Part 1
2006 Fluoride Abstracts

2006 Fluoride Abstracts. Part 1.

Abstracts for the following years:
Part 1 - mainly biochemistry and physiology (brain, hormonal, G-proteins, etc.)
Part 2 ("b") - all other



















1976 -
1970 -



















1974 -
1968 -



2005-b continued










1990 -b







1972 -
Up to


Full free study available at

World J Gastroenterol. 2006 Feb 21;12(7):1144-8.
DNA damage, apoptosis and cell cycle changes induced by fluoride in rat oral mucosal cells and hepatocytes.

He LF, Chen JG.

Department of Dental Medicine, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China.

AIM: To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes.
METHODS: Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in fluoride group had free access to deionized water containing 150 mg/L sodium fluoride (NaF). The animals in control group were given distilled water. Four weeks later, the animals were killed. Reactive oxygen species (ROS) in oral mucosa and liver were measured by Fenton reaction, lipid peroxidation product, malondialdehyde (MDA), was detected by thiobarbituric acid (TBA) reaction, reduced glutathione (GSH) was assayed by dithionitrobenzoic acid (DTNB) reaction. DNA damage in oral mucosal cells and hepatocytes was determined by single cell gel (SCG) electrophoresis or comet assay. Apoptosis and cell cycle in oral mucosal cells and hepatocytes were detected by flow cytometry.
RESULTS: The contents of ROS and MDA in oral mucosa and liver tissue of fluoride group were significantly higher than those of control group (P<0.01), but the level of GSH was markedly decreased (P<0.01). The contents of ROS, MDA and GSH were (134.73+/-12.63) U/mg protein, (1.48+/-0.13) mmol/mg protein and (76.38+/-6.71) mmol/mg protein in oral mucosa respectively, and (143.45+/-11.76) U/mg protein, (1.44+/-0.12) mmol/mg protein and (78.83+/-7.72) mmol/mg protein in liver tissue respectively. The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higher than those in the control group (P<0.01). The apoptosis rate in oral mucosal cells was (13.63+/-1.81) % in fluoride group, and (12.76+/-1.67)% in hepatocytes, higher than those in control group. Excess fluoride could differently lower the number of oral mucosal cells and hepatocytes at G(0)/G(1) and S G(2)/M phases (P<0.05).
CONCLUSION: Excess fluoride can induce oxidative stress and DNA damage and lead to apoptosis and cell cycle change in rat oral mucosal cells and hepatocytes.

PMID: 16534862 [PubMed - in process]

J Occup Environ Med. 2006 Mar;48(3):275-282.
Incidence of Asthma Among Aluminum Workers.

Taiwo OA, Sircar KD, Slade MD, Cantley LF, Vegso SJ, Rabinowitz PM, Fiellin MG, Cullen MR.

From the Yale University School of Medicine (Dr Taiwo, Dr Sircar, Mr Slade, Ms Cantley, Ms Vegso, Dr Rabinowitz, Ms Fiellin, Dr Cullen), New Haven, Connecticut; and the Respiratory Disease Surveillance Branch, Division of Respiratory Disease Studies (Dr Sircar), National Institute for Occupational Safety and Health, Morgantown, West Virginia.

Exposures to respiratory irritants encountered in aluminum smelters in Europe, Australia, and New Zealand have been suggested as the cause of "potroom asthma." However, there remains disagreement in North America regarding the existence of this entity. This study was designed to assess whether asthma occurs excessively among potroom workers and if so, delineate dose-response relationships for possible causal risk factors. The asthma incidence ratio between potroom and nonpotroom workers after adjusting for smoking was 1.40. Although bivariate analyses showed a relationship between asthma incidence and exposure to total fluoride, gaseous fluoride, particulate fluoride, sulfur dioxide, and smoking, only the effects of gaseous fluoride (relative risk [RR] = 5.1) and smoking (RR = 7.7) remained significant in a multivariate model. Potroom asthma appears to occur at the studied U.S. aluminum smelters at doses within regulatory guidelines.

PMID: 16531831 [PubMed - as supplied by publisher]

Adv Med Sci. 2006;51 Suppl1:91-5.

Effect of sodium fluoride on the morphological picture of the rat liver exposed to NaF in drinking water.

Dabrowska E, Letko R, Balunowska M.

Department of Social and Preventive Dentistry, Medical University of Bialystok, Poland.

