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Metabolic Reprogramming Triggered by Fluoride in U-87 Glioblastoma Cells: Implications for Tumor Progression?
Wojciech Żwierełło1, Agnieszka Maruszewska2, Marta Skórka-Majewicz1
1Department of Medical Chemistry, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Physiologically high fluoride concentrations increase oxidative stress and inflammation in glioblastoma cells. This study reveals how fluoride impacts reactive oxygen species (ROS) and inflammatory cytokines, potentially affecting glioma progression.
Area of Science:
- Neuro-oncology
- Toxicology
- Cell Biology
Background:
- Chronic inflammation is characteristic of brain tumors, particularly gliomas.
- The role of fluoride in inducing metabolic disturbances and oxidative stress in aggressive glioma cells is not well understood.
Purpose of the Study:
- To investigate the effects of physiologically elevated fluoride concentrations on oxidative stress and pro-inflammatory responses in U-87 human glioblastoma cells.
Main Methods:
- U-87 glioblastoma cells were exposed to varying concentrations of sodium fluoride (NaF) (0.1-10 µM) for short-term and long-term periods.
- Analysis included assessment of reactive oxygen species (ROS) levels, antioxidant defenses, and key cytokines/chemokines in cells and culture medium.
Main Results:
- Fluoride exposure at physiologically relevant concentrations significantly increased ROS levels in U-87 cells.
- Elevated levels of pro-inflammatory cytokines, including IL-6 and TNF-α, were observed, correlating with fluoride concentration and exposure duration.
Conclusions:
- Fluoride compounds can induce oxidative stress by generating ROS and impairing antioxidant defenses in glioblastoma cells.
- This disruption contributes to the initiation and progression of inflammatory states within the tumor microenvironment.
- Prolonged NaF exposure may trigger adaptive responses in U-87 glioblastoma cells.
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