ArticleOxidative medicine and cellular longevity2017
Arsenite Effects on Mitochondrial Bioenergetics in Human and Mouse Primary Hepatocytes Follow a Nonlinear Dose Response.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Positive Association of Cardiovascular Disease (CVD) with Chronic Exposure to Drinking Water Arsenic (As) at Concentrations below the WHO Provisional Guideline Value: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2020Pooled it
- Alzheimer's Disease Risk AllelebioRxiv : the preprint server for biology · 2026Article
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- Exposure of Primary Human Skin Fibroblasts to Carbon Dioxide-Containing Solution Significantly Reduces TGF-β-Induced Myofibroblast Differentiation In Vitro.International journal of molecular sciences · 2024Article
- Proteomic-miRNA Biomics Profile Reveals 2D Cultures of Human iPSC-Derived Neural Progenitor Cells More Sensitive than 3D Spheroid System Against the Experimental Exposure to Arsenic.Molecular neurobiology · 2024Article
- Exposure of Bladder Cancer Cells to Blue Light (λ = 453 nm) in the Presence of Riboflavin Synergistically Enhances the Cytotoxic Efficiency of Gemcitabine.International journal of molecular sciences · 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
- Mitochondria in the Spotlight:Cells · 2023Review
- Effects of Sodium Arsenite on the Myocardial Differentiation in Mouse Embryonic Bodies.Toxics · 2023Article
- Mitochondrial ROS, ER Stress, and Nrf2 Crosstalk in the Regulation of Mitochondrial Apoptosis Induced by Arsenite.Antioxidants (Basel, Switzerland) · 2022Review
- Role of tubular epithelial arginase-II in renal inflammaging.NPJ aging and mechanisms of disease · 2021Article
- G3BP1-linked mRNA partitioning supports selective protein synthesis in response to oxidative stress.Nucleic acids research · 2020Article
- Non-redox cycling mechanisms of oxidative stress induced by PM metals.Free radical biology & medicine · 2020Review
- Alternol eliminates excessive ATP production by disturbing Krebs cycle in prostate cancer.The Prostate · 2019Article
- Hypoxia Enhances Endothelial Intercellular Adhesion Molecule 1 Protein Level Through Upregulation of Arginase Type II and Mitochondrial Oxidative Stress.Frontiers in physiology · 2019Article
- Preliminary observations of mitochondrial dysfunction in Prader-Willi syndrome.American journal of medical genetics. Part A · 2018Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Arsenite is a known carcinogen and its exposure has been implicated in a variety of noncarcinogenic health concerns. Increased oxidative stress is thought to be the primary cause of arsenite toxicity and the toxic effect is thought to be linear with detrimental effects reported at all concentrations of arsenite. But the paradigm of linear dose response in arsenite toxicity is shifting. In the present study we demonstrate that arsenite effects on mitochondrial respiration in primary hepatocytes follow a nonlinear dose response. In vitro exposure of primary hepatocytes to an environmentally relevant, moderate level of arsenite results in increased oxidant production that appears to arise from changes in the expression and activity of respiratory Complex I of the mitochondrial proton circuit. In primary hepatocytes the excess oxidant production appears to elicit adaptive responses that promote resistance to oxidative stress and a propensity to increased proliferation. Taken together, these results suggest a nonlinear dose-response characteristic of arsenite with low-dose arsenite promoting adaptive responses in a process known as mitohormesis, with transient increase in ROS levels acting as transducers of arsenite-induced mitohormesis.
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