ArticleExperimental biology and medicine (Maywood, N.J.)2015
Comparative evaluation of N-acetylcysteine and N-acetylcysteineamide in acetaminophen-induced hepatotoxicity in human hepatoma HepaRG cells.
Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Redefining the role of the thiol-based agentRSC medicinal chemistry · 2026Review
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- IL-37 ameliorates acetaminophen-induced acute liver injury by limiting MAPK/NFκB signaling-mediated liver inflammation.Scientific reports · 2025Article
- Minimizing Oxidative Stress in the Lens: Alternative Measures for Elevating Glutathione in the Lens to Protect against Cataract.Antioxidants (Basel, Switzerland) · 2024Review
- Fructose as a novel nutraceutical for acetaminophen (APAP)-induced hepatotoxicity.Metabolism and target organ damage · 2023Article
- Malting barley carbon dots-mediated oxidative stress promotes insulin resistance in mice via NF-κB pathway and MAPK cascade.Journal of nanobiotechnology · 2022Article
- The Protective Effects of Ganoderic Acids fromFoods (Basel, Switzerland) · 2022Article
- Thiol antioxidants protect human lens epithelial (HLE B-3) cells againstBiochemistry and biophysics reports · 2022Article
- Post-treatment with glycyrrhizin can attenuate hepatic mitochondrial damage induced by acetaminophen in mice.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Novel Therapies for the Treatment of Drug-Induced Liver Injury: A Systematic Review.Frontiers in pharmacology · 2021Review
- Medicinal Thiols: Current Status and New Perspectives.Mini reviews in medicinal chemistry · 2020Review
- Silicon dioxide nanoparticles induce insulin resistance through endoplasmic reticulum stress and generation of reactive oxygen species.Particle and fibre toxicology · 2019Article
- γ-glutamylcysteine exhibits anti-inflammatory effects by increasing cellular glutathione level.Redox biology · 2019Article
- Ascorbic acid alters cell fate commitment of human neural progenitors in a WNT/β-catenin/ROS signaling dependent manner.Journal of biomedical science · 2017Article
- MicroRNA regulation of CYP 1A2, CYP3A4 and CYP2E1 expression in acetaminophen toxicity.Scientific reports · 2017Article
- Prevention and reversal of selenite-induced cataracts by N-acetylcysteine amide in Wistar rats.BMC ophthalmology · 2017Article
- Effect of amlodipine, lisinopril and allopurinol on acetaminophen-induced hepatotoxicity in rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2016Article
- A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: Application to acetaminophen.Toxicology and applied pharmacology · 2016Article
- N-Acetylcysteine Amide Protects Against Oxidative Stress-Induced Microparticle Release From Human Retinal Pigment Epithelial Cells.Investigative ophthalmology & visual science · 2016Article
- Experimental models of hepatotoxicity related to acute liver failure.Toxicology and applied pharmacology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen (N-acetyl-p-aminophenol, APAP) is one of the most widely used over-the-counter antipyretic analgesic medications. Despite being safe at therapeutic doses, an accidental or intentional overdose can result in severe hepatotoxicity; a leading cause of drug-induced liver failure in the U.S. Depletion of glutathione (GSH) is implicated as an initiating event in APAP-induced toxicity. N-acetylcysteine (NAC), a GSH precursor, is the only currently approved antidote for an APAP overdose. Unfortunately, fairly high doses and longer treatment times are required due to its poor bioavailability. In addition, oral and intravenous administration of NAC in a hospital setting are laborious and costly. Therefore, we studied the protective effects of N-acetylcysteineamide (NACA), a novel antioxidant, with higher bioavailability and compared it with NAC in APAP-induced hepatotoxicity in a human-relevant in vitro system, HepaRG. Our results indicated that exposure of HepaRG cells to APAP resulted in GSH depletion, reactive oxygen species (ROS) formation, increased lipid peroxidation, mitochondrial dysfunction (assessed by JC-1 fluorescence), and lactate dehydrogenase release. Both NAC and NACA protected against APAP-induced hepatotoxicity by restoring GSH levels, scavenging ROS, inhibiting lipid peroxidation, and preserving mitochondrial membrane potential. However, NACA was better than NAC at combating oxidative stress and protecting against APAP-induced damage. The higher efficiency of NACA in protecting cells against APAP-induced toxicity suggests that NACA can be developed into a promising therapeutic option for treatment of an APAP overdose.
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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.