 2020Article
- Role of the Intracellular Sodium Homeostasis in Chemotaxis of Activated Murine Neutrophils.Frontiers in immunology · 2020Article
- Mito-tempo protects against acute liver injury but induces limited secondary apoptosis during the late phase of acetaminophen hepatotoxicity.Archives of toxicology · 2019Article
- Gut microbiota mediates diurnal variation of acetaminophen induced acute liver injury in mice.Journal of hepatology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen (APAP) overdose induces acute liver injury. The aim of the present study was to analyze the difference of susceptibility between immature and adult mice to APAP-induced acute liver injury. Weanling immature and adult mice were injected with APAP (300 mg/kg). As expected, immature mice were more susceptible than adult mice to APAP-induced acute liver injury. APAP-evoked hepatic c-Jun N-terminal kinase phosphorylation was stronger in immature mice than in adult mice. Hepatic receptor-interacting protein (RIP)1 was obviously activated at APAP-exposed immature and adult mice. Interestingly, hepatic RIP3 activation was more obvious in APAP-treated immature mice than adult mice. Although there was no difference on hepatic GSH metabolic enzymes between immature and adult mice, immature mice were more susceptible than adult mice to APAP-induced hepatic GSH depletion. Of interest, immature mice expressed a much higher level of hepatic Cyp2e1 and Cyp3a11 mRNAs than adult mice. Correspondingly, immature mice expressed a higher level of hepatic CYP2E1, the key drug metabolic enzyme that metabolized APAP into the reactive metabolite NAPQI. These results suggest that a higher level of hepatic drug metabolic enzymes in immature mice than adult mice might contribute to the difference of susceptibility to APAP-induced acute liver injury.
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