ArticleBiological trace element research2023
Fluoride Exposure Provokes Mitochondria-Mediated Apoptosis and Increases Mitophagy in Osteocytes via Increasing ROS Production.
Article in Biological trace element research, 2023. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Fluoride Damages the Ovary by Inhibiting LKB1-AMPK Signaling to Promote Mitochondrial Injury-Induced Inflammation and Oxidative Stress.Biological trace element research · 2026Article
- Integrated network toxicology and molecular docking revealed that 2-ethylhexyldiphenylphosphoric acid induces nephrotoxicity in chickens by activating the ROS/JNK pathway.Poultry science · 2026Article
- Rosa roxburghii Tratt Juice Inhibits Fluoride Exposure-Induced Bone Damage in Male Rats by Regulating the Homeostasis of the ROS/TNF-α/NF-κB Pathway.Biological trace element research · 2026Article
- Thyroid/parathyroid function and fluoride: role of mitochondrial DNA and SOD genetic variations.Journal of endocrinological investigation · 2026Article
- The Effects of Exercise on Fluorosis: A Comprehensive Multisystem Review.Veterinary sciences · 2026Review
- Dehydrocostus lactone induces apoptosis and mitophagy in gastric cancer cells through the ROS-mediated mitochondrial pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pollutant-regulated mitophagy: new perspectives in environmental toxicology.Apoptosis : an international journal on programmed cell death · 2026Review
- Metabolic programming in tooth development: a regulatory network from energy substrates to signaling instructions.Frontiers in cell and developmental biology · 2026Review
- Melatonin Supplementation Relieves Fluoride-Induced Bone Injury via Ion Homeostasis Disorder and PINK1/Parkin-Mediated Mitophagy.Foods (Basel, Switzerland) · 2025Article
- The NRF2/HO- 1 Pathway: a Potential Regulatory Factor in Fluoride-Induced Colonic Injury under Estrogen Deficiency.Biological trace element research · 2025Article
- In-vitro-cytotoxicity of cariostatic agents based on fluorides and lanthanide salts in L-929 fibroblasts.Clinical oral investigations · 2025Article
- Knockdown of SMYD3 by RNA Interference Regulates the Expression of Autophagy-Related Proteins and Inhibits Bone Formation in Fluoride-Exposed Osteoblasts.Biological trace element research · 2025Article
- Interruption of mitochondrial symbiosis is associated with the development of osteoporosis.Frontiers in endocrinology · 2025Review
- Sirtuin 3-activated superoxide dismutase 2 mediates fluoride-induced osteoblastic differentiation in vitro and in vivo by down-regulating reactive oxygen species.Archives of toxicology · 2024Article
- Origin recognition complex 6 overexpression promotes growth of glioma cells.Cell death & disease · 2024Article
- Reactive Oxygen Species-Mediated Mitophagy and Cell Apoptosis are Involved in the Toxicity of Aluminum Chloride Exposure in GC-2spd.Biological trace element research · 2024Article
- The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fluoride is a persistent environmental pollutant, and its excessive intake causes skeletal and dental fluorosis. However, few studies focused on the effects of fluoride on osteocytes, making up over 95% of all bone cells. This study aimed to investigate the effect of fluoride on osteocytes in vitro, as well as explore the underlying mechanisms. CCK-8, LDH assay, fluorescent probes, flow cytometry, and western blotting were performed to examine cell viability, apoptosis, mitochondria changes, reactive oxygen species (ROS) and mitochondrial ROS (mtROS), and protein expressions. Results showed that sodium fluoride (NaF) exposure (4, 8 mmol/L) for 24 h inhibited the cell viability of osteocytes MLO-Y4 and promoted G0/G1 phase arrest and increased cell apoptosis. NaF treatment remarkably caused mitochondria damage, loss of MMP, ATP decrease, Cyto c release, and Bax/Bcl-2 ratio increase and elevated the activity of caspase-9 and caspase-3. Furthermore, NaF significantly upregulated the expressions of LC-3II, PINK1, and Parkin and increased autophagy flux and the accumulation of acidic vacuoles, while the p62 level was downregulated. In addition, NaF exposure triggered the production of intracellular ROS and mtROS and increased malondialdehyde (MDA); but superoxide dismutase (SOD) activity and glutathione (GSH) content were decreased. The scavenger N-acetyl-L-cysteine (NAC) significantly reversed NaF-induced apoptosis and mitophagy, suggesting that ROS is responsible for the mitochondrial-mediated apoptosis and mitophagy induced by NaF exposure. These findings provide in vitro evidence that apoptosis and mitophagy are cellular mechanisms for the toxic effect of fluoride on osteocytes, thereby suggesting the potential role of osteocytes in skeletal and dental fluorosis.
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Registered trials
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.