Żwierełło Wojciech, Maruszewska Agnieszka, Skórka-Majewicz Marta, Wszołek Agata, Gutowska Izabela
Department of Medical Chemistry, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Institute of Biology, University of Szczecin, 71-415 Szczecin, Poland.
Cells. 2025 May 29;14(11):800. doi: 10.3390/cells14110800.
Chronic inflammation is a hallmark of brain tumors, especially gliomas, which exhibit elevated levels of pro-inflammatory mediators within the tumor and its microenvironment. Metabolic disturbances triggered by fluoride as a pro-oxidative agent in glioma cells, known for their high aggressiveness and resistance to therapy-remain poorly understood. Therefore, investigating the impact of physiologically elevated fluoride concentrations on oxidative stress and pro-inflammatory responses in glioma cells represents a relevant and timely research objective.
U-87 human glioblastoma cells were subjected to short-term and long-term exposure to physiologically high concentrations of NaF (0.1-10 µM). Both the cells and the culture medium were analyzed. We assessed levels of reactive oxygen species (ROS), antioxidant defenses, and a panel of cytokines and chemokines.
Our results demonstrated that oxidative stress and inflammatory conditions in U-87 cells varied with fluoride concentration and exposure time. This led to an increase in ROS levels and key pro-inflammatory cytokines, including IL-6 and TNF-α.
Fluoride compounds can generate ROS and disrupt the antioxidant defense system in U-87 human glioblastoma cells, leading to the initiation and progression of inflammatory states. Furthermore, prolonged exposure to NaF may induce adaptive mechanisms in U-87 cells.
慢性炎症是脑肿瘤尤其是胶质瘤的一个标志，胶质瘤在肿瘤及其微环境中表现出促炎介质水平升高。氟作为胶质瘤细胞中的一种促氧化剂所引发的代谢紊乱，因其高侵袭性和对治疗的抗性而仍未被充分理解。因此，研究生理浓度升高的氟对胶质瘤细胞氧化应激和促炎反应的影响是一个相关且及时的研究目标。
将U - 87人胶质母细胞瘤细胞短期和长期暴露于生理高浓度的NaF（0.1 - 10 μM）。对细胞和培养基都进行了分析。我们评估了活性氧（ROS）水平、抗氧化防御以及一组细胞因子和趋化因子。
我们的结果表明，U - 87细胞中的氧化应激和炎症状况随氟浓度和暴露时间而变化。这导致ROS水平以及关键促炎细胞因子（包括IL - 6和TNF - α）增加。
氟化合物可在U - 87人胶质母细胞瘤细胞中产生ROS并破坏抗氧化防御系统，导致炎症状态的起始和进展。此外，长期暴露于NaF可能会在U - 87细胞中诱导适应性机制。
