Sodium Fluoride
(Synonyms: 氟化钠) 目录号 : GC10594
Sodium Fluoride作为氟的另一种形式，经口服后可蓄积于生殖器官，干扰激素调控并激活氧化应激通路，从而导致生殖毒性。
Cas No.:7681-49-4
Sample solution is provided at 25 µL, 10mM.
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Sodium Fluoride, another form of fluorine, is orally bioavailable and can accumulate in reproductive organs and interfere with hormonal regulation and oxidative stress pathways, contributing to reproductive toxicity[1]. Sodium Fluoride is extensively used for the prevention of dental caries and tooth decay in the form of fluorinated drinking water, salts, or milk, tooth pastes, mouth washes, and fluo-ride tablets[2]. The acute Fluoride toxicosis usually occurs by soluble forms of Sodium Fluoride upon ingestion in large doses[3].
In vitro, bone mesenchymal stem cells (BMSCs) grew well in media containing 0-240μM Sodium Fluoride, whereas exposure to 480μM or 1200μM Sodium Fluoride caused a decline in cell viability—first evident at day 7 for 480μM and from day 3 onward for 1200μM—accompanied by reduced cell density and a marked rise in reactive oxygen species (ROS) on day 7[4]. After 12h of exposure to 0, 0.5, 5 or 10mM Sodium Fluoride, OCCM-30 cells treated with 5 or 10mM Sodium Fluoride exhibited apoptotic morphological changes and DNA fragmentation; 5mM Sodium Fluoride up-regulated Fas-L mRNA, whereas 10mM Sodium Fluoride induced the expression of cleaved caspase-3, -8, -9 and cleaved Poly (ADP-ribose) polymerase (PARP) and provoked a significant rise in intracellular ROS[5].
In vivo, oral administration of Sodium Fluoride to ICR mice at 12, 24, and 48mg/kg body weight for 42 consecutive days elicited dose- and time-dependent histopathological lesions in the liver, and dose-dependent elevate of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AKP) activities, and total bilirubin (TBIL) contents on days 21 and 42[6]. Intragastric administration of 0, 12, 24 and 48mg/kg Sodium Fluoride to ICR mice, Sodium Fluoride in excess of 12mg/kg activated the mitogen-activated protein kinases (MAPKs) signaling pathway by markedly increasing mRNA and protein levels of apoptosis signal-regulating kinase 1 (ASK1), mitogen-activated protein kinase kinases 1/2 (MEK1/2), extracellular signal-regulated protein kinases 1/2 (Erk1/2), mitogen-activated protein kinase kinases 4/7 (MEK4/7), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38) and mitogen-activated protein kinase kinases 3/6 (MEK3/6), and the nuclear factor-kappa B (NF-κB) signaling pathway by increasing the production of NF-κB and inhibitor of nuclear factor kappa-B kinase subunit beta (IKK-β) and reducing the production of the inhibitory kappa B (IκB)[7].
References:
[1] Talebi SF, Seify M, Bhandari RK, et al. Fluoride-induced testicular and ovarian toxicity: evidence from animal studies. Biol Res. 2025;58(1):6.
[2] A.A. Oyagbemi, T.O. Omobowale, O.E. Ola-Davies, et al. Luteolin-mediated Kim-1/NF-kB/Nrf2 signaling pathways protects sodium fluoride-induced hypertension and cardiovascular complications. BioFactors. 2018;44(6):518-531.
[3] Giri D K, Ghosh R C, Mondal M, et al. Pathology of acute oral toxicity of sodium fluoride in Wistar rats. Indian Journal of Veterinary Pathology. 2014;38(1):33-38.
[4] Wu S, Xia B, Mai S, et al. Sodium Fluoride under Dose Range of 2.4-24 μM, a Promising Osteoimmunomodulatory Agent for Vascularized Bone Formation. ACS Biomater Sci Eng. 2019;5(2):817-830.
[5] Ni J, Li Y, Zhang W, et al. Sodium fluoride causes oxidative stress and apoptosis in cementoblasts. Chem Biol Interact. 2018;294:34-39.
[6] Lu Y, Luo Q, Cui H, et al. Sodium fluoride causes oxidative stress and apoptosis in the mouse liver. Aging (Albany NY). 2017;9(6):1623-1639.
[7] Chen L, Kuang P, Liu H, et al. Sodium Fluoride (NaF) Induces Inflammatory Responses Via Activating MAPKs/NF-κB Signaling Pathway and Reducing Anti-inflammatory Cytokine Expression in the Mouse Liver. Biol Trace Elem Res. 2019;189(1):157-171.
