Different Concentrations Of Sodium Fluoride Research Articles

Ameliorative Effects of Orange Juice on Sodium Fluoride Induced Gastro-Hepatic Toxicity in Mice

Floride toxicity has been under discussion and investigations when taken in excess amounts. Floride leaching into the water bodies as a result of industrialization is a common issue facing most of the developing countries like Pakistan, India, Bangladesh etc. This leached fluoride has the ability to cause a myriad of disorders when incorporated in animal bodies. Objective: To find out the ameliorative effect of orange juice against toxic effects of sodium fluoride influencing damaging effect on liver and stomach. Methods: The mice were divided in six groups. The control group was only Nestle’s water, while different concentrations of sodium fluoride (2.50µg/g, 5.00µg/g and 7.50µg/g body weight) were prepared and administered orally in mice for 30 days. Then all treated groups were supplied with fresh natural orange juice for next 30 days to test its ameliorative potential. Results: The data revealed the significant reduction of body weight (p<0.001), stomach length, stomach diameter (p < 0.05) while hepato- somatic and gastro-somatic index increased (p < 0.05) in treated groups as compared to control group after sodium fluoride administration. Morphological studies revealed different abnormalities in treated groups such as spots on the liver and stomach, swelling of stomach, constriction of fundic and cardiac regions and lobes of liver. Conclusions: This study clearly revealed that sodium fluoride is potentially toxic to organs of albino mice, especially liver and stomach and that orange juice demonstrated ameliorative potential against the toxicity due to sodium fluoride.

HIF-1α-mediated autophagy and canonical Wnt/β-catenin signalling activation are involved in fluoride-induced osteosclerosis in rats

Fluoride (F) exposure can cause osteosclerosis, which is characterised by a high bone mass, but its mechanism is not fully illustrated. Here, we aimed to evaluate the effects of excessive F exposure on the bone lesion by treating female Sprague–Dawley rats with different concentrations of sodium fluoride (NaF) (0, 55, 110 and 221 mg/L) for 90 days and the corresponding concentrations of fluorine ion (0, 25, 50 and 100 mg/L, respectively). Histopathological results showed that excessive F exposure caused the enlargement of trabeculae and their integration into one large piece, growth plate thickening, articular cartilage impairment and bone collagen abnormality. Meanwhile, F promoted calcium deposition and bone mineralisation, and induced abnormal osteogenesis increased. The results of micro-computed tomography also confirmed that excessive F destroyed the bone microstructure and induced a high-bone-mass phenotype, consistent with the results of pathomorphology. Mechanistically, excessive amounts of F led to angiogenesis inhibition and HIF-1α signalling enhancement. Subsequently, F induced autophagy and canonical Wnt/β-catenin signalling pathway activation. Collectively, these results manifested that F enhanced the hypoxia inducible factor-1α signalling, which in turn triggered autophagy and canonical Wnt/β-catenin signalling activation, ultimately leading to osteosclerosis in the rats.

Excessive fluoride impairs autophagy flux in ameloblasts which is prevented by the autophagy activator rapamycin.

Excessive fluoride intake can cause dental fluorosis during teeth development and growth. However, the mechanisms underlying fluoride-induced enamel damage are still not fully elucidated. Previously, we observed fluoride-induced autophagy in ameloblasts, but the effects of fluoride on autophagy flux in ameloblasts remain unclear. Hence, this study aimed to clarify the effects of fluoride and rapamycin, an autophagy activator, on autophagy flux in ameloblasts. This in vitro study used the murine ameloblast-derived cell line LS8. Cells were treated with different concentrations of sodium fluoride (NaF) to evaluate NaF-induced cytotoxicity. Using transmission electron microscopy, we observed an increase in the number of autophagosomes with increasing fluoride concentrations. Western blot analyses showed increases in microtubule-associated protein 1 light chain 3 (LC3) and SQSTM1 (p62) expression after NaF treatment and an increase in LC3II expression after bafilomycin A1 administration. Together with changes in RFP-GFP-LC3 lentivirus expression, this demonstrated that fluoride impaired autophagy flux. Furthermore, we evaluated whether rapamycin can alleviate fluoride-induced cytotoxicity by restoring autophagy flux. Compared to the NaF-treated group, LS8 cells cotreated with NaF and rapamycin grew considerably better and had significantly decreased p62 expression. Taken together, these data suggest that fluoride-induced impaired autophagosome degradation may damage ameloblasts. This provides experimental in vitro evidence and an explanation for the observed NaF-induced toxicity of ameloblasts. Rapamycin probably alleviates this impairment by decreasing the expression of p62, thereby preventing autophagy defects.

