ReviewBiological trace element research2024
Fluoride-Induced Mitochondrial Dysfunction and Approaches for Its Intervention.
Review in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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
6 citing papers in PubMed, 11 citations in OpenAlex.
- An overview of fluoride stress: physiological and biochemical responses of plants.Plant signaling & behavior · 2026Review
- Bioaccumulation and nutritional impact of fluoride in Pleurotus ostreatus and Pleurotus djamor with human health risk assessment.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Fluoride Damages the Ovary by Inhibiting LKB1-AMPK Signaling to Promote Mitochondrial Injury-Induced Inflammation and Oxidative Stress.Biological trace element research · 2026Article
- Cytotoxicity and Genotoxicity of Fluoride Toothpastes in Buccal Cells.Acta stomatologica Croatica · 2026Article
- Benchmark Approach to Unravel Fluoride Toxicity: Liver and Kidney Disruptions in Subacutely Exposed Rats.Journal of xenobiotics · 2026Article
- Effect of naringin on sodium fluoride‑induced neurobehavioral deficits in Wistar rats.Biomedical reports · 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fluoride is present everywhere in nature. The primary way that individuals are exposed to fluoride is by drinking water. It's interesting to note that while low fluoride levels are good for bone and tooth growth, prolonged fluoride exposure is bad for human health. Additionally, preclinical studies link oxidative stress, inflammation, and programmed cell death to fluoride toxicity. Moreover, mitochondria play a crucial role in the production of reactive oxygen species (ROS). On the other hand, little is known about fluoride's impact on mitophagy, biogenesis, and mitochondrial dynamics. These actions control the growth, composition, and organisation of mitochondria, and the purification of mitochondrial DNA helps to inhibit the production of reactive oxygen species and the release of cytochrome c, which enables cells to survive the effects of fluoride poisoning. In this review, we discuss the different pathways involved in mitochondrial toxicity and dysfunction induced by fluoride. For therapeutic approaches, we discussed different phytochemical and pharmacological agents which reduce the toxicity of fluoride via maintained by imbalanced cellular processes, mitochondrial dynamics, and scavenging the ROS.
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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.