Time‐dependent Changes of Blood Parameters and Fluoride Kinetics in Rats after Acute Exposure to Subtoxic Hydrofluoric Acid

Imanishi, Masafumi; Dote, Tomotaro; Tsuji, Hiroshi; Tanida, Eri; Yamadori, Emi; Kono, Koichi

doi:10.1539/joh.m8016

Cited by 9 publications

(4 citation statements)

References 17 publications

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“…Frequently used syringe-based devices are available from Penn Century Ltd and deliver aerosols generated from dry powder or from suspensions. MicroSprayer® IA-1C aerosolizer for liquid aerosols and DP-4 Dry Powder Insufflator™ for powder aerosols have been used for intratracheal delivery of nanoparticles and occupational and environmental toxicants to mice and rats [63][64][65][66]. Both devices have also been used in cellular studies [35,61,[67][68][69][70][71][72][73][74].…”

Section: Exposure With Particlesmentioning

confidence: 99%

In Vitro Assessment of Chronic Nanoparticle Effects on Respiratory Cells

Frőhlich¹,

Meindl²

2015

Nanomaterials - Toxicity and Risk Assessment

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Nanoparticles (NPs) are included in a variety of consumer products including cosmetics, food, and food packaging. They are also used in medical products for dermal and oral application and for inhalation. The thinness of the air-blood barrier, the large absorption area of the lung, and the relatively low inactivation by enzymes provide fast entry to the systemic blood circulation at high drug concentrations. In addition to intended uptake, exposure to airborne particles from the environment and to NPs released during the manufacturing process may occur. Cytotoxicity is routinely studied for 4-48 h of exposure, but NPs may accumulate in cells and can cause cellular effects after longer times. Both extent and consequences of cellular NP accumulation are currently largely unknown. In vitro studies could help estimating the extent and the consequences of cellular accumulation and classify NPs according to their potential to cause adverse effects upon chronic exposure. Furthermore, such information could help to decrease the amount of labor-and cost-intensive and ethically problematic animal studies. Important parameters for representative chronic cytotoxicity testing in vitro include choice of the appropriate cells and of physiological relevant culture and exposure conditions, verification of uptake, and identification of cell damage. Calu-3 bronchial epithelial cells are a suggested cell line for physiologically relevant testing when cultured on membranes, which allows supplying the cells with nutrients only from the basal side (culture at an air-liquid interface). This culturing also enables the exposure to NPs by aerosol. Cytotoxicity can be identified by changes in cell number, membrane integrity, amount of DNA or protein, and metabolic activity.

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Section: Exposure With Particlesmentioning

confidence: 99%

In Vitro Assessment of Chronic Nanoparticle Effects on Respiratory Cells

Frőhlich¹,

Meindl²

2015

Nanomaterials - Toxicity and Risk Assessment

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“…Acute exposure to fluoride through injection of hydrofluoric acid (1.6mg/Kg) in rats led to a decrease in serum ionized calcium and total calcium after 30 and 300mins respectively [Santoyo-Sanchez et al, 2013]. Similar decrease in plasma calcium was observed in rats due to acute fluoride exposure [Imanishi et al, 2009]. The reduced serum calcium is hypothesized to be due to the formation of CaF 2 complexes resulting into a net reduction in calcium levels leading to a hypocalcemic response.…”

