ArticleToxicological sciences : an official journal of the Society of Toxicology2011
The cytoprotective effect of N-acetyl-L-cysteine against ROS-induced cytotoxicity is independent of its ability to enhance glutathione synthesis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 128 citations in OpenAlex.
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- Enhancing Escin's Therapeutic Efficacy: A Nanoformulation Approach for Improved Stability and Anticancer Potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Potential Anti-Inflammatory Effects of Gintonin-Enriched Fraction in TNF-α-Stimulated Keratinocytes.International journal of molecular sciences · 2025Article
- Aniline TFPA enhances camptothecin-induced anti-NSCLC by modulating oxidative stress and impairing autophagy.Cancer cell international · 2025Article
- Synergistic protective effects of TCM formula NRICM102 andFrontiers in pharmacology · 2025Article
- Neuropsychiatric Manifestations of COVID-19 Disease and Post COVID Syndrome: The Role of N-acetylcysteine and Acetyl-L-carnitine.Current neuropharmacology · 2025Review
- Mitochondrial Dysfunction in Systemic Lupus Erythematosus: Insights and Therapeutic Potential.Diseases (Basel, Switzerland) · 2024Review
- The presence of cancer-associated fibroblast in breast cavity side margins is in correlation with the expression of oncoproteins by adjacent epithelial cells: a new era in cancerous potential.Journal of cancer research and clinical oncology · 2024Article
- Thioredoxin is a metabolic rheostat controlling regulatory B cells.Nature immunology · 2024Article
- Reactive oxygen species in biological systems: Pathways, associated diseases, and potential inhibitors-A review.Food science & nutrition · 2024Review
- Oxidative stress in the brain-lung crosstalk: cellular and molecular perspectives.Frontiers in aging neuroscience · 2024Review
- Role of CD14+ monocyte-derived oxidised mitochondrial DNA in the inflammatory interferon type 1 signature in juvenile dermatomyositis.Annals of the rheumatic diseases · 2023Article
- A novel algicidal properties of fermentation products fromFrontiers in microbiology · 2023Article
- Renoprotective effect of N-acetylcystein and vitamin E in bisphenol A-induced rat nephrotoxicity; Modulators of Nrf2/ NF-κB and ROS signaling pathway.Acta bio-medica : Atenei Parmensis · 2022Article
- Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells.Investigative ophthalmology & visual science · 2022Article
- Cystine reduces mitochondrial dysfunction in C2C12 myotubes under moderate oxidative stress induced by HAmino acids · 2022Article
- Single Dose of N-Acetylcysteine in Local Anesthesia Increases Expression of HIF1α, MAPK1, TGFβ1 and Growth Factors in Rat Wound Healing.International journal of molecular sciences · 2021Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
2,3,5-Tris(glutathion-S-yl)-hydroquinone (TGHQ), a metabolite of hydroquinone, is toxic to renal proximal tubule epithelial cells. TGHQ retains the ability to redox cycle and create an oxidative stress. To assist in elucidating the contribution of reactive oxygen species (ROS) to TGHQ-induced toxicity, we determined whether the antioxidant, N-acetyl-L-cysteine (NAC), could protect human kidney proximal tubule epithelial cells (HK-2 cell line) against TGHQ-induced toxicity. NAC provided remarkable protection against TGHQ-induced toxicity to HK-2 cells. NAC almost completely inhibited TGHQ-induced cell death, mitochondrial membrane potential collapse, as well as ROS production. NAC also attenuated TGHQ-induced DNA damage and the subsequent activation of poly (ADP-ribose) polymerase and ATP depletion. Moreover, NAC significantly attenuated c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinase phosphorylation induced by TGHQ. In contrast, NAC itself markedly increased extracellular regulated kinase1/2 (ERK1/2) activation, and the upstream mitogen-activated protein/extracellular signal-regulated kinase kinase inhibitor, PD-98059, only partially inhibited this activation, suggesting that NAC can directly activate ERK1/2 activity. However, although NAC is frequently utilized as a glutathione (GSH) precursor, the cytoprotection afforded by NAC in HK-2 cells was not a consequence of increased GSH levels. We speculate that NAC exerts its protective effect in part by directly scavenging ROS and in part via ERK1/2 activation.
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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.