Some
studies reporting effects on the brain from sodium fluoride
Note:
the following are a limited number of
studies that have found adverse effects on the brain
with NaF. Not included are numerous studies on G-Proteins
and NaF due to lack of time to condense results. Also not
included are the many studies on aluminum fluoride. |
Date |
Effects........................................... |
Study |
ATSDR
(2003) response to studies |
UPDATE
NRC
2006 REPORT
Studies cited |
2003
RAT |
Fluoride
concentration in rat hippocampus was significantly correlated
with the dosage of fluoride, and
there were significant differences among high dosage group [(13.03
+/- 1.79) micro g/g], low dosage group [(9.83 +/- 0.92) micro
g/g] and control |
Zhonghua
Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2003
Apr;21(2):102-4.
[Studies on fluoride concentration and
cholinesterase activity in rat hippocampus]
Zhai JX, Guo ZY, Hu CL, Wang QN, Zhu
QX.
School of Public Health, Anhui Medical University, Hefei 230032,
China.
Article
in Chinese. Suggest NRC translate |
Not
cited by ATSDR |
Not
cited by NRC |
2003
RABBIT
NaF 0,
5, 10, 20, and 50 mg
15 weeks |
Neuropathological
changes occurred with loss of the molecular
layer and glial cell layer in the brain tissues of rabbits
exposed to the three higher fluoride doses. The Purkinje
neurones exhibited chromatolysis and acquired a "ballooned"
appearance. Nissl substance showed various degrees of decrease
and even complete loss. Fragmented
particles were retained in the perinuclear zone. The
perikaryon showed vacuolization,
and spheroid bodies were present in the neoplasm. These cytoplasmic
inclusions appeared as various sized ovoid bodies or elongated
eosinophilic masses due to which the nucleus was shifted to
the periphery. |
Fluoride
36: 95-105.2003
Histopathological
investigation of fluoride-induced neurotoxicity in rabbits.
Shashi
A. |
Not cited
by ATSDR |
Not
cited by NRC |
2003
NaF
recombinant
human prion protein |
Chemical
unfolding studies in urea show that at low concentrations
(below approximately 50 mM), all salts
tested (sodium
sulfate, sodium fluoride, sodium
acetate and sodium chloride) significantly
reduce the thermodynamic stability of the protein.
The observed
decrease in the thermodynamic stability of huPrP90-231 in
the presence of sodium fluoride, sulfate, acetate and chloride
is highly unusual since these salts are generally known to
have a stabilizing effect on proteins.
The present
study provides direct experimental evidence that, at relatively
low concentrations, a variety of salts including sodium fluoride,
sodium sulfate, sodium acetate, and sodium chloride decrease
the thermodynamic stability of the recombinant human prion
protein.
To the
best of our knowledge, no other protein has been reported
to be destabilized by kosmotropes such as fluoride, sulfate
or acetate. Therefore, the present finding points to rather
unique properties of the prion protein.
The present
data indicate that electrostatic interactions play
an unusually important role in the stability of the prion
protein. The abnormal effect of salts is likely due
to the ion-induced destabilization of salt bridges (Asp144-Arg148
and/or Asp147-Arg151) in the extremely hydrophilic helix 1. |
J Biol Chem 2003. Apr
3
Atypical effect of salts on
the thermodynamic stability of human prion protein
Apetri AC, Surewicz WK.
Physiology and Biophysics, Case Western Reserve University,
Cleveland, OH 44106.
Free
full text article
|
Not cited
by ATSDR |
Not
cited by NRC |
2003
high-frequency
synaptic stimulation in the rat hippocampal CA1-isolated slice
preparations |
intracellular
loading of the GABA(A) receptor blocker fluoride abolished the
oscillatory responses in the pyramidal cells. |
Neuroscience
2003.
119(1):265-75
Excitatory gaba input directly
drives seizure-like rhythmic synchronization in mature hippocampal
CA1 pyramidal cells.
Fujiwara-Tsukamoto Y, Isomura Y, Nambu
A, Takada M.
Dept. of System Neuroscience, Tokyo Metropolitan Institute for
Neuroscience, 2-6 Musashidai, Fuchu, 183-8526, Tokyo, Japan
|
Not cited
by ATSDR |
Not
cited by NRC |
2003 |
In an attempt
to elucidate the mechanism by which excessive fluoride damages
the central nervous system, the effects of exposure of PC12
cells to different concentrations of fluoride for 48 h on nicotinic
acetylcholine receptors (nAChRs) were characterized here. Significant
reductions in the number of binding sites for both [3H]epibatidine
and [125I]alpha-bungarotoxin, as well as a significant decrease
in the B(max) value for the high-affinity of epibatidine binding
site were observed in PC12 cells subjected to high levels of
fluoride. On the protein level, the alpha 3 and alpha 7 subunits
of nAChRs were also significantly decreased in the cells exposed
to high concentrations of fluoride. In contrast, such exposure
had no significant effect on the level of the beta 2 subunit.