PURPOSE: Due to its efficacy in caries prophylaxis and easy application, sodium fluoride (NaF) is still used for caries prevention in the form of fluoridated drinking water, fluoride tablets, fluoridated salt or milk. Effect of fluorides on various metabolic levels in hard and soft tissues, namely respiration as well as carbohydrate, protein, enzymatic and vascular metabolism, can disturb detoxication of fluorine compounds administered orally. The study objective was morphological examination of the liver of young and mature rats exposed to NaF in drinking water from conception till maturity, as well as after its withdrawal.
MATERIAL AND METHODS: In the initial stage of the experiment, 30 female Wistar rats, 180-200 g body weight, were divided into 3 groups: one control and two experimental groups (I, II). Female rats in the experimental groups received fluorine in aqueous solutions of sodium fluoride (NaF) at a concentration of 10.6 mg NaF/dm3 (group I) and 32.0 mg NaF/dm3 (group II).
RESULTS: The pathomorphological changes observed in the liver, particularly of young rats exposed,to fluorides at superoptimal doses can help determine to what degree oral fluoride caries prevention is safe and whether it should be implemented. The transitory nature of pathomorphological changes in hepatocytes indicates adaptive potentials or defence mechanisms against orally administered sodium fluoride.

PMID: 17458067 [PubMed - in process]

Full free study available at

J Biol Chem. 2006 Mar 9; [Epub ahead of print]
Role of Arf6 GDP/GTP cycle and Arf6GAP in actin remodeling and intracellular transport.

Klein S, Franco M, Chardin P, Luton F.

Institut de Pharmacologie Moleculaire et Cellulaire, Valbonne 06560.

We have analysed both biochemically and functionally a series of Arf6 mutants providing new insights into the molecular mode of Arf6 action. First, by comparing a fast-cycling mutant (Arf6T157N) and a GTPase-deficient mutant (Arf6Q67L), our data suggests the necessity for completion of the Arf6 GDP/GTP cycle for plasma membrane and cortical actin cytoskeleton rearrangement, as well as for the recycling of MHCI molecules. Second, we found that aluminum fluoride (AlFx), known for inducing membrane protrusion in cells expressing exogenous Arf6WT, can stabilize an Arf6WT-AlFx-GAP complex in vitro. Third, we found that the tandem mutation Q37ES38I prevents the binding of the GAP and the formation of membrane protrusion and actin reorganization. Collectively, our results establish the requirement of the GDP/GTP cycle and suggest a central role for ArfGAP in Arf6-regulated actin cytoskeleton remodeling and intracellular transport. Finally, competition experiments conducted in vivo suggest the existence of a membrane receptor for Arf6GDP.

PMID: 16527809 [PubMed - as supplied by publisher]

Gig Sanit. 2006 Jan-Feb;(1):69-72.

[Quantitative comparison of human percutaneous and inhalational exposures to uranium and fluorine with uranium hexafluoride and its hydrolysis products]

[Article in Russian]

[No authors listed]

PMID: 16491805 [PubMed - in process]

Full article available at Science Direct

Biochemical and Biophysical Research Communications - 2006 Feb 28

A role for Rho kinase in vascular contraction evoked by sodium fluoride

Jeon SB (a), Jin F (a), Kim JI (a), Kim SH (a), Suk K (a), Chae SC (b), Jun JE (b), Park WH (b), Kim IK (a).

(a) Department of Pharmacology, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea
(b) Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea

Agonist and depolarization-induced vascular smooth muscle contractions involve the activation of Rho-kinase pathway. However, there are no reports addressing the question whether this pathway is involved in NaF-induced vascular contractions. We hypothesized that Rho-kinase plays a role in vascular contraction evoked by sodium fluoride in rat aortae. In both physiological salt solution and calcium-free solution with 2 mM EGTA, cumulative addition of NaF increased vascular tension in concentration-dependent manners. Effects of Rho-kinase inhibitor (Y27632) on phosphorylation of myosin light chain (MLC20) and myosin targeting subunit (MYPT1Thr696) of myosin light chain phosphatase as well as NaF-induced contractions were determined using isolated tissue and the Western blot experiments. Y27632 inhibited NaF-induced contractions in a concentration-dependent manner. NaF increased phosphorylation of MLC20 and MYPT1Thr696, which were also inhibited by Y27632. However, MLCK inhibitor (ML-7) or PKC inhibitor (Ro31-8220) did not inhibit the NaF-induced contraction. These results indicate that activation of Rho-kinase and the subsequent phosphorylation of MYPT1Thr696 play important roles in NaF-induced contraction of rat aortae.

