ArticleBiological trace element research2021
Fluoride Can Damage the Spleen of Mice by Perturbing Th1/Th2 Cell Balance.
Article in Biological trace element research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Exposure to Fluoride During Pregnancy and Lactation Induces Metabolic Imbalance in Pancreas: A Toxicological Insight Using the Rat Model.International journal of molecular sciences · 2025Article
- Article
- Progress in research on the role of fluoride in immune damage.Frontiers in immunology · 2024Review
- Molecular basis of fluoride toxicities: Beyond benefits and implications in human disorders.Genes & diseases · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
To investigate the mechanism of fluoride-induced splenic toxicity, 0, 25, 50, and 100 mg/L sodium fluoride (NaF) were administered in male mice via drinking water for 90 days. After NaF treatment, the histological structure of the spleen, the proportion of helper T 1 cell (Th1) and helper T 2 cell (Th2), and the relative expression levels of cytokines and T-bet and GATA3 were analyzed. The results showed that 50 and 100 mg/L NaF consumption can change the normal structure of mouse spleen and the proportion of Th1/Th2 cells. It also decreased the mRNA expression levels of IL-2, INF-γ, and TGF-β, but increased the levels of IL-4, IL-6, and IL-10. Importantly, fluoride increased the protein expression of GATA3 but decreased the expression of T-bet. Our findings indicate that superfluous fluoride intake damages the balance of Th1/Th2 cells by changing the levels of T-bet and GATA3 in the spleen, and further changes the expression of Th1/Th2 cell-related cytokines in the spleen microenvironment, eventually leading to spleen injury.
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Registered trials
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