title: The Effect of Sodium Fluoride on Cell Apoptosis and the Mechanism of Human Lung BEAS-2B Cells In Vitro.
abstract: Sodium fluoride (NaF) is a source of fluoride ions used in many applications. Previous studies found that NaF suppressed the proliferation of osteoblast MC3T3 E1 cells and induced the apoptosis of chondrocytes. However, little is known about the effects of NaF on human lung BEAS-2B cells. Therefore, we investigated the mode of cell death induced by NaF and its underlying molecular mechanisms. BEAS-2B cells were treated with NaF at concentrations of 0, 0.25, 0.5, 1.0, 2.0, and 4.0 mmol/L. Cell viability decreased and apoptotic cells significantly increased as concentrations of NaF increased over specific periods of time. The IC50of NaF was 1.9 and 0.9 mM after 24 and 48 h, respectively. The rates of apoptosis increased from 4.8 to 37.7% after NaF exposure. HE staining, electron microscopy, and single cell gel electrophoresis revealed that morphological changes of apoptosis increased with exposure concentrations. RT-PCR and Western blotting were used to detect the apoptotic pathways. The expressions of bax, caspase-3, caspase-9, p53, and the cytoplasmic CytC of the NaF groups increased, while bcl-2 and mitochondrial CytC decreased compared with that of the control group (P < 0.05). Further, the fluorescence intensities of ROS in the NaF groups were higher than those in the control group, and the membrane potential of mitochondria in the NaF group was significantly lower than that of the control group (P < 0.05). These findings suggested that NaF induced apoptosis in the BEAS-2B cells through mitochondria-mediated signal pathways. Our study provides the theoretical foundation and experimental basis for exploring the mechanisms of human lung epithelial cell damage and cytotoxicity induced by fluorine.
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Forensic Medicine, Xi'an Jiaotong University, Xi'an, 710000, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Ying
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Xu
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Liping
authors.initials: L
authors.lastname: Shen
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Zhijie
authors.initials: Z
authors.lastname: Mao
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Jingchen
authors.initials: J
authors.lastname: Liang
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Shuangxiang
authors.initials: S
authors.lastname: Lin
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China.|School of Renji, Wenzhou Medical University, Wenzhou, 325035, China.
authors.forename: Xinyan
authors.initials: X
authors.lastname: Yu
authors.affiliation: 118 Hospital of PLA, Wenzhou, 325000, China.
authors.forename: Ruowang
authors.initials: R
authors.lastname: Pan
authors.affiliation: School of Forensic Medicine, Xi'an Jiaotong University, Xi'an, 710000, China.
authors.forename: Chunxia
authors.initials: C
authors.lastname: Yan
authors.affiliation: School of Forensic Medicine, Xi'an Jiaotong University, Xi'an, 710000, China.
authors.forename: Shengbin
authors.initials: S
authors.lastname: Li
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China. baoqy@genomics.cn.
authors.forename: Qiyu
authors.initials: Q
authors.lastname: Bao
authors.affiliation: School of Laboratory Medicine and Life Science/Institute of Biomedical Informatics, Wenzhou Medical University, Wenzhou, 325035, China. lpz@wmu.edu.cn.|School of Forensic Medicine, Xi'an Jiaotong University, Xi'an, 710000, China. lpz@wmu.edu.cn.
authors.forename: Peizhen
authors.initials: P
authors.lastname: Li
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D006801:Humans; D008855:Microscopy, Electron, Scanning; D017382:Reactive Oxygen Species / Q000378:metabolism; D012969:Sodium Fluoride / Q000494:pharmacology*
chemical_list: D017382:Reactive Oxygen Species; D012969:Sodium Fluoride
keywords: Cell apoptosis; Human bronchial epithelial BEAS-2B cells; Mitochondrial membrane potential; Reactive oxygen species; Sodium fluoride