ArticleOncoTargets and therapy2013
Arsenic trioxide-mediated oxidative stress and genotoxicity in human hepatocellular carcinoma cells.
Article in OncoTargets and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Short-term actions of arsenic trioxide on metabolic fluxes in the isolated perfused rat liver.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Arsenic Trioxide Underpins Delayed Neuroinflammation and Impaired Synaptic Integrity involving Integrative Stress Response Signaling.bioRxiv : the preprint server for biology · 2025Article
- Multiple roles of arsenic compounds in phase separation and membraneless organelles formation determine their therapeutic efficacy in tumors.Journal of pharmaceutical analysis · 2024Review
- Arsenic and Human Health: Genotoxicity, Epigenomic Effects, and Cancer Signaling.Biological trace element research · 2022Review
- Melatonin: a pleiotropic hormone as a novel potent therapeutic candidate in arsenic toxicity.Molecular biology reports · 2021Review
- p62-containing, proteolytically active nuclear condensates, increase the efficiency of the ubiquitin-proteasome system.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation.Frontiers in public health · 2020Review
- Inhibition of FEN1 Increases Arsenic Trioxide-Induced ROS Accumulation and Cell Death: Novel Therapeutic Potential for Triple Negative Breast Cancer.Frontiers in oncology · 2020Article
- Risk assessment of low arsenic exposure using biomarkers of oxidative and genotoxic stress in a piscine model.Ecotoxicology (London, England) · 2019Article
- Association of Vitamin BProbiotics and antimicrobial proteins · 2019Article
- Hepatic Arterial Chemoembolization With Arsenic Trioxide Eluting CalliSpheres Microspheres Versus Lipiodol Emulsion: Pharmacokinetics And Intratumoral Concentration In A Rabbit Liver Tumor Model.Cancer management and research · 2019Article
- Effects of Proanthocyanidins on Arsenic Methylation Metabolism and Efflux in Human Hepatocytes L-02.BioMed research international · 2019Article
- Trisenox induces cytotoxicity through phosphorylation of mitogen-activated protein kinase molecules in acute leukemia cells.Journal of biochemical and molecular toxicology · 2018Article
- Substantial Evidences Indicate That Inorganic Arsenic Is a Genotoxic Carcinogen: a Review.Toxicological research · 2018Review
- Low dosage of arsenic trioxide (AsJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018Article
- Mitochondrial toxicity of organic arsenicals: membrane permeability transition pore opening and respiratory dysfunction.Toxicology research · 2018Article
- Low-level arsenic causes proteotoxic stress and not oxidative stress.Toxicology and applied pharmacology · 2018Article
- The consequence of NAC on sodium arsenite-induced uterine oxidative stress.Toxicology reports · 2018Article
- Low dosage of arsenic trioxide inhibits vasculogenic mimicry in hepatoblastoma without cell apoptosis.Molecular medicine reports · 2018Article
- Arsenic trioxide induces ROS activity and DNA damage, leading to G0/G1 extension in skin fibroblasts through the ATM-ATR-associated Chk pathway.Environmental science and pollution research international · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundArsenic is a ubiquitous environmental toxicant, and abnormalities of the skin, lung, kidney, and liver are the most common outcomes of long-term arsenic exposure. This study was designed to investigate the possible mechanisms of genotoxicity induced by arsenic trioxide in human hepatocellular carcinoma cells. METHODS AND
resultsA mild cytotoxic response of arsenic trioxide was observed in human hepatocellular carcinoma cells, as evident by (3-(4,5-dimethyl thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide) and lactate dehydrogenase assays after 24 and 48 hours of exposure. Arsenic trioxide elicited a significant (P < 0.01) reduction in glutathione (15.67% and 26.52%), with a concomitant increase in malondialdehyde level (67.80% and 72.25%; P < 0.01), superoxide dismutase (76.42% and 81.09%; P < 0.01), catalase (73.33% and 76.47%; P < 0.01), and reactive oxygen species generation (44.04% and 56.14%; P < 0.01) after 24 and 48 hours of exposure, respectively. Statistically significant (P < 0.01) induction of DNA damage was observed by the comet assay in cells exposed to arsenic trioxide. It was also observed that apoptosis occurred through activation of caspase-3 and phosphatidylserine externalization in human hepatocellular carcinoma cells exposed to arsenic trioxide.
conclusionThe results demonstrate that arsenic trioxide induces apoptosis and genotoxicity in human hepatocellular carcinoma cells through reactive oxygen species and oxidative stress.
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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.