Section: Discussionmentioning

confidence: 99%

Fluoride Modulates Parathyroid Hormone Secretion in vivo and in vitro

Puranik¹,

Ryan

Yin³

et al. 2014

Cells Tissues Organs

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The study objective was to investigate the effects of fluoride on intact parathyroid hormone (iPTH) secretion. Thyro-parathyroid complexes (TPC) from C3H (n = 18) and B6 (n = 18) mice were cultured in Ca²⁺-optimized medium. TPC were treated with 0, 250, or 500 µM NaF for 24 h and secreted iPTH assayed by ELISA. C3H (n = 78) and B6 (n = 78) mice were gavaged once with distilled or fluoride (0.001 mg [F^-]/g of body weight) water. At serial time points (0.5-96 h) serum iPTH, fluoride, total calcium, phosphorus, and magnesium levels were determined. Expression of genes involved in mineral regulation via the bone-parathyroid-kidney (BPK) axis, such as parathyroid hormone (Pth), calcium-sensing receptor (Casr), vitamin D receptor (Vdr), parathyroid hormone-like hormone (Pthlh), fibroblast growth factor 23 (Fgf23), α-Klotho (αKlotho), fibroblast growth factor receptor 1c (Fgf1rc), tumor necrosis factor 11 (Tnfs11), parathyroid hormone receptor 1 (Pth1r), solute carrier family 34 member 1 (Slc34a1), solute carrier 9 member 3 regulator 1 (Slc9a3r1), chloride channel 5 (Clcn5), and PDZ domain-containing 1 (Pdzk1), was determined in TPC, humeri, and kidneys at 24 h. An in vitro decrease in iPTH was seen in C3H and B6 TPC at 500 µM (p < 0.001). In vivo levels of serum fluoride peaked at 0.5 h in both C3H (p = 0.002) and B6 (p = 0.01). In C3H, iPTH decreased at 24 h (p < 0.0001), returning to baseline at 48 h. In B6, iPTH increased at 12 h (p < 0.001), returning to baseline at 24 h. Serum total calcium, phosphorus, and magnesium levels did not change significantly. Pth, Casr,αKlotho,Fgf1rc,Vdr, and Pthlh were significantly upregulated in C3H TPC compared to B6. In conclusion, the effects of fluoride on TPC in vitro were equivalent between the 2 mouse strains. However, fluoride demonstrated an early strain-dependent effect on iPTH secretion in vivo. Both strains demonstrated differences in the expression of genes involved in the BPK axis, suggesting a possible role in the physiologic handling of fluoride.

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“…Although acute toxic effects of fluoride on heart are fairly well known, information about the exact nature of these effects is still very limited. In experimental animals given massive doses of fluoride, cardiac dysfunction and low BP have been reported (Imanishi et al 2009;Mclvor 1990;Takamori et al 1956). In humans, changes in the electrocardiogram and heart enlargement has been positively correlated to fluoride in the drinking water (Kant et al 2010, Mclvor et al 1987Luoma and Aromaa 1983;Okushi 1954), however there is less certainty about the nature of these effects.…”

Section: Introductionmentioning

confidence: 99%

Interactive effect of arsenic and fluoride on cardio-respiratory disorders in male rats: possible role of reactive oxygen species

et al. 2011

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Epidemiological evidence demonstrates positive correlation between environmental and occupational arsenic or fluoride exposure and risk to various cardio-respiratory disorders. Arsenic-exposure has been associated with atherosclerosis, hypertension, cerebrovascular diseases, ischemic heart disease, and peripheral vascular disorders, whereas Fluoride-exposure manifests cardiac irregularities and low blood pressure (BP). Present study aims to study the combined effects of these toxicants on various cardio-respiratory variables in male rats. Single intravenous (i.v.) dose of arsenic (1, 5, 10 mg/kg) or fluoride (5, 10, 20, 36.5 mg/kg) either alone or in combination were administered. Individual exposure to arsenic or fluoride led to a significant depletion of mean arterial pressure, heart rate (HR), respiration rate and neuromuscular (NM) transmission in a dose-dependent manner. These changes were accompanied by increased levels of blood reactive oxygen species (ROS) and decreased glutathione (GSH) concentrations. An increase in the blood acetyl cholinesterase (AChE) activity was observed in both arsenic or fluoride exposed rats. These changes were significantly more pronounced in arsenic-exposed animals than in fluoride. During combined exposure to arsenic (5 mg/kg) + fluoride (20 mg/kg) or arsenic (10 mg/kg) + fluoride (36.5 mg/kg) the toxic effects were more pronounced compared to individual toxicities of arsenic or fluoride alone. However, combined exposure to arsenic (5 mg/kg) + fluoride (36.5 mg/kg) resulted in antagonistic effects on variables suggestive of altered cardio-respiratory function and oxidative stress. The results from the present study suggest that arsenic or fluoride individually demonstrate cardio-respiratory failure at all doses whereas during combination exposure these toxins show variable toxicities; both synergistic and antagonistic effects depending upon the dose. Moreover, it may be concluded that arsenic and/or fluoride cardio-respiratory toxicity may be mediated via oxidative stress. However, these results are new in the discipline thus requires further exploration.

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Time‐dependent Changes of Blood Parameters and Fluoride Kinetics in Rats after Acute Exposure to Subtoxic Hydrofluoric Acid

Cited by 9 publications

References 17 publications

In Vitro Assessment of Chronic Nanoparticle Effects on Respiratory Cells

In Vitro Assessment of Chronic Nanoparticle Effects on Respiratory Cells

Fluoride Modulates Parathyroid Hormone Secretion in vivo and in vitro

Interactive effect of arsenic and fluoride on cardio-respiratory disorders in male rats: possible role of reactive oxygen species

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