These findings suggest that selective
decreases in the number of nAChRs may play an important role
in the mechanism(s) by which fluoride causes dysfunction of
the central nervous system. |
Toxicology.
2003 Feb 1;183(1-3):235-42.
Selective decreases of nicotinic acetylcholine
receptors in PC12 cells exposed to fluoride.
Chen J, Shan KR, Long YG, Wang YN, Nordberg A, Guan ZZ.
Department of Pathology, Guiyang Medical College, Guiyang 550004,
Guizhou, PR China. |
Not cited
by ATSDR |
Not
cited by NRC |
2002
MOUSE
(Female) |
Ultrastructural
studies revealed neurodegenrative characteristics
like involution of cell membranes, swelling of mitochondria,
clumping of chromatin material
etc, can be observed in cell bodies of CA3, CA4 and dentate
gyrus (Dg).
Fluoride
intoxicated animals also performed poorly
in motor co-ordination tests and maze tests |
Indian
J Exp Biol. 2002 May;40(5):546-54.
Neurotoxicity of fluoride: neurodegeneration
in hippocampus of female mice.
Bhatnagar M, Rao P, Sushma J, Bhatnagar R.
Dept. of Zoology, M.L.S. University, Udaipur 313 001, India.
mbhatnagar@yahoo.com |
Not cited
by ATSDR |
CITED
BY NRC |
2002
RAT
NaF |
The
DNA damage in pallium neurons
in rats of the fluoride group was much more serious compared
with those of the control group
TUNEL
positive cells were found in pallium,
hippocampus and cerebellar granule cells in rats of
fluoride group, whereas those in the control group were rare |
Zhonghua
Yu Fang Yi Xue Za Zhi. 2002 Jul;36(4):222-4.
[Studies on DNA damage and apoptosis in rat brain induced
by fluoride]
Chen
J, Chen X, Yang K, Xia T, Xie H.
Dept. of Environmental Health, Tongji Medical College, Huazhong
University of Science and Technology, Wuhan 430030, China.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
2002
RAT
NaF |
results
suggest that fluoride enhances oxidative
stress in the brain, thereby disturbing the antioxidant
defense of rats Increased oxidative stress could be one of the
mediating factors in the pathogenesis of fluoride toxicity in
the brain. |
Fluoride
2002; 35(3):153-160.
Brain
lipid peroxidation and antioxidant systems of young rats in
chronic fluoride intoxication.
Shivarajashankara YM, Shivashankara AR, Bhat PG, Rao SH
Correspondence:
YM Shivarajashankara, Dept. of Biochemistry, MR Medical College,
Gulbarga-585105, Karnataka, India. shivrajsym@yahoo.com |
Not cited
by ATSDR |
Not
cited by NRC |
2002
RAT
100 ppm
F |
rats
exposed to 100 ppm fluoride showed significant neurodegenerative
changes in the hippocampus, amygdala, motor cortex, and cerebellum.
Changes included decrease in size and number of neurons in all
the regions, decrease in the number of Purkinje cells in the
cerebellum, and signs of chromatolysis and gliosis in the motor
cortex. |
Full
report
Fluoride 2002; 35(1):12-21
Histological changes in the brain
of young fluoride-intoxicated rats
YM Shivarajashankara, AR Shivashankara,
P Gopalakrishna Bhat, S Muddanna Rao, S Hanumanth Rao
Correspondence:
YM Shivarajashankara, Dept. of Biochemistry, MR Medical College,
Gulbarga-585105, Karnataka, India. shivrajsym@yahoo.com |
Not cited
by ATSDR |
CITED
BY NRC |
2002
RAT
30
or 100 ppm F in their drinking water for 7 months |
There was a significant reduction in the number of [3H]epibatidine
binding sites in the brain of rats exposed 100 ppm of fluoride...
the number of [125I]alpha-BTX binding sites was significantly
decreased in the brains of rats exposed to both levels of
fluoride. Western blotting revealed that the level of the
nAChR alpha4 subunit protein in the brains of rats was significantly
lowered by exposure to 100 ppm, but not 30 ppm fluoride; whereas
the expression of the alpha7 subunit
protein was significantly decreased by both levels of exposure.
