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Sodium fluoride (NaF) causes toxic effects on splenic development in mice
Ping Kuang1, Huidan Deng1, Hengmin Cui1,2
1College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China.
Oncotarget
|December 22, 2016
Summary
Sodium fluoride (NaF) exposure impairs mouse splenic development, reducing immune cells and impacting humoral and cellular immunity. Cell cycle arrest is identified as the underlying molecular mechanism.
Area of Science:
- Toxicology
- Immunology
- Cell Biology
Background:
- Limited research exists on sodium fluoride's (NaF) toxic effects on splenic development.
- The spleen plays a crucial role in immune responses, filtering blood and housing immune cells.
Purpose of the Study:
- To investigate the toxic effects of NaF on mouse splenic development in vivo.
- To elucidate the molecular mechanisms underlying NaF-induced splenic toxicity.
Main Methods:
- Histopathology, flow cytometry (FCM), western blot (WB), and ELISA were employed.
- 240 ICR mice were exposed to varying doses of NaF (12, 24, 48 mg/kg) or distilled water for 42 days.
- Assessed splenic growth index, lymphocyte populations, immunoglobulin levels, cytokine expression, and cell cycle proteins.
Main Results:
- NaF exposure (≥12 mg/kg) reduced splenic growth index and lymphocyte counts.
- NaF treatment increased G0/G1 phase cell percentage and decreased S phase percentage, indicating cell cycle arrest.
- T and B cell populations, IgA, IgG, and IgM levels were significantly reduced.
- Pro-inflammatory cytokines (IL-2, TGF-β, TNF-α, IFN-γ) and cell cycle proteins (cyclin E/D, CDK2/4) decreased, while IL-10 increased.
Conclusions:
- NaF induces toxic effects on splenic development, impairing both cellular and humoral immunity.
- Cell cycle arrest is the primary molecular mechanism responsible for NaF-induced splenic toxicity.
- These findings highlight the potential risks of NaF exposure on immune system development.