DNA Methylation Profiles of Ovarian Granular Cells from Fluorosis Female Patients Suffering Reproductive Dysfunctions.

Fluorosis often causes female reproductive dysfunction. A rapid turnover of DNA methylation is a pathological change in many human diseases, including female reproductive dysfunction. The role of DNA methylation in fluorosis was unknown and investigated in this experiment. Fifty fluorosis women patients were selected as High F group and forty-six healthy women were recruited as Control group were enrolled. In addition, ovarian granulosa cells were obtained from five women in High F group and five women in Control group. All ten women went through in vitro fertilization (IVF) process with DNA methylation sequencing. KGN cells (human granulosa cell line) were cultured with different concentrations of sodium fluoride (0-8mM NaF) for 24h for the in vitro study. The level of DNA methylation in blood samples was significantly higher in High F group than that in Control group. The level of serum estradiol (E2) was significantly lower in women from High F group, while the levels of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in High F group were significantly higher than that in Control group. The methylation sequences of KGN cells relating to autophagy were significantly changed by NaF treatment dose-dependently. Based on these results, it is concluded that DNA methylation and autophagy may play a significant role in the pathophysiology of reproductive dysfunction caused by fluorosis.

Fluoride exposure decreased neurite formation on cerebral cortical neurons of SD rats in vitro.

Fluoride, a geochemical element, can damage the brain and result in dysfunction of the central nervous system. In recent years, fluoride-induced neurotoxicity has become one of research focuses of environmental toxicology. Our previous study showed that fluoride could induce the structural damages of the cerebral cortex and reduce the learning and memory abilities of mice offspring. However, the underlying mechanisms of these effects remain unclear. In this study, primary neurons were isolated from the cerebral cortices of postnatal 1-day SD rats. The primary cultured cerebral cortical neurons were adherent and the cellular network was obvious. Neurons were identified by Nissl's staining and were used for experiments. Different concentrations of sodium fluoride (0.5, 1.0, 1.5, 2.0 and 2.5 mM) were chosen to explore its toxic effects on neuron of SD rats in vitro. Results showed that neuronal morphology was obviously damaged in 2.0 and 2.5 mM, but was not adversely affected in 0.5 and 1 mM. Further studies revealed that the neurites of neuron were shrunken and even became fractured with the increase in NaF dose, which have been detected by scanning electron microscopy (SEM). Meanwhile, TEM showed marginated chromatin, widened nuclear gaps, damaged nuclei and swollen or even absent mitochondria in 1.5, 2 and 2.5 mM group. The cytoskeletal staining was consistent with the above results. The number of neurites of cerebral cortical neuron significantly decreased after fluoride exposure by immunofluorescent assay. In summary, high fluoride (1.5, 2 and 2.5 mM) concentrations exerted a significant toxic effect on the cellular morphologies and neural formation of primary cultured cortical neurons. These findings provide new insights into the roles of NaF in neuronal damage and can contribute to an improved understanding of fluoride-induced neurotoxicity.

MiR-378d is Involved in the Regulation of Apoptosis and Autophagy of and E2 Secretion from Cultured Ovarian Granular Cells Treated by Sodium Fluoride.

Taking excessive sodium fluoride may cause female reproductive dysfunction, but underlying molecular mechanism is unclear. The ovarian granulosa cells are the key endocrine cells releasing reproductive hormones. The miRNAs in the granulosa cells play an important function in regulating reproduction. The aim of this study is to explore the role of miRNAs in granulosa cell apoptosis and autophagy, as well as estradiol (E2) release in response to excessive sodium fluoride. The ovarian granulosa cells (KGN cells) were treated in vitro by different concentrations of sodium fluoride (NaF) for 24 h. The level of estradiol (E2) in the incubation medium was measured by ELISA kits. The total RNA and protein were collected and purified from KGN cells. The expression of miRNAs was detected by the real-time PCR. The signal molecules involved in cell apoptosis and autophagy were detected by the real-time PCR and Western blotting. Six miRNAs in granulosa cells were significantly up- or downregulated by NaF and selected for real-time PCR analysis. The miR-378d was the most significantly upregulated one dose dependently by NaF. It was positively correlated to the extent of apoptosis but negatively correlated to the level of autophagy in KGN cells in response to NaF. In addition, miR-378d promoted E2 release in response to 1 and 2 mM NaF but reduced E2 release in response to 4 and 8 mM NaF treatments. It is concluded that expression of miR-378d in ovarian granulosa cells is negatively correlated to the autophagy and E2 release and positively correlated to cell apoptosis under the influence of NaF.