Since
nAChRs play major roles in cognitive processes such as
learning and memory, the decrease in the number of
nAChRs caused by fluoride toxicity may be an important factor
in the mechanism of brain dysfunction in the disorder. |
Neurotoxicol
Teratol 2002 Nov-Dec;24(6):751-7
Chronic fluoride toxicity decreases the number of nicotinic
acetylcholine receptors in rat brain.
Long YG, Wang YN, Chen J, Jiang SF, Nordberg
A, Guan ZZ.
Dept. of Pathology, Guiyang Medical College, 550004, Guizhou,
Guiyang, PR China
|
Not
cited by ATSDR |
CITED
BY NRC |
2001
MICE
NaF |
The
main results showed that the learning
capability of mice drinking higher concentration of fluoride
presented remarkable deterioration.
The
results suggested that selenium might antagonize the neurotoxicity
of fluoride on behavior and morphology. |
Wei
Sheng Yan Jiu 2001 May;30(3):144-6
[Effects of selenium on
the damage of learning-memory ability of mice induced by fluoride]
Zhang Z, Shen X, Xu X.
College of Life and Environmental Science, Zhejiang Normal
University, Jinhua 321004, China.
Article
in Chinese. Suggest NRC translate
|
Not cited
by ATSDR |
Not
cited by NRC |
2001
MICE
NaF in
drinking water (0.5 g/L) to pregnant and lactating mice, from
the 15th day of pregnancy to the 14th day after delivery. |
Compared
to the control group, reductions in
the cerebellar and cerebral protein concentrations by 27%
and 17%, respectively.
Consistent
histological changes were present in
the cerebellum of the treated mice with the external
granular layer being markedly reduced or absent, the
Purkinje cell bodies being poorly differentiated and
arranged in a single layer at the surface of the internal
granular layer, and with more apoptotic
Purkinje cells being present. |
Full
report
Fluoride
2001; 34(3 ):165-173
Effect of fluoride on thyroid function
and cerebellar development in mice
Mahmoud Trabelsi, Fadhel Guermazi, Najiba
Zeghal
Correspondence:
Dr N Zeghal, Animal Physiology Laboratory, Dept. of Biology,
Faculty des Sciences de Sfax-Route de la Soukra-Km 3.5, 3038
Sfax BP802, Tunisia.
Nejiba.Zghal@fss.rnu.tn |
Not cited
by ATSDR |
CITED
BY NRC
Cited
in Appendix E: "Detailed information on endocrine studies
of fluoride" |
2001
RAT
12 one-month-old
albino rats were administered 100-ppm fluoride (as NaF) in
their drinking water for 4 months. |
In
the brain and liver, MDA and GSH levels
increased, as did the activities of
GSH-Px and glutathione S-transferase (GST). The level
of ascorbic acid increased in the brain,
but it decreased in the liver. These results suggest
that fluoride enhances lipid peroxidation in the red blood cells,
brain and liver of rats and causes increased or decreased
enzyme activity associated with free radical metabolism. |
Full
report
Fluoride
2001; 34(2):108-113
Effect of fluoride intoxication
on lipid peroxidation and antitoxidant systems in rats
YM Shivarajashankara, AR Shivashankara,
P Gopalakrishna Bhat, S Hanumanth Rao |
Not cited
by ATSDR |
Not
cited by NRC |
2001 |
General
serine-threonine phosphatase inhibitors
such sodium fluoride, or ss-glycerophosphate
and sodium pyrophosphate, or specific PP1 and PP2A inhibitors
including microcystin-LR, protein phosphatase 2A inhibitor I(1)
or protein phosphatase inhibitor 2 all
abrogate H-Ras and K-Ras dependent Raf-1 activation in vitro. |
Oncogene.
2001 Jul 5;20(30):3949-58.
Protein
phosphatases 1 and 2A promote Raf-1 activation by regulating
14-3-3 interactions.
Jaumot M, Hancock JF.
Laboratory
of Experimental Oncology, Department of Pathology, University
of Queensland Medical School, Herston Road, Queensland 4006,
Australia. |
Not cited
by ATSDR |
Not
cited by NRC |
2000
RAT |
The
results showed that the degree of DNA damage in the fluoride
group and the selenium group were significantly
greater than that in control group(P < 0.01). The damage
in the fluoride group was even more serious.
It
suggested that fluoride and selenium could induce DNA damage
in pallium neural cells of rats respectively. Moreover, the
joint antagonistic effect of selenium and zinc against fluoride
was more obvious.
