ArticleScientific reports2016
Cr(VI) induces premature senescence through ROS-mediated p53 pathway in L-02 hepatocytes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026Review
- Decoding Short- and Long-Term Cellular Adaptations to Cr(VI) Exposure Through High-Throughput Transcriptomics.International journal of medical sciences · 2026Article
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Employing a Toxic Aging Coin approach to assess hexavalent chromium (Cr[VI])-induced neurotoxic effects on behavior: Heads for age differences.Toxicology and applied pharmacology · 2024Article
- Activated cGAS/STING signaling elicits endothelial cell senescence in early diabetic retinopathy.JCI insight · 2023Article
- Proteasome inhibitor MG132 enhances the sensitivity of human OSCC cells to cisplatin via a ROS/DNA damage/p53 axis.Experimental and therapeutic medicine · 2023Article
- Among Gerontogens, Heavy Metals Are a Class of Their Own: A Review of the Evidence for Cellular Senescence.Brain sciences · 2023Review
- Inflammatory effects of hexavalent chromium in the lung: A comprehensive review.Toxicology and applied pharmacology · 2022Review
- Oxidative stress-induced premature senescence and aggravated denervated skeletal muscular atrophy by regulating progerin-p53 interaction.Skeletal muscle · 2022Article
- A protocol for rapid construction of senescent cells.Frontiers in integrative neuroscience · 2022Article
- Regulation of Cr(VI)-Induced Premature Senescence in L02 Hepatocytes by ROS-CaOxidative medicine and cellular longevity · 2022Article
- Current understanding of hexavalent chromium [Cr(VI)] neurotoxicity and new perspectives.Environment international · 2022Review
- CDK5RAP2 loss-of-function causes premature cell senescence via the GSK3β/β-catenin-WIP1 pathway.Cell death & disease · 2021Article
- Chromium (VI)-Induced Alterations in Physio-Chemical Parameters, Yield, and Yield Characteristics in Two Cultivars of Mungbean (Frontiers in plant science · 2021Article
- Cellular and molecular mechanisms of xenobiotics-induced premature senescence.Toxicology research · 2020Review
- Protection of the Retinal Ganglion Cells: Intravitreal Injection of Resveratrol in Mouse Model of Ocular Hypertension.Investigative ophthalmology & visual science · 2020Article
- Chromium-Induced Reactive Oxygen Species Accumulation by Altering the Enzymatic Antioxidant System and Associated Cytotoxic, Genotoxic, Ultrastructural, and Photosynthetic Changes in Plants.International journal of molecular sciences · 2020Review
- Acute myeloid leukemia induces protumoral p16INK4a-driven senescence in the bone marrow microenvironment.Blood · 2019Article
- Redox control of senescence and age-related disease.Redox biology · 2017Review
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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
Hexavalent Chromium [Cr(VI)], which can be found of various uses in industries such as metallurgy and textile dying, can cause a number of human disease including inflammation and cancer. Unlike previous research that focused on Cr(VI)-induced oxidative damage and apoptosis, this study placed emphasis on premature senescence that can be induced by low-dose and long-term Cr(VI) exposure. We found Cr(VI) induced premature senescence in L-02 hepatocytes, as confirmed by increase in senescence associated-β-galactosidase (SA-β-Gal) activity. Cr(VI) stabilized p53 through phosphorylation at Ser15 and increased expression of p53-transcriptional target p21. Mechanism study revealed Cr(VI) targeted and inhibited mitochondrial respiratory chain complex (MRCC) I and II to enhance reactive oxygen species (ROS) production. By applying antioxidant Trolox, we also confirmed that ROS mediated p53 activation. A tetracycline-inducible lentiviral expression system containing shRNA to p53 was used to knockout p53. We found p53 could inhibit pro-survival genes B-cell lymphoma-2 (Bcl-2), myeloid leukemia-1 (Mcl-1) and S phase related cell cycle proteins cyclin-dependent kinase 2 (CDK2), Cyclin E to induce premature senescence, and the functional role of ROS in Cr(VI)-induced premature senescence is depend on p53. The results suggest that Cr(VI) has a role in premature senescence by promoting ROS-dependent p53 activation in L-02 hepatocytes.
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