ReviewFrontiers in veterinary science2022
Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism.
Review in Frontiers in veterinary science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Fluoride as a Modifier of Metallome Homeostasis: A Systematic Review of Animal Studies.Basic & clinical pharmacology & toxicology · 2026Pooled it
- An overview of fluoride stress: physiological and biochemical responses of plants.Plant signaling & behavior · 2026Review
- Chronic Fluoride Exposure Disrupts Calcium-Dependent Neurodevelopmental Signalling and Brain Proteomic Architecture: Multi-Target Modulation by Naringin.Biological trace element research · 2026Article
- Microplastic-Induced DRP1-BAX Interaction Contributes to Mitochondrial Apoptosis in Lung Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Article
- Fluoride Damages the Ovary by Inhibiting LKB1-AMPK Signaling to Promote Mitochondrial Injury-Induced Inflammation and Oxidative Stress.Biological trace element research · 2026Article
- Melatonin attenuates fluoride-induced neurotoxicity and cognitive dysfunction through modulation of oxidative stress, neuroinflammation, and SIRT1 signaling in Wistar rats.Veterinary world · 2026Article
- The Effects of Exercise on Fluorosis: A Comprehensive Multisystem Review.Veterinary sciences · 2026Review
- Benchmark Approach to Unravel Fluoride Toxicity: Liver and Kidney Disruptions in Subacutely Exposed Rats.Journal of xenobiotics · 2026Article
- Article
- Intersecting and intricacy pathways of Vitamin D and Fluoride in obesity.Journal of family medicine and primary care · 2025Article
- The Role of SIRT1-BDNF Signaling Pathway in Fluoride-Induced Toxicity for Glial BV-2 Cells.Biological trace element research · 2025Article
- Fluoride: Toxicity, Mechanism and Role of Bioremediation in Detoxification.Current microbiology · 2025Review
- In-vitro-cytotoxicity of cariostatic agents based on fluorides and lanthanide salts in L-929 fibroblasts.Clinical oral investigations · 2025Article
- Dose-dependent developmental fluoride exposure leads to neurotoxicity and impairs excitatory synapse development.Archives of toxicology · 2025Article
- Comparative safety profile of levofloxacin versus moxifloxacin in first-line tuberculosis therapy: a pharmacovigilance study of the FAERS database.Frontiers in pharmacology · 2025Article
- The MAPK/ERK signaling pathway involved in Raddeanin A induces apoptosis via the mitochondrial pathway and G2 phase arrest in multiple myeloma.Scientific reports · 2024Article
- Fluoride-Induced Mitochondrial Dysfunction and Approaches for Its Intervention.Biological trace element research · 2024Review
- Elevated Level of PINK1/Parkin-Mediated Mitophagy Pathway Involved to the Inhibited Activity of Mitochondrial Superoxide Dismutase in Rat Brains and Primary Hippocampal Neurons Exposed to High Level of Fluoride.Biological trace element research · 2024Article
- Inhibitory effects of NaF on mitochondrial energy generation in human plateletsFrontiers in toxicology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.
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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.