Excerpt from full article at Science Direct:
The mechanism by which F- activates G-proteins has been clearly established [14], [15], [16] and [17]. It has been reported that the effect of NaF on heterotrimeric G protein is the result of formation of AlF4- from fluoride and trace amounts of aluminum, which can come from contamination of glassware [32] and [33]. The cellular mechanism by which fluoroaluminates activate G proteins is based on the structural similarity of AlF4- to PO43-, enabling the former to interact with GDP situated on the ?-subunit of the G proteins where it can mimic GTP [34]. NaF is also a classical Ser/Thr phosphatase inhibitor [35] and is routinely included in extraction buffers to prevent dephosphorylation of proteins on Ser and Thr residues by endogenous phosphatases. Since it has been known that Rho-kinase plays a role in hypertension, coronary artery spasm, and basilar artery vasospasm [3], [36] and [37], NaF is a useful chemical to activate Rho-kinase pathway for research.


[3] M. Uehata, T. Ishizaki, H. Satoh, T. Ono, T. Kawahara, T. Morishita, H. Tamakawa, K. Yamagami, J. Inui, M. Maekawa and S. Narumiya, Calcium sensitization of smooth muscle mediated by a Rho-associated protein kinase in hypertension, Nature 389 (1997), pp. 990–994.

[14] A.G. Gilman, Guanine nucleotide-binding regulatory proteins and dual control of adenylate cyclase, J. Clin. Invest. 73 (1984), pp. 1–4.

[15] Y. Kanaho, J. Moss and M. Vaughan, Mechanism of inhibition of transducin GTPase activity by fluoride and aluminum, J. Biol. Chem. 260 (1985), pp. 11493–11497.

[16] P.F. Blackmore and J.H. Exton, Studies on the hepatic calcium-mobilizing activity of aluminum fluoride and glucagon. Modulation by cAMP and phorbol myristate acetate, J. Biol. Chem. 261 (1986), pp. 11056–11063.

[17] S. Cockcroft and J.A. Taylor, Fluoroaluminates mimic guanosine 5?-[gamma-thio]triphosphate in activating the polyphosphoinositide phosphodiesterase of hepatocyte membranes. Role for the guanine nucleotide regulatory protein Gp in signal transduction, Biochem. J. 241 (1987), pp. 409–414.

[32] Y.Y. Zeng, C.G. Benishin and P.K. Pang, Guanine nucleotide binding proteins may modulate gating of calcium channels in vascular smooth muscle. I. Studies with fluoride, J. Pharmacol. Exp. Ther. 250 (1989), pp. 343–351.

[33] M. Chabre, Aluminofluoride and beryllofluoride complexes: a new phosphate analogs in enzymology, Trends Biochem. Sci. 15 (1990), pp. 6–10.

[34] J. Bigay, P. Deterre, C. Pfister and M. Chabre, Fluoroaluminates activate transducin-GDP by mimicking the gamma-phosphate of GTP in its binding site, FEBS Lett. 191 (1985), pp. 181–185.

[35] S. Shenolikar and A.C. Nairn, Protein phosphatases: recent progress, Adv. Second Messenger Phosphoprotein Res. 23 (1991), pp. 1–121.

[36] H. Shimokawa, M. Seto, N. Katsumata, M. Amano, T. Kozai, T. Yamawaki, K. Kuwata, T. Kandabashi, K. Egashira, I. Ikegaki, T. Asano, K. Kaibuchi and A. Takeshita, Rho-kinase-mediated pathway induces enhanced myosin light chain phosphorylations in a swine model of coronary artery spasm, Cardiovasc. Res. 43 (1999), pp. 1029–1039.

[37] I. Kim, B.D. Leinweber, M. Morgalla, W.E. Butler, M. Seto, Y. Sasaki, J.W. Peterson and K.G. Morgan, Thin and thick filament regulation of contractility in experimental cerebral vasospasm, Neurosurgery 46 (2000), pp. 440–447.

In Vivo. 2006 Jan-Feb;20(1):103-8.

Enhancement of sodium fluoride-induced cell death by centrifugal force.

Chien CH, Ali Chowdhury S, Sakagami H, Kanegae H.

Division of Orthodontics, Department of Human Development and Fostering, Meikai University School of Dentistry, Sakado, Saitama 350-0283, Japan.

As an initial step in the study of the influence of orthodontic force on cellular function in vitro, the effects of centrifugal force on the cytotoxicity induced by various apoptosis inducers were investigated. When human oral squamous cell carcinoma (HSC-2) and human promyelocytic leukemia (HL-60) cell lines were treated with increasing magnitudes of centrifugal force (evaluated by g-value), the viability assessed by the MTT method and trypan blue dye exclusion began to decline. Centrifugal force enhanced the cytotoxicity of sodium fluoride (NaF), but not that of redox compounds (hydrogen peroxide, sodium ascorbate, gallic acid) or chemotherapeutic agents (daunorubicin, doxorubicin, idarubicin, mitoxantrone, peplomycin, 5-FU). The combination of NaF and centrifugal force enhanced caspase-3 activity. The present study suggests that centrifugal force is an additional factor that modifies the biological activity of NaF.