Toxicity of fluoride on isolated rat liver mitochondria

Fluoride is abundant in the environment and exists mostly in combination with other elements as fluoride compounds. Several studies showed that exposing to irregular level of fluoride could impair the normal function of mitochondria that have major contribution for producing of reactive oxygen species (ROS). However, information about the exact mechanism behind the fluoride-induced mitochondrial damage has not been fully understood. In the present study, isolated rat liver mitochondria were exposed to different concentrations of sodium fluoride (NaF) for 30 min and their functionality was assessed at the presence of different concentrations of N-acetylcysteine (NAC) and IC50 concentration of NaF. Mitochondrial dehydrogenase activity, glutathione (GSH) content, lipid peroxidation, ROS production and mitochondrial membrane potential (MMP) assay in the presence of these two substances were evaluated. Our findings demonstrated that, NaF reduced the GSH content of mitochondria, increased ROS and lipid peroxidation which led to a decrease in the dehydrogenase activity (complex II) of mitochondria. NAC considerably inhibited those noxious effects of NaF on mitochondria and prevented NaF toxicity on mitochondria isolated from rat liver.

NANOCOMPLEJO DE FOSFOPÉPTIDO DE CASEÍNA-FOSFATO DE CALCIO AMORFO (CPP-ACP) EN ODONTOLOGÍA: ESTADO DEL ARTE

Saliva and external agents containing different concentrations of sodium fluoride (NaF) promote the dental remineralization process. However, these resources may not be sufficient to counteract the multiple factors involved in the process of dental caries, especially in high-risk patients. There are alternatives that have been extensively researched, such as casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) which provides essential ions, like phosphate and calcium, acting as an adjuvant in the remineralization process. Manufacturers of CPP-ACP-based products also suggest that it can produce desensitizing effects. This nanocomplex has been used experimentally with some dental cements and adhesive systems, but it is important to clarify the effects of this procedure, and the remineralizing/desensitizing advantages it offers. The objective of this topic review was to present the state of the art on CPP-ACP nanocomplex. In terms of dental caries prevention, this remineralizing option is not better than NaF. CPP-ACP provides a dental desensitizing action, but it is temporary and less effective than other alternatives such as potassium nitrate or NaF. The experimental incorporation of CPP-ACP into dental cements should be controlled for not to compromise the physico-chemical properties of the material. The use of dental products based on this nanocomplex as dental surface pretreatment may decrease the bond strength of adhesive materials, but this effect is material dependent.

Effects of fluoride on primary cultured haemocytes from the marine gastropod Haliotis tuberculata

As a consequence of human’s activities, fluoride concentration in many aquatic ecosystems is significantly increasing. Nevertheless, little is known about fluoride toxicity to aquatic life. In this study the effect of exposure to different concentrations of sodium fluoride (2, 10, 50, 250 and 1,250 μg mL−1) during 24 h on primary cultured haemocytes of the gastropod Haliotis tuberculata was realized. Results indicate no significant effect of NaF on cell viability, Lysosomal membrane stability, phagocytosis and ROS production at concentrations of 2, 10, 50 and 250 μg mL−1. Nevertheless, lysosomal membrane alterations, a decrease of phagocytosis and morphological changes of H. tuberculata haemocytes were observed at concentration of 1,250 μg mL−1 NaF suggesting a potential impact of NaF at high concentration in the environment.

Assessment of the electrochemical behaviour of Nickel-Titanium-based orthodontic wires: Effect of some natural corrosion inhibitors in comparison with fluoride.

