Alizarin complexone-lanthanide(III)-fluoride system: Revised speciation and the origin of the analytical signal

Potentiometric titrations of alizarin complexone (ALC) in the presence of La(III), Eu(III) and Y(III) in 50% vol. DMSO reveal formation of mostly binuclear complexes with monoprotonated (LH) and completely deprotonated (L) forms of the ligand of the type M₂L₂H₂, M₂L₂H and M₂L₂. Only for La(III) a single mononuclear complex LaLH is observed in acidic media. Titrations of the same mixtures with added fluoride show that with Eu(III) and Y(III), fluoride forms ternary complexes without shifting the distribution profile of complexes with differently protonated forms of bound ALC, but with La(III) a strong shift in distribution in favor of complexes with the deprotonated ligand occurs, which explains the appearance of blue colored species in acidic medium giving rise to the analytical signal employed for quantitative determination of fluoride. Detailed analysis of the spectral properties of La(III)-ALC-fluoride system on the basis of the established species distribution diagrams demonstrate the following factors to be involved: (1) fluoride-induced conversion of LaLH to La₂L₂HF around pH 3; (2) anomalously high affinity of La(III)-ALC complexes to fluoride and (3) some sort of mutual effect of fluoride and ALC ligands in ternary La(III) complexes, probably involving change in the metal coordination number, leading to enhanced absorptivity of La₂L₂HF as compared to La₂L₂H.     

Influence of dietary lead on fluoride bioavailability in the rat

A factorial experiment was conducted with weanling rats fed a purified diet to determine the influence of dietary lead (0 or 100 ppm) as either lead acetate or lead carbonate on fluoride bioavailability (2 or 10 ppm as sodium fluoride). During the 6-wk study, both forms of lead depressed weight gain, regardless of the fluoride level, despite the fact that food intake was similar for all treatment groups. Both forms of lead produced a small, but significant, reduction in femur and second molar fluoride. This effect, however, could only be demonstrated in rats fed diets containing 10 ppm fluoride, indicating a significant interaction between lead and fluoride for these indices of fluoride bioavailability. This interactive effect between fluoride and lead was also demonstrated for apparent fluoride absorption. Both forms of dietary lead significantly increased the lead concentration of plasma, femur, liver, and kidney, and both forms of lead significantly increased the urinary excretion of delta-aminolevulinic acid. The level of dietary fluoride failed to influence these measurements. We therefore conclude that, although small amounts of dietary lead reduce fluoride bioavailability, small amounts of dietary fluoride do not appear to significantly influence the utilization of dietary lead.     

Variations in the metabolism and maturation of collagen after fluorine ingestion

This study described the effect of fluoride ingestion (10 mg NaF/kg body weight per day) for up to 180 days, on the biosynthesis, maturation and degradation of rabbit skin collagen. Higher intake of fluoride interferes with the collagen biosynthesis resulting in a reduction in the collagen content (in terms of hydroxyproline). Fluoride administration increases the solubility of collagen by reducing the amount of cross-link precursors, thus impairing the cross-linking and maturation of tissue collagen fibers. Collagen degradation by the collagen-bound collagenase is increased due to the accumulation of higher pools of soluble collagen.     

Health risk assessment in children living in an urban area with hydrofluorosis: San Luis Potosí Mexico case study

BackgroundFluoride is an inorganic element, which can be found in high concentrations in groundwater. Its consumption and exposure have consequences on human health. The objective of this study was to evaluate fluoride exposure and develop a health risk assessment in children from an urban area with hydrofluorosis in Mexico.MethodsWater fluoride levels in active wells were provided by the Water State Agency and divided into three zones: agriculture zone (Zone A), metallurgical zone (Zone B), and industrial zone (Zone C). Urinary fluoride levels were determined by potentiometric method using an ion-selective electrode. Health risk assessment was performed through Monte Carlo model analysis and hazard quotient was calculated.ResultsAccording to fluoride well concentration, all zones have high concentration especially Zone B (2.55 ± 0.98 mg/L). Urinary fluoride concentrations were highest in children in Zone B (1.42 ± 0.8 mg/L). The estimated median daily intake dose of fluoride was 0.084 mg/Kg-day for the children living in zone B. The highest mean HQ value was to Zone B (1.400 ± 0.980), followed by Zone C (0.626 ± 0.443).ConclusionThe levels of fluoride exposure registered are a potential risk to generate adverse health effects in children in the San Luis Potosi metropolitan area.     