PMID: 16433036 [PubMed - in process]

Am J Physiol Lung Cell Mol Physiol. 2006 Jan 13; [Epub ahead of print]

The mechanism of fluoride-induced MAP kinase activation in pulmonary artery endothelial cells.

Bogatcheva NV, Wang P, Birukova AA, Verin AD, Garcia JG.

Department of Medicine, University of Chicago, Chicago, IL, USA.

In this study, we demonstrate that endothelial cells (EC) challenge with NaF, a recognized G protein activator and protein phosphatase inhibitor, leads to a significant Erk activation, with increased phosphorylation of the well-known Erk substrate, caldesmon. Inhibition of the Erk MAPK kinase, MEK, by UO126 produces a marked decrease in NaF-induced caldesmon phosphorylation. NaF transiently increases the activity of the MEK kinase known as Raf-1 (~3-4 fold increase over basal level), followed by a sustained Raf-1 inhibition (~3-4 fold decrease). Selective Raf-1 inhibitors (ZM 336372 and Raf-1 inhibitor 1) significantly attenuate NaF-induced Erk and caldesmon phosphorylation. Because we have previously shown that Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) participates in Erk activation in thrombin-challenged cells, we next explored if CaMKII is involved in NaF-induced EC responses. We found that in NaF-treated EC, CaMKII activity increases in a time-dependent manner with maximal activity at 10 min (~4 fold increase over a basal level). Pretreatment with KN-93, a specific CaMKII inhibitor, attenuates NaF-induced barrier dysfunction and Erk phosphorylation. The Rho inhibitor, C3 exotoxin, completely abolishes NaF-induced CaMKII activation. Collectively, these data suggest that sequential activation of Raf-1, MEK, and Erk is modulated by Rho-dependent CaMKII activation and represents important NaF-induced signaling response. Caldesmon phosphorylation occurring by Erk-dependent mechanism in NaF-treated pulmonary EC may represent a link between NaF stimulation and contractile responses of endothelium.

PMID: 16414982 [PubMed - as supplied by publisher]

Biochemistry. 2006 Jan 24;45(3):793-800.

Fluoride inhibition of enolase: crystal structure and thermodynamics.

Qin J, Chai G, Brewer JM, Lovelace LL, Lebioda L.

Department of Chemistry and Biochemistry and Center for Colon Cancer Research, University of South Carolina, Columbia, South Carolina 29208, and Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia 30602.

Enolase is a dimeric metal-activated metalloenzyme which uses two magnesium ions per subunit: the strongly bound conformational ion and the catalytic ion that binds to the enzyme-substrate complex inducing catalysis. The crystal structure of the human neuronal enolase-Mg(2)F(2)P(i) complex (enolase fluoride/phosphate inhibitory complex, EFPIC) determined at 1.36 A resolution shows that the combination of anions effectively mimics an intermediate state in catalysis. The phosphate ion binds in the same site as the phosphate group of the substrate/product, 2-phospho-d-glycerate/phosphoenolpyruvate, and induces binding of the catalytic Mg(2+) ion. One fluoride ion bridges the structural and catalytic magnesium ions while the other interacts with the structural magnesium ion and the ammonio groups of Lys 342 and Lys 393. These fluoride ion positions correspond closely to the positions of the oxygen atoms of the substrate's carboxylate moiety. To relate structural changes resulting from fluoride, phosphate, and magnesium ions binding to those that are induced by phosphate and magnesium ions alone, we also determined the structure of the human neuronal enolase-Mg(2)P(i) complex (enolase phosphate inhibitory complex, EPIC) at 1.92 A resolution. It shows the closed conformation in one subunit and a mixture of open and semiclosed conformations in the other. The EPFIC dimer is essentially symmetric while the EPIC dimer is asymmetric. Isothermal titration calorimetry data confirmed binding of four fluoride ions per dimer and yielded K(b) values of 7.5 x 10(5) +/- 1.3 x 10(5), 1.2 x 10(5) +/- 0.2 x 10(5), 8.6 x 10(4) +/- 1.6 x 10(4), and 1.6 x 10(4) +/- 0.7 x 10(4) M(-)(1). The different binding constants indicate negative cooperativity between the subunits; the asymmetry of EPIC supports such an interpretation.