Sodium Fluoride作为氟的另一种形式，经口服后可蓄积于生殖器官，干扰激素调控并激活氧化应激通路，从而导致生殖毒性[1]。Sodium Fluoride被广泛用于预防龋齿和牙釉质脱矿，常以氟化饮水、食盐、牛奶、牙膏、漱口水及含氟片剂等形式存在[2]。急性氟中毒通常由大剂量摄入可溶性Sodium Fluoride引起[3]。
在体外，骨髓间充质干细胞（BMSCs）在含0-240μM的Sodium Fluoride的培养基中生长良好；而暴露于480μM或1200μM的Sodium Fluoride时，细胞活力从第7天（480μM）或第3天（1200μM）开始下降，细胞密度减少，并于第7天出现活性氧（ROS）显著升高[4]。0、0.5、5或10mM的Sodium Fluoride处理OCCM-30细胞12h后，5mM与10mM的Sodium Fluoride组出现凋亡形态学改变及DNA片段化；5mM的Sodium Fluoride上调Fas-L mRNA表达，而10mM的Sodium Fluoride诱导cleaved caspase-3、-8、-9及cleaved聚ADP核糖聚合酶（PARP）表达，并显著增加胞内ROS水平[5]。
在体内，以12、24和48mg/kg的Sodium Fluoride连续灌胃ICR小鼠42天，可诱发肝脏呈剂量和时间依赖性组织病理学损伤，并于第21和42天剂量依赖性地升高丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、碱性磷酸酶（AKP）活性及总胆红素（TBIL）含量[6]。对ICR小鼠灌胃0、12、24和48mg/kg的Sodium Fluoride后，≥12mg/kg的Sodium Fluoride通过显著升高凋亡信号调节激酶1（ASK1）、丝裂原活化蛋白激酶激酶1/2（MEK1/2）、胞外信号调节蛋白激酶1/2（Erk1/2）、丝裂原活化蛋白激酶激酶4/7（MEK4/7）、c-Jun N-末端激酶（JNK）、p38丝裂原活化蛋白激酶（p38）及丝裂原活化蛋白激酶激酶3/6（MEK3/6）的mRNA和蛋白水平，激活MAPKs信号通路；同时通过升高 NF-κB和核因子κB抑制激酶β（IKK-β）的表达并降低抑制性κB（IκB）的表达，激活NF-κB信号通路[7]。
| Cell experiment [1]: | |
Cell lines | Bone mesenchymal stem cells (BMSCs) |
Preparation Method | A series of concentrations of fluoride was prepared (0, 0.24, 2.4, 24, 120, 240, 480, 1200μM Sodium Fluoride) with complete medium. Cells were plated in 96-well plates at a density of 2,000 per well and incubated overnight. The culture medium was removed and replaced with complete medium with Sodium Fluoride. To evaluate proliferation, at days 1, 3, 5, and 7, the medium was removed, followed by adding 10% cell counting kit-8 (CCK-8) solution. After 2h incubation, the absorbance of each well was detected by a microplate reader at a wavelength of 450nm. The morphologies of BMSCs were also observed using a light microscope. To evaluate reactive oxygen species (ROS) production, at days 3 and 7, the medium was removed, followed by adding 10μM 2,7-dichlorofluorescin diacetate (DCFH-DA) for 3min. The medium was then removed, and the plates were rinsed with phosphate buffer. The cellular fluorescence was measured on a fluorescence microplate reader with excitation and emission wavelengths at 500 and 530nm, respectively. |
Reaction Conditions | 0, 0.24, 2.4, 24, 120, 240, 480, 1200μM; 1, 3, 5, and 7 days |
Applications | The BMSCs grew well in the complete medium with 0, 0.24, 2.4, 24, 120, and 240μM Sodium Fluoride. The CCK-8 assay showed significantly decreased cell vitality in the 1200μM group at days 3, 5, and 7, whereas significantly decreased cell vitality was found at day 7 in the 480μM group. The BMSC density decreased in groups of 480 and 1200μM, while the cells grew well in other groups with lower fluoride concentration. The production of ROS was observed in all Sodium Fluoride-treated groups at day 3 and there was a significant increase in the 480 and 1200μM groups at day 7. |
| Animal experiment [2]: | |
Animal models | ICR mice |
Preparation Method | 240 ICR mice were randomly divided into 4 equal groups, and housed in separate cages. The control group received distilled water. The low-, medium-, and high-fluoride groups were oral administered with Sodium Fluoride at a dose of 12, 24 and 48mg/kg body weight for consecutively 42 days, and the gavage volume was 1ml/100g body weight respectively. All of the mice had free access to food and water. |
Dosage form | 12, 24, and 48mg/kg; orally |
Applications | Sodium Fluoride resulted in histopathological lesions in a dose- and time-dependent manner. Lesions included hepatocellular granular degeneration, vacuolar degeneration, and necrosis. In the granular and vacuolar degenerated hepatocytes, tiny particles and small or large vacuoles appeared in the cytoplasm. Karyorrhexis, karyolysis, and hypochromatosis appeared in the necrotic hepatocytes. Alanine amino transferase (ALT), aspartic acid transferase (AST), alkaline phosphatase (AKP) activities, and TBIL contents were increased in a dose-dependent manner in the Sodium Fluoride groups when compared with those in the control group at 21 and 42 days of the experiment. |
References: | |
| Cas No. | 7681-49-4 | SDF | |
| 别名 | 氟化钠 | ||
| 化学名 | sodium fluoride | ||
| Canonical SMILES | [F-].[Na+] | ||
| 分子式 | FNa | 分子量 | 41.99 |
| 溶解度 | ≥ 4.2mg/mL in Water | 储存条件 | Store at RT |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 23.8152 mL | 119.076 mL | 238.1519 mL |
| 5 mM | 4.763 mL | 23.8152 mL | 47.6304 mL |
| 10 mM | 2.3815 mL | 11.9076 mL | 23.8152 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
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