BackgroundThe aim of this study is to assess the corrosion resistance behaviour of Nickel-Titanium-based orthodontic wires (NiTi) in different concentrations of Sodium Fluoride (NaF) and the corrosion’s inhibitory effect of the extracts of some medicinal plants (essential oils, hydrosols and extract).Material and MethodsIn this study we used NiTi (3M) and CuNiTi (ORMCO, 35°C, California) orthodontic wires. The following electrolytes were prepared: Lactate Ringer solution with additions of 0.1%, 0.5% or 1% of Sodium Fluoride and the extracts of different plants: Artemisia, Syzygium aromaticum (Clove) and Celtis australis. Corrosion resistance was studied using anodic potentiodynamic polarisation and electrochemical impedance spectroscopy measurements. At the end of the experiment, microscopic images of wires were performed. ANOVA test with the comparison of Bonferroni and Tukey tests were performed to elucidate comparisons among all groups.ResultsThe higher sodium fluoride concentration is related to negative corrosion potential for both NiTi and CuNiTi orthodontic wire. Hydrosols are associated to positive values of corrosion potential. CuNiTi has a lower corrosion resistance than NiTi.ConclusionsThe prescription of toothpastes containing sodium fluoride should be reduced especially for patients wearing fixed orthodontic appliances. Eugenol may be considered as alternative of sodium fluoride for orthodontic patients for its anti-microbial and anti-corrosive effects. Key words:Corrosion behaviour, Sodium Fluoride, Nickel-Tatanium, orthodontic wires, corrosion inhibitors, aromatical plants.

Abnormal spermatogenesis following sodium fluoride exposure is associated with the downregulation of CREM and ACT in the mouse testis.

cAMP response element modulator (CREM) is involved in regulating gene expression in normal spermatogenesis. The transcriptional activity of CREM is partly regulated by activator of CREM in the testis (ACT). To investigate the effects of different concentrations of sodium fluoride (NaF) on the gene and protein expression of CREM and ACT in the mouse testis, sexually mature male Kunming mice were exposed to 50, 100, or 150 mg/L NaF in their drinking water for 90 days. NaF reduced the sperm count and viability and increased the percentage of malformed sperm in a dose-dependent manner. The mRNA expression of CREM and ACT was markedly downregulated in the NaF-treated groups. Furthermore, immunohistochemistry revealed that CREM and ACT proteins were decreased significantly in the 50, 100, and 150 mg/L NaF-treated groups compared to the control group. These findings indicate that the decreased gene and protein expression of CREM and ACT in the testis is associated with an impairment of reproductive functions by NaF.

Fluoride induces apoptosis in H9c2 cardiomyocytes via the mitochondrial pathway

Numerous studies have shown that chronic excessive fluoride intake can adversely affect different organ systems. In particular, the cardiovascular system is susceptible to disruption by a high concentration of fluoride. The objectives of this study were to explore the mechanism of apoptosis by detecting the toxic effects of different concentrations of sodium fluoride (NaF) in H9c2 cells exposed for up to 96 h. NaF not only inhibited H9c2 cell proliferation but also induced apoptosis and morphological damage. With increasing NaF concentrations, early apoptosis of H9c2 cells was increased while the mitochondrial membrane potential was decreased. Compared with the control group, the mRNA levels of caspase-3, caspase-9, and cytochrome c all increased with increasing concentrations of NaF. In summary, these data suggest that apoptosis is involved in NaF-induced H9c2 cell toxicity and that activation of the mitochondrial pathway may occur.

234 - Evaluation of Antioxidant System in Kidney of Rats Treated with Different Concentrations of Sodium Fluoride in Drinking Water for Twenty Days

234 - Evaluation of Antioxidant System in Kidney of Rats Treated with Different Concentrations of Sodium Fluoride in Drinking Water for Twenty Days

Effect of fluoride sodium mouthwash solutions on cpTI: evaluation of physicochemical properties

The effects of fluoride, which is present in different oral hygiene products, deserve more investigation because little is known about their impact on the surface of titanium, which is largely used in Implantology. This study evaluated the surface of commercially pure titanium (cpTi) after exposure to different concentrations of sodium fluoride (NaF). The hypothesis tested in this study was that different concentrations of NaF applied at different time intervals can affect the titanium surface in different ways. The treatments resulted in the following groups: GA (control): immersion in distilled water; GB: immersion in 0.05% NaF for 3 min daily; GC: immersion in 0.2% NaF for 3 min daily; GD: immersion in 0.05% NaF for 3 min every 2 weeks; and GE: immersion in 0.2% NaF for 3 min every 2 weeks. The experiment lasted 60 days. Roughness was measured initially and every 15 days subsequently up to 60 days. After 60 days, corrosion analysis and anodic polarization were done. The samples were examined by scanning electron microscopy (SEM). The roughness data were analyzed by ANOVA and there was no significant difference among groups and among time intervals. The corrosion data (i(corr)) were analyzed by the Mann-Whitney test, and significant differences were found between GA and GC, GB and GC, GC and GD, GC and GE. SEM micrographs showed that the titanium surface exposed to NaF presented corrosion that varied with the different concentrations. This study suggests that the use of 0.05% NaF solution on cpTi is safe, whereas the 0.2% NaF solution should be carefully evaluated with regard to its daily use.