PMID: 16411755 [PubMed - in process]

Biol Trace Elem Res. 2006 Jan;109(1):55-60.
Effect of sodium fluoride on the expression of bcl-2 family and osteopontin in rat renal tubular cells.

Xu H, Jin XQ, Jing L, Li GS.

Institute of Endemic Diseases, Jilin University, 828 Xinmin, ChangChun 130021, China.

Our earlier studies showed that the apoptosis of renal tubules can be induced by sodium fluoride (NaF). The present study was designed to estimated the effects of B-cell lymphoma/leukemia 2 (Bcl-2), Bcl-2-associated protein X (Bax), and osteopontin (OPN) on the apoptosis of renal tubular cells induced by NaF at different levels. The technique of reverse transcription-polymerase chain reaction and densitometer scanning volume density were used to evaluate the changes of Bcl-2, Bax, and OPN mRNA in tubular cells treated with different doses of NaF (0, 1, 5, 7.5, 12.5 mgF-/L) for 48 h. Compared to control, the level of Bax mRNA significantly increased at cells of the 7.5- and 12.5-mg F-/L groups and the expression of Bcl-2 mRNA obviously decreased at cells of the 5- and 7.5-mg F-/L groups. The NaF also enhanced the expression of OPN mRNA in a dose-dependent manner, but the strongest expression of OPN mRNA was observed at cells of the 7.5-mg F-/L group. The results suggested that NaF induces the apoptosis in renal tubules via activation of the Bax expression and Bcl-2 suppression; OPN probably acts as protective role against apoptosis in fluoride-treated renal cells.

PMID: 16388103 [PubMed - in process]

J Zoo Wildl Med. 2006 Dec;37(4):477-86.

Fluorosis as a probable cause of chronic lameness in free ranging eastern grey kangaroos (Macropus giganteus).

Clarke E, Beveridge I, Slocombe R, Coulson G.

Departments of Veterinary Science and Zoology, The University of Melbourne, Parkville, Victoria 3052, Australia.

A population of eastern grey kangaroos (Macropus giganteus) inhabiting heathland and farmland surrounding an aluminum smelter at Portland, Victoria, Australia, exhibited clinical signs of lameness. An investigation was undertaken to determine the cause of this lameness. Hematology, necropsy, histopathology, fecal egg count, total worm count, reproductive status, and the population age range were examined and failed to reveal any additional underlying disease state. The specific problem of lameness was addressed with bone histopathology, radiography, quantitative ultrasonography, microradiography, and multielement analysis of bone ash samples. The significant lesions observed were: osteophytosis of the distal tibia and fibula, tarsal bones, metatarsus IV, and proximal coccygeal vertebrae; osteopenia of the femur, tibia, and metatarsus IV; incisor enamel hypoplasia; stained, uneven, and abnormal teeth wear; abnormal bone matrix mineralization and mottling; increased bone density; and elevated bone fluoride levels. Microradiography of affected kangaroos exhibited "black osteons," which are a known manifestation of fluorosis. Collectively, these lesions were consistent with a diagnosis of fluorosis.

PMID: 17315432 [PubMed - indexed for MEDLINE]

Folia Morphol (Warsz). 2006 Nov;65(4):359-66.

Fluoride alters type I collagen expression in the early stages of odontogenesis.

Maciejewska I, Spodnik JH, Domaradzka-Pytel B, Sidor-Kaczmarek J, Bereznowski Z.

Department of Oral Implantology, Medical University, Gdansk, Poland.

Fluoride alters the expression and post-translational modifications of extracellular matrix proteins in dentin. The aim of our study was to determine the effects of fluoride on type I collagen expression during the early stages of tooth germ development in rats. Pregnant dams were divided into three groups and fed a standard diet. From the fifth day of pregnancy the three groups received tap water with, respectively, trace amounts of fluoride (C), a low fluoride concentration (FL) or and a high fluoride concentration (FH). Changes in type I collagen expression and distribution were evaluated. The expression of type I collagen was restricted to the extracellular spaces of cells of mesenchymal origin. In the youngest animals the most intense immunoreactivity for type I collagen was detected in predentin of the FL group. Although the intensity of immunostaining increased in proportion to the age of the animals, the largest increase in the groups investigated was detected in the FL group. We concluded that a low concentration of fluoride can act as a stimulator of type I collagen deposition in the extracellular matrix of dentin, while high concentrations of fluoride have an opposite effect, acting as an inhibitor of type I collagen formation in dentin.

