Full
free study available at http://www.wjgnet.com/1007-9327/12/1144.pdf
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. helingfei.wh@163.com.
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]
|
|
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16531831&query_hl=1&itool=pubmed_docsum
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]
|
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17458067&query_hl=7&itool=pubmed_docsum
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. helpdentamb@tlen.pl
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 http://www.jbc.org/cgi/reprint/M601021200v1?ijkey=50be4e0889009f2c23145732d1721e48d80fa26f
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16491805&query_hl=34&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16527249&query_hl=1&itool=pubmed_docsum
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.
References:
[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.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16433036&query_hl=1&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16414982&query_hl=3&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16411755&query_hl=3&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16388103&query_hl=1&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17315432&query_hl=1&itool=pubmed_DocSum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17171616&query_hl=1&itool=pubmed_DocSum
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. Izabelam@amg.gda.pl
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16388101&query_hl=1&itool=pubmed_docsum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17086699&query_hl=1&itool=pubmed_DocSum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17075705&query_hl=1&itool=pubmed_DocSum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17243499&query_hl=1&itool=pubmed_DocSum
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. alex.p@centrum.cz
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17319268&query_hl=1&itool=pubmed_DocSum
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. yurian.tj@163.com
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17150117&query_hl=1&itool=pubmed_DocSum
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. wangwwb@yahoo.com.cn.
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17089519&query_hl=1&itool=pubmed_DocSum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17176997&query_hl=1&itool=pubmed_DocSum
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.
NO ABSTRACT AVAILABLE
Department of Biological Sciences, Laboratory of Biochemistry,
Bauru School of Dentistry, USP, SP, Brazil.
PMID: 17176997 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17176839&query_hl=1&itool=pubmed_DocSum
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17176823&query_hl=1&itool=pubmed_DocSum
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. Lorna@creh.demon.co.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]