Increased level of apoptosis in rat brains and SH-SY5Y cells exposed to excessive fluoride—A mechanism connected with activating JNK phosphorylation

In order to reveal the mechanism of the brain injury induced by chronic fluorosis, the levels of apoptosis and c-Jun N-terminal kinases (JNK) in brains of rats and SH-SY5Y cells exposed to different concentrations of sodium fluoride (NaF) were detected. The dental fluorosis and fluoride contents in blood, urine and bones of rats were measured to evaluate the exhibition of fluorosis. The apoptotic death rate was measured by flow cytometry and the expression of JNK at protein level by Western blotting. The results showed that as compared with controls, the apoptotic death rate was obviously increased in brains of the rats exposed to high-fluoride (50ppm) for 6 months with a concentration dependent manner, but no significant change for 3 months. In SH-SY5Y cells treated with high concentration (50ppm) of fluoride, the increased apoptotic death rate was obviously observed as compared to controls. In addition, the expressions of phospho-JNK at protein level were raised by 20.5% and 107.6%, respectively, in brains of the rats exposed to low-fluoride (5ppm) and high-fluoride for 6 months; while no significant changes were found between the rats exposed to fluoride and the controls for 3 months. The protein level of phospho-JNK was also increased in SH-SY5Y cells exposed to high-fluoride. There were no changes of total-JNK both in the rats and in the SH-SY5Y cells exposed to excessive fluoride as compared to controls. When SH-SY5Y cells were singly treated with SP600125, an inhibitor of phospho-JNK, the decreased expression of phospho-JNK, but no apoptosis, was detected. Interestingly, after JNK phosphorylation in the cultured cells was inhibited by SP600125, the treatment with high-fluoride did not induce the increase of apoptosis. In addition, there was a positive correlation between the expression of phospho-JNK and the apoptotic death rate in rat brains or SH-SY5Y cells treated with high-fluoride. The results indicated that exposure to excessive fluoride resulted in the increase of apoptosis in rat brains and SH-SY5Y cells, in which one of the mechanisms might be activating JNK phosphorylation.

Alteration of osteocalcin mRNA expression in ovine osteoblasts in dependence of sodium fluoride and sodium selenite medium supplementation

Objective of this study was to assess the quantification of osteocalcin (OCN) expression by ovine osteoblasts cultured with different concentrations of sodium fluoride (F) and sodium selenite (Se) to evaluate the interaction of these agents on OCN expression in vitro . We wanted to demonstrate a possible protective effect of selenium on the toxic effect of fluoride. Osteoblasts were isolated by complete trypsin and collagenase digestion from ovine calvarial bone and cultured in DMEM supplemented with 15% FBS at 37 degrees C in a humidified 5% CO 2 incubator. Identified osteoblasts were divided into one control group (C) and eight experimental groups, which were exposed to different concentrations of sodium fluoride (F; 0, 0.5, 1 mM) sodium selenite (Se; 0, 0.1, 1 microM). At different time points after treatment total RNA was extracted and reverse transcribed into first-strand cDNA. OCN mRNA was indirectly measured by real-time fluorescent quantitative PCR (qPCR). OCN mRNA expression in F 1 mM with Se 1 microM group was found to have a high peak at day seven and was lower before and afterwards. Expression of OCN mRNA in all groups except control could be promoted by F and/or Se showing a general upregulation. Furthermore, the toxicity from excessive exposure of osteoblast with F could be circumvented by usage of moderate concentration of Se. Osteoblasts cultured in vitro may have stressful responses to F and Se at the first few days. Low concentrations of Se inhibit the toxic effects of high concentrations of F. Therefore, F and Se could be used as antagonistic factors, which could regulate osteocalcin expression.