PMID: 17171616 [PubMed - indexed for MEDLINE]

Biol Trace Elem Res. 2006 Jan;109(1):35-48.
Influence of Sodium Fluoride and Caffeine on the Kidney Function and Free-Radical Processes in that Organ in Adult Rats.

Birkner E, Grucka-Mamczar E, Zwirska-Korczala K, Zalejska-Fiolka J, Stawiarska-Pieta B, Kasperczyk S, Kasperczyk A.

Department of Biochemistry, Silesian Medical University in Katowice, Jordana 19, 41-808 Zabrze, Poland.

An experiment was carried out on Sprague-Dawley rats (adult males) that for 50 days were administered, in the drinking water, NaF and NaF with caffeine (doses, respectively: 4.9 mg of NaF/kg body mass/24 h and 3 mg of caffeine/kg body mass/24 h). Disturbances were noted in the functioning of kidneys, which were particularly noticeable after the administration of NaF with caffeine. Changes in the functioning of kidneys were also confirmed by such parameters as the level of creatinine, urea, protein, and calcium. Modifications of the enzymatic antioxidative system (superoxide dismutase, catalase, and glutathione peroxidase) and lipid peroxidation (malondialdehyde) were also observed. Changes in the contents of the above parameters as well as pathomorphological examinations suggest increased diuresis, resulting in dehydration of the rats examined.

PMID: 16388101 [PubMed - in process]

Wei Sheng Yan Jiu. 2006 Sep;35(5):546-8.

[Research in the relation between telomerase reverse transcriptase expression in spermatogenic cells and serum levels of estradiol of fluorotic rats]

[Article in Chinese]

Li Y, Zhu JY, Zhuang DG, Cheng XM.

Department of Environmental Health, College of Public Health, Zhengzhou University, Zhengzhou 450052, China.

OBJECTIVE: To study the relation between telomerase reverse transcriptase (TERT) activity expression in spermatogenic cells and serum levels of estradiol of fluorotic rats.
METHODS: We randomly divided thirty SD male rats into control group, low-dose group and high-dose group, then inject sodium fluoride (0, 10, 20 mg/kg bw) into celiac of rats. We respectively observed changes of estrogen and TERT using methods of radioimmunoassay, in situ hybridization. In addition, we observed the quality of spermatozoa.
RESULTS: The level of estrogen, the expression of telomerase and the number and the livability of the spermatozoon in low-dose and high-dose fluorotic rats were lower than those of control rats (P < 0.05). Therefore,the above indexes decreased with the increase of dosage. In addition, sperm aberration of each fluorotic group was higher than control group (P < 0.05). And it increased with the increase of dosage. The content of E2 in serum of different fluoride treatment groups was positively correlated with the expression of telomerase in seminiferous tubule significantly, respectively (low-dose fluoride treatment groups, r = 0.941, P < 0.01, high-dose fluoride treatment groups, r = 0.929, P < 0.01).
CONCLUSION: NaF possibly damaged the male reproductive system by the approach of E2/ER-TERT-spermotozoon, relation between TERT expression in spermatogenic cells and serun levels of estradiol is positive correlation.

PMID: 17086699 [PubMed - in process]

Eur Spine J. 2006 Oct 31; [Epub ahead of print]

Thoracic ossification of ligamentum flavum caused by skeletal fluorosis.

Wang W, Kong L, Zhao H, Dong R, Li J, Jia Z, Ji N, Deng S, Sun Z, Zhou J.

Spinal Surgery Department, Tianjin Hospital, No. 406 Jiefangnan Road, Hexi District, Tianjin City, 300211, People's Republic of China.