Gramicidin D enhances the antibacterial activity of fluoride

Fluoride is a toxic anion found in many natural environments. One of the major bacterial defenses against fluoride is the cell envelope, which limits passage of the membrane-impermeant fluoride anion. Accordingly, compounds that enhance the permeability of bacterial membranes to fluoride should also enhance fluoride toxicity. In this study, we demonstrate that the pore-forming antibiotic gramicidin D increases fluoride uptake in Bacillus subtilis and that the antibacterial activity of this compound is potentiated by fluoride. Polymyxin B, another membrane-targeting antibiotic with a different mechanism of action, shows no such improvement. These results, along with previous findings, indicate that certain compounds that destabilize bacterial cell envelopes can enhance the toxicity of fluoride.     

Influence of sodium fluoride and caffeine on the concentration of fluoride ions, glucose, and urea in blood serum and activity of protein metabolism enzymes in rat liver

The aim of the study was examining the effect of fluoride ions and caffeine administration on glucose and urea concentration in blood serum and the activity of protein metabolism enzymes and selected enzymes of the urea cycle in rat liver. The study was carried out using 18 male Sprague-Daowley rats (4.5 mo old). Rats were divided into three groups. Group I received distilled water ad libitum. Group II received 4.9 mg F⁻/kg body mass/d of sodium fluoride in the water, and group III received sodium fluoride (in the above-mentioned dose) and 3 mg/kg body mass/d of caffeine in the water. After 50 d, the rats were anesthetized with thiopental and fluoride ions, glucose, and urea concentration in blood serum were determined. Also determined were the activities of aspartate aminotransferase, alanine aminotransferase glutamate dehydrogenase, ornithine carbamoylotransferase and arginase in liver homogenates. Liver was taken for pathomorphological examinations. The applied doses of F⁻ (4.9 mg/kg body mass/d) and F⁻+ caffeine (4.9 mg F⁻/kg body mass/d+3 mg caffeine/kg body mass/d) resulted in a statistically significant increase of fluoride ion concentration in blood serum, a slight increase of the glucose concentration, and no changes in the concentration of urea in blood serum. This might testify to the absence of kidney lesions for the applied concentrations of F⁻. No change in the functioning of hepatocytes was observed; however, slight disturbances have been noted in the functioning of the liver, connected with the activation of urea cycle, increase of arginase activity, and accumulation of F⁻ in this organ. There was no observed significant influence of caffeine supplementation on the obtained results.     

Sodium fluoride induces apoptosis and alters bcl-2 family protein expression in MC3T3-E1 osteoblastic cells

Chronic excessive fluoride intake is known to be toxic and can lead to fluorosis and bone pathologies. However, the cellular mechanisms underlying NaF-induced cytotoxicity in osteoblasts are not well understood. The objectives of this study were to determine the effects of fluoride treatment on MC3T3-E1 osteoblastic cell viability, cell cycle analysis, apoptosis and the expression levels of bcl-2 family members: bcl-2 and bax. MC3T3-E1 cells were treated with 10⁻⁵; 5 × 10⁻⁵; 10⁻⁴; 5 × 10⁻⁴ and 10⁻³ M NaF for up to 48 h. NaF was found to reduce cell viability in a temporal and concentration dependent manner and promote apoptosis even at low concentrations (10⁻⁵ M). This increased apoptosis was due to alterations in the expression of both pro-apoptotic bax and anti-apoptotic bcl-2. The net result was a decrease in the bcl-2/bax ratio which was found at both the mRNA and protein levels. Furthermore, we also noted that NaF-induced S-phase arrest during the cell cycle of MC3T3-E1 cells. These data suggest that fluoride-induced osteoblast apoptosis is mediated by direct effects of fluoride on the expression of bcl-2 family members.     

Urinary Fluoride Reference Values Determined by a Fluoride Ion Selective Electrode

As fluoride has a very short half-life in the body and the major route for fluoride excretion is via the kidney, human exposure is best measured in urine, where the concentration is expected to be highest. The urinary fluoride concentrations of 167 healthy Japanese adults were determined by means of a fluoride ion selective electrode. When the results were corrected for a specific gravity ρ = 1.024 g cm⁻³, the histogram of urinary fluoride concentrations highly skewed toward low values with sharp peakedness (skewness = 1.56, kurtosis = 3.08). The normality of the log-transformed histogram (skewness = 0.12, kurtosis = 0.07) and the straight line on log-probability paper clearly showed a key feature of lognormal distribution of urinary fluoride. A geometric mean (GM) of 613.8 μg/l and 95% confidential interval (CI) of 241.0–1633.1 μg/l were established as reference values for urinary fluoride. The results presented in this study will be useful as guidelines for the biological monitoring of fluoride in normal subjects and individuals at risk of occupational or environmental fluoride exposure.