Quantitative 19 F imaging using inductively coupled reference signal injection

This report describes recent efforts on our continuous development of a synthetic signal injection method for quantification of metabolite content in MR spectroscopy and MRI. Previous work showed that conversion of spectral peaks to quantitative units of metabolite content could be achieved with a calibrated synthetic free induction decay generated by an inductively coupled injection coil. This work demonstrates that calibrated synthetic voxels, injected in the same manner, can be used to quantify metabolite content in real (19)F image voxels. Images of vials containing different concentrations of sodium fluoride (NaF) were converted to units of moles by reference to precalibrated synthetically injected voxels. Additional images of vials containing variable sodium chloride (NaCl) demonstrate that the quantification process is robust and immune to changes in coil loading conditions.

Alterations of nAChRs and ERK1/2 in the brains of rats with chronic fluorosis and their connections with the decreased capacity of learning and memory

In order to reveal the mechanism of the decreased ability of learning and memory induced by chronic fluorosis, nicotinic acetylcholine receptors (nAChRs) and the pathway of extracellular signal regulated protein kinase (ERK1/2) were investigated by using the rats fed with different concentrations of sodium fluoride for 6 months. Spatial learning and memory of the rats were evaluated by Morris Water Maze test. The expressions of nAChRs, ERK1/2 and mitogen-induced extracellular kinase (MEK1/2) at protein and mRNA levels were detected by Western blotting and real-time PCR, respectively. The results showed that as compared with controls, the learning and memory capacity in the rats with fluorosis was decreased. The protein expressions of α7 and α4 nAChR subunits in rat brains with fluorosis were decreased by 35% and 33%, whereas the corresponding receptor subunit mRNAs did not exhibit any changes. The increases of phospho- and total-ERK1/2 as well as phospho-MEK1/2 at the protein levels were found in the brains of rats with fluorosis as compared to controls, and no difference of ERK1/2 mRNA was found. In addition, the activation rate of phospho-ERK1/2 was decreased in the brains affected with fluorosis. The modifications of nAChRs and ERK1/2 pathway might be connected with the molecular mechanisms in the decreased capacity of learning and memory of the rats with fluorosis.

Caries incidence after topical application of varnishes containing different concentrations of sodium fluoride: 3-year results

Previous studies have shown that topical application of the fluoride varnish Duraphat reduces caries incidence. The aim of the present study was to compare the caries inhibiting effect of a new fluoride varnish (Carex) containing 1.8% fluoride (F) with that of Duraphat (2.26% F). Informed consent was obtained from the guardians of 495 children 10-12 yr old in Voss Dental Health District (low F area). The children were randomly allocated to two groups. One group of subjects received 6-monthly application of Duraphat (n = 185), the other Carex (n = 165). Ethical considerations precluded the use of a placebo varnish. All participants received dental examinations including one pair of posterior bitewing radiographs and necessary dental care annually. One trained examiner interpreted bitewing radiographs blindly. Total 3-yr net DFS increment for 24 posterior approximal surfaces was 2.63 (SD = 3.81) in the Duraphat group and 2.12 (SD = 3.50) in the Carex group. DMFS increments based on 40 posterior occlusal and approximal surfaces were 5.21 (SD = 5.79) and 4.04 (SD = 4.92), respectively. Thus the results indicate a comparable efficacy for Carex and Duraphat at the caries activity level exhibited by these study participants.

Short-term toxicity of fluoride ion (F-) in soft water to rainbow trout and brown trout

Short-term static bioassays were conducted in duplicate to determine the toxicity of fluoride ion (F-) in soft water (hardness average value of 22 ppm CaCO 3) to fingerlings (two months old) of Oncorhynchus mykiss Richardson and Salmo trutta fario Linnaeus. Animals were exposed to five different concentrations of sodium fluoride (NaF) for 8 days. They were also exposed to a high concentration of sodium chloride (NaCl) (800 ppm for O. mykiss and 1,000 ppm for S. trutta fario) as sodium and conductivity toxicity controls. No significant effect was obseved during NaCl tests, indicating that toxic effects generated by NaF were fundamentally due to fluoride ion. Fish in fluoride aquaria showed hypoexcitability, darkened backs and a decrease in respiration before their death. The 120, 144, 168 and 192 hour LC 50 values were respectively 92.4, 85.1, 73.4 and 64.1 ppm F- for rainbow trout and 135.6, 118.5, 105.1 and 97.5 ppm F- for brown trout. O. mykiss appears significantly ( P <0.05) more sensitive to fluoride ion than S. trutta fario.