Thoracic ossification of ligamentum flavum (OLF) caused by skeletal fluorosis is rare. Only six patients had been reported in the English literature. This study reports findings from the first clinical series of this disease. This was a retrospective study of patients with thoracic OLF due to skeletal fluorosis who underwent surgical management at the authors' hospital between 1993 and 2003. Diagnosis of skeletal fluorosis was made based on the epidemic history, clinical symptoms, radiographic findings, and urinalysis. En bloc laminectomy decompression of the involved thoracic levels was performed in all cases. Cervical open door decompression or lumbar laminectomy decompression was performed if relevant stenosis was present. Neurological status was evaluated preoperatively, at the third day postoperatively, and at the end point of follow-up using the Japanese Orthopaedic Association (JOA) scoring system of motor function of the lower extremities. A total of 23 cases were enrolled, 16 (69.6%) males and 7 (30.4%) females, age ranging from 42 to 72 years (mean 54.8 years). All patients came from a high-fluoride area, and 22 (95.7%) had dental fluorosis. Medical imaging showed OLF together with ossification of many ligaments and interosseous membranes, including interosseous membranes of the forearm (18/23 patients 78.3%), leg (14/23 patients 60.9%), and ribs (11/23 patients 47.8%). OLF was classified into five types based on MRI findings: localized (4/23 patients 17.4%), continued (12/23 patients 52.2%), skip (3/23 patients 13.0%), combining with anterior pressure (2/23 patients 8.7%), and combining with cervical and/or lumbar stenosis (2/23 patients, 8.7%). Urinalysis showed a markedly high urinary fluoride level in 14 of 23 patients (60.9%). Patients were followed up for an average duration of 4 years, 5 months. Paired t-test showed that the JOA score was slightly but nonsignificantly increased relative to preoperative measurement 3 days after surgery (P = 0.0829) and significantly increased at the end of follow-up (P = 0.0001). In conclusion, Fluorosis can cause ossification of thoracic ligamentum flavum, as well as other ligaments. Comparing with other OLF series, a larger number of spinal segments were involved. The diagnosis of skeletal fluorosis was made by the epidemic history, clinical symptom, imaging study findings, and urinalysis. En bloc laminectomy decompression was an effective method.

PMID: 17075705 [PubMed - as supplied by publisher]

Cent Eur J Public Health. 2006 Dec;14(4):189-92.

Orofacial dysfunctions, drinking regimen and quality of life--long-term prospective study.

Pilinova A, Matejickova E, Lendova E, Foltinova J, Pisa J.

Institute of Dental Research, 1st Faculty of Medicine of the Charles University, Prague and General University Hospital, Prague, Czech Republic.

The care for mentally ill patients with combined impairment deals with orofacial dysfunctions of the mentally ill, especially children suffering from Down syndrome and cerebral palsy. Objective of the study was to assess urine fluoride excretion in disabled patients with orofacial dysfunctions in relation to prevention of dental caries. The urine fluoride concentrations in disabled people were analysed to assess their fluoride exposure and possibly preventive contribution of fluoride intake. The patients for the study were recruited from the clients of three day-stay establishments from two regions in the Czech Republic. All the clients from the selected establishments were examined except for a small number of clients, whose statutory representatives (usually parents) did not agree with oral examination. Signed informed consents were obtained from the statutory representatives of all the examined patients. Totally 95 mentally disabled patients were examined with the mean age of 11.8 years (ranging from 6 months to 28 years) for orofacial dysfunctions using the Castillo Morales concept. Fluoride concentrations were measured by fluoride-selective electrode. The urine density was measured by means of hydrostatic weighing. The above-mentioned analytical methods were chosen since urine density reflects the overall liquids intake by the person and the fluoride excretion by the urine reflects its intake from all environmental sources. Atypical swallowing act was found in 98% of the cohort. Mean urine density was 1.038 g/ml ranging from 1.002 to 1.069 (77 samples). The mean urine fluoride concentration was 0.816 mg/l ranging from 0.045 to 3.225 (82 samples). Orofacial dysfunctions decrease the quality of life. Among other aspects, they influence liquids intake due to an impaired swallowing act. Moreover, patients are often dependent on the assistance of the other persons.

PMID: 17243499 [PubMed - indexed for MEDLINE]

Biomed Environ Sci. 2006 Dec;19(6):439-44.

Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats.

Yu RA, Xia T, Wang AG, Chen XM.

Department of Occupational and Environmental Health, School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, Guangdong, China.

OBJECTIVE: To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride.
METHODS: Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 x 7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4 x 7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry.
RESULTS: NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine gamma-glutamyl transpeptidase (gamma-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly.
CONCLUSION: Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.

PMID: 17319268 [PubMed - indexed for MEDLINE]

J Orthop Surg. 2006 Nov 2;1:10.

Thoracic myelopathy caused by ossification of ligamentum flavum of which fluorosis as an etiology factor.

Wang W, Kong L, Zhao H, Dong R, Zhou J, Lu Y.

Spine surgery department, Tianjin hospital, No, 406 Jiefangnan Road, Hexi District, Tianjin City, 300211, People's Republic of China.

