ArticleChemico-biological interactions2015
Reactive oxygen species and c-Jun N-terminal kinases contribute to TEMPO-induced apoptosis in L5178Y cells.
Article in Chemico-biological interactions, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- The role of trace N-Oxyl compounds as redox mediator in enhancing antiviral ribavirin elimination in UV/Chlorine process.Applied catalysis. B, Environmental · 2022Article
- Actein contributes to black cohosh extract-induced genotoxicity in human TK6 cells.Journal of applied toxicology : JAT · 2022Article
- Genotoxicity evaluation using primary hepatocytes isolated from rhesus macaque (Macaca mulatta).Toxicology · 2021Article
- Mechanistic Evaluation of Black Cohosh Extract-Induced Genotoxicity in Human Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Glucocorticoids induce femoral head necrosis in rats through the ROS/JNK/c-Jun pathway.FEBS open bio · 2021Article
- Size-Dependent Cytotoxicity and Reactive Oxygen Species of Cerium Oxide Nanoparticles in Human Retinal Pigment Epithelia Cells.International journal of nanomedicine · 2021Article
- F1012-2 Induced ROS-Mediated DNA Damage Response through Activation of MAPK Pathway in Triple-Negative Breast Cancer.BioMed research international · 2021Article
- Evaluation of pyrrolizidine alkaloid-induced genotoxicity using metabolically competent TK6 cell lines.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Article
- Abamectin induces cytotoxicity via the ROS, JNK, and ATM/ATR pathways.Environmental science and pollution research international · 2020Article
- Benchmark Dose Modeling ofToxicological research · 2018Review
- DNA damage-induced apoptosis and mitogen-activated protein kinase pathway contribute to the toxicity of dronedarone in hepatic cells.Environmental and molecular mutagenesis · 2018Article
- Comparative Genotoxicity of TEMPO and 3 of Its Derivatives in Mouse Lymphoma Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- ROS generation and JNK activation contribute to 4-methoxy-TEMPO-induced cytotoxicity, autophagy, and DNA damage in HepG2 cells.Archives of toxicology · 2018Article
- Oxidative stress regulates mitogen‑activated protein kinases and c‑Jun activation involved in heat stress and lipopolysaccharide‑induced intestinal epithelial cell apoptosis.Molecular medicine reports · 2017Article
- Activation of the Nrf2 signaling pathway in usnic acid-induced toxicity in HepG2 cells.Archives of toxicology · 2017Article
- Oblongifolin C and guttiferone K extracted from Garcinia yunnanensis fruit synergistically induce apoptosis in human colorectal cancer cells in vitro.Acta pharmacologica Sinica · 2017Article
- BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells.Veterinary research · 2016Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
The biological consequences of exposure to piperidine nitroxides is a concern, given their widespread use in manufacturing processes and their potential use in clinical applications. Our previous study reported that TEMPO (2,2,6,6-tetramethylpiperidine-1-oxyl), a low molecular weight free radical, possesses pro-oxidative activity in L5178Y cells. In this study, we investigated and characterized the role of reactive oxygen species (ROS) in TEMPO-induced toxicity in L5178Y cells. We found that TEMPO induced time- and concentration-dependent intracellular ROS production and glutathione depletion. TEMPO also induced apoptosis as demonstrated by increased caspase-3/7 activity, an increased proportion of annexin V stained cells, and decreased expression of anti-apoptotic proteins including Bcl-2, Bcl-xL and Mcl-1. N-acetylcysteine, a ROS scavenger, attenuated the ROS production and apoptosis induced by TEMPO. Moreover, Western blot analyses revealed that TEMPO activated γ-H2A.X, a hallmark of DNA damage, and c-Jun N-terminal kinases (JNK), a key member in the mitogen-activated protein kinase (MAPK) signaling pathway. Addition of SP600125, a JNK-specific inhibitor, blocked TEMPO-mediated JNK phosphorylation and also attenuated TEMPO-induced apoptosis. These findings indicate that both ROS production and JNK activation are involved in TEMPO-induced apoptosis, and may contribute to the toxicity of TEMPO in L5178Y cells.
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