ArticleToxicology and applied pharmacology2010
Cr(VI) induces mitochondrial-mediated and caspase-dependent apoptosis through reactive oxygen species-mediated p53 activation in JB6 Cl41 cells.
Article in Toxicology and applied pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 101 citations in OpenAlex.
- Long-Term Impact of Cr(VI) Exposure in Swiss Albino Mice: ROS-Driven Modulation of Autophagy and Cellular Fate.Biological trace element research · 2025Article
- Environmental Insults to Glucose Metabolism: The Role of Pollutants in Insulin Resistance.International journal of molecular sciences · 2025Review
- Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Review
- Marine Staurosporine Analogues: Activity and Target Identification in Triple-Negative Breast Cancer.Marine drugs · 2024Article
- Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria.International journal of molecular sciences · 2023Review
- Neuroprotective effect of tangeretin against chromium-induced acute brain injury in rats: targeting Nrf2 signaling pathway, inflammatory mediators, and apoptosis.Inflammopharmacology · 2023Article
- Article
- Hexavalent-Chromium-Induced Oxidative Stress and the Protective Role of Antioxidants against Cellular Toxicity.Antioxidants (Basel, Switzerland) · 2022Review
- Selenium Alleviates Chromium(VI)-Induced Ileum Damage and Cecal Microbial Disturbances in Mice.Biological trace element research · 2022Article
- T63 induces apoptosis in nasopharyngeal carcinoma cells through mitochondrial dysfunction and inhibition of PI3K/Akt signaling pathway.Translational cancer research · 2020Article
- Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study.Medical science monitor basic research · 2018Article
- Roles of ROS, Nrf2, and autophagy in cadmium-carcinogenesis and its prevention by sulforaphane.Toxicology and applied pharmacology · 2018Article
- Grapevine VpPR10.1 functions in resistance to Plasmopara viticola through triggering a cell death-like defence response by interacting with VpVDAC3.Plant biotechnology journal · 2018Article
- Ascorbic acid protects male rat brain from oral potassium dichromate-induced oxdative DNA damage and apoptotic changes: the expression patterns of caspase-3, P 53, Bax, and Bcl-2 genes.Environmental science and pollution research international · 2018Article
- Mitochondria targeting by environmental stressors: Implications for redox cellular signaling.Toxicology · 2017Review
- Protection from Cr(VI)-induced malignant cell transformation and tumorigenesis of Cr(VI)-transformed cells by luteolin through Nrf2 signaling.Toxicology and applied pharmacology · 2017Article
- Mitochondrial Biogenesis in Response to Chromium (VI) Toxicity in Human Liver Cells.International journal of molecular sciences · 2017Article
- Environmental Presence of Hexavalent but Not Trivalent Chromium Causes Neurotoxicity in Exposed Drosophila melanogaster.Molecular neurobiology · 2017Article
- Different roles of ROS and Nrf2 in Cr(VI)-induced inflammatory responses in normal and Cr(VI)-transformed cells.Toxicology and applied pharmacology · 2016Article
- Inhibitory effects and molecular mechanisms of tetrahydrocurcumin against human breast cancer MCF-7 cells.Food & nutrition research · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Cr(VI) compounds are known to cause serious toxic and carcinogenic effects. Cr(VI) exposure can lead to a severe damage to the skin, but the mechanisms involved in the Cr(VI)-mediated toxicity in the skin are unclear. The present study examined whether Cr(VI) induces cell death by apoptosis or necrosis using mouse skin epidermal cell line, JB6 Cl41 cells. We also investigated the cellular mechanisms of Cr(VI)-induced cell death. This study showed that Cr(VI) induced apoptotic cell death in a dose-dependent manner, as demonstrated by the appearance of cell shrinkage, the migration of cells into the sub-G1 phase, the increase of Annexin V positively stained cells, and the formation of nuclear DNA ladders. Cr(VI) treatment resulted in the increases of mitochondrial membrane depolarization and caspases activation. Electron spin resonance (ESR) and fluorescence analysis revealed that Cr(VI) increased intracellular levels of reactive oxygen species (ROS) such as hydrogen peroxide and superoxide anion radical in dose-dependent manner. Blockage of p53 by si-RNA transfection suppressed mitochondrial changes of Bcl-2 family composition, mitochondrial membrane depolarization, caspase activation and PARP cleavage, leading to the inhibition of Cr(VI)-induced apoptosis. Further, catalase treatment prevented p53 phosphorylation stimulated by Cr(VI) with the concomitant inhibition of caspase activation. These results suggest that Cr(VI) induced a mitochondrial-mediated and caspase-dependent apoptosis in skin epidermal cells through activation of p53, which are mainly mediated by reactive oxidants generated by the chemical.
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