PURPOSE: To evaluate the clinical feature, operative method and prognosis of thoracic ossification of ligamentum flavum caused by skeletal fluorosis.
METHODS: All the patients with thoracic OLF, who underwent surgical management in the authors' hospital from 1993-2003, were retrospectively studied. The diagnosis of skeletal fluorosis was made by the epidemic history, clinical symptoms, radiographic findings, and urinalysis. En bloc laminectomy decompression of the involved thoracic levels was performed in all cases. Cervical open door decompression or lumbar laminectomy decompression was performed if relevant stenosis existed. The neurological statuses were evaluated with the Japanese Orthopaedic Association (JOA) scoring system preoperatively and at the end point of follow up. Also, the recovery rate was calculated.
RESULTS: 23 cases have been enrolled in this study. Imaging study findings showed all the cases have ossification of ligamentum flavum together with ossification of many other ligaments and interosseous membranes, i.e. interosseous membranes of the forearm in 18 of 23 (78.3%), of the leg in 14 of 23 (60.1%) and of the ribs in 11 of 23 (47.8%). Urinalysis showed markedly increased urinary fluoride in 14 of 23 patients (60.9%). All the patients were followed up from 12 months to 9 years and 3 months, with an average of 4 years and 5 months. The JOA score increased significantly at the end of follow up (P = 0.0001). The recovery rate was 51.83 +/- 32.36%. Multiple regression analysis revealed that the preoperative JOA score was an important predictor of surgical outcome (p = 0.0022, r = 0.60628). ANOVA analysis showed that patients with acute onset or too long duration had worse surgical result (P = 0.0003).
CONCLUSION: Fluorosis can cause ossification of thoracic ligamentum flavum, as well as other ligaments. En bloc laminectomy decompression was an effective method. Preoperative JOA score was the most important predictor of surgical outcome. Patients with acute onset or too long duration had worse surgical outcome.

PMID: 17150117 [PubMed - in process]

Med Tr Prom Ekol. 2006;(9):6-9.

[Toxicologic characteristics of ammonium fluoroberyllate and its distribution in body after various intake methods]

[Article in Russian]

Urikh AA, Leshukov AV, Shin RB.

The authors present materials on toxic influence and distribution of ammonium fluoroberyllate after various intake ways in white rats, on decontamination of skin wound surface.

PMID: 17089519 [PubMed - indexed for MEDLINE]

Bull Environ Contam Toxicol. 2006 Nov;77(5):700-6.

Absence of DNA damage in multiple organs after oral exposure to fluoride in Wistar rats.

Buzalaf MA, Salvadori DM, Marques ME, Caroselli EE, Leite AL, Camargo EA, Ribeiro DA.


Department of Biological Sciences, Laboratory of Biochemistry, Bauru School of Dentistry, USP, SP, Brazil.

PMID: 17176997 [PubMed - indexed for MEDLINE]

Fiziol Zh. 2006;52(5):47-54.

[State of the adaptation reactions in the correction process of the negative effect of the stress-factors of chemical nature]

[Article in Ukrainian]

Hzhehots'kyi MR, Fedorenko IuV.

The prolonged influence of lead and fluorine lowers gradually adaptative reserves of organism. Gradual diet supplementation with such bioprotectors as pectin, calcium and triovitum results in renewal of prooxidant-antioxidant balance, that is confirmed by the elevation of antioxidant defence' integral coefficient from 0,09 to 1. The method of estimation of the states of the organism adaptive reactions and the power of action of chemical nature stress-factors in the process of correction of the adaptive violations, using the value of antioxidant defence' integral coefficient is offered. This method is based on correlation of indexes of antioxidant system activity and intensity of lipoperoxidation products.

PMID: 17176839 [PubMed - indexed for MEDLINE]

J Water Health. 2006 Dec;4(4):533-42.

An attempt to estimate the global burden of disease due to fluoride in drinking water.

Fewtrell L, Smith S, Kay D, Bartram J.

Centre for Research into Environment and Health, 5 Quakers Coppice, Crewe Gates Farm, Crewe, Cheshire, UK.

A study was conducted to examine the feasibility of estimating the global burden of disease due to fluoride in drinking water. Skeletal fluorosis is a serious and debilitating disease which, with the exception of one area in China, is overwhelmingly due to the presence of elevated fluoride levels in drinking water. The global burden of disease due to fluoride in drinking water was estimated by combining exposure-response curves for dental and skeletal fluorosis (derived from published data) with model-derived predicted drinking water fluoride concentrations and an estimate of the percentage population exposed. There are few data with which to validate the output but given the current uncertainties in the data used, both to form the exposure-response curves and those resulting from the prediction of fluoride concentrations, it is felt that the estimate is unlikely to be precise. However, the exercise has identified a number of data gaps and useful research avenues, especially in relation to determining exposure, which could contribute to future estimates of this problem.

PMID: 17176823 [PubMed - indexed for MEDLINE]


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