Definition
of Pallium: - the central cortex with
the subajacent white substance. |
Wei
Sheng Yan Jiu 2000 Jul;29(4):216-7
[Effects of selenium and zinc on
the DNA damage caused by fluoride in pallium
neural cells of rats]
Chen J, Chen X, Yang K.
Dept. of Environmental Health, Tongji Medical University,
Wuhan 430030, China.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
2000
MICE |
Results:
Learning and memory abilities of high-fluoride exposed groups
were significantly lower
than that of the control group, while the brain
ChE activities of high-fluoride exposed groups were significantly
higher.
Conclusions: High fluoride concentration in drinking water can
decrease the cerebral functions of mice. Fluoride is a neurotoxicant.
|
Chinese
Journal of Endemiology 2000;19(4):262-3
As cited
and abstracted in Fluoride 2001;
34(1):80
Effects
of high fluoride drinking water on the cerebral functions
of mice
Sun Z-R, Liu F-Z, Wu L-N, et al.
Correspondence: Dept. of Environmental Health, Tianjin Medical
University, Tianjin 300070, China. |
Not cited
by ATSDR |
Not
cited by NRC |
2000
RAT |
Conclusions:
There is a tendency for neurone apoptosis
in chronic fluorosis in rats. It is most evident with
changes in pathology. It is not likely that only one form of
neurone damage exist in the process of chronic fluorosis. There
are recessive changes and apoptosis in the process at the same
time. |
Chinese
Journal of Endemiology 2000;19(2):96-8
As cited
and abstracted in Fluoride 2001;
34(1):82
Study
of the mechanism of neurone apoptosis in rats from the chronic
fluorosis
Lu X-H, Li G-S, Sun B
Correspondence: Institute of Endemi c Diseases in Nornman
Bethune University of Medical Sciences, Changchun 130021,
China |
Not cited
by ATSDR |
Not
cited by NRC |
2000
MICE
NaF (20mg/kg/body
weight) for 14 days |
fluoride
levels were significantly increased
(p<0.01) in both brain and gastrocnemius muscle.
This
study therefore shows that both brain and muscle are affected
by fluoride with inhibition of
some enzymes associated with free-radical metabolism, energy
production and transfer, membrane transport, and synaptic
transmission, but with an enhanced activity of XOD. |
Fluoride
2000. Vol. 33 No. 1:17-26.
Effects
of fluoride accumulation on some enzymes of brain and gastrocnemius
muscle of mice
M
Lakshmi Vani and K Pratap Reddy |
Not cited
by ATSDR |
Not
cited by NRC |
2000
RAT |
CONCLUSION:
Over uptake of fluoride for a long term
could cause potential increase in the
level of oxidative stress in the brain tissue. |
Zhonghua
Yu Fang Yi Xue Za Zhi 2000 Nov;34(6):330-2
[Influence of free radical inducer on the level of oxidative
stress in brain of rats with fluorosis]
Shao Q, Wang Y, Guan Z.
Dept. of Neurology, Guiyang Medical College, Guizhou 550004,
China.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1999
MICE
F in drinking
water |
the
learning ability of mice drinking high concentration of fluoride
presented remarkable deterioration,
the thickness of post-synaptic density (PSD) was decreased,
and the width of synaptic cleft was remarkably increased. The
results suggested that the impairment on the learning capability
induced by fluorosis may be closely related with the pathological
changes of synaptic structure in the brain of mice. |
Wei Sheng
Yan Jiu. 1999 Jul;28(4):210-2.
[Effect of fluoride exposure
on synaptic structure of brain areas related to learning-memory
in mice]
Zhang Z, Xu X, Shen X, Xu X.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1999
in
vitro system of cultured hippocampal neurons from foetal rats |
It
was concluded that aluminium interferes with the metabolism
of the neuronal cytoskeleton and that this interference is potentiated
by fluoride. |
Arch
Physiol Biochem. 1999
Feb;107(1):15-21.
Fluoride enhances the effect of aluminium
chloride on interconnections between aggregates of hippocampal
neurons.
van der Voet GB, Schijns O, de Wolff FA.
Toxicology Laboratory Leiden University Medical Center Leiden,
The Netherlands.
|
Not cited
by ATSDR |
Not
cited by NRC |
1999
RAT |
Fluoride,
which is used commonly as a pharmacological tool to activate
phosphoinositide-phospholipase C coupled to the heterotrymeric
Gq/11 proteins, inhibited the phosphorylation
of phosphatidylinositol (PtdIns) to polyphosphoinositides
(PtdIns4P and PtdIns4,5P2) in membranes from rat brain cortex.
our
data show that fluoride, at a concentration similar to that
used to stimulate directly Gq/11-coupled phospholipase C,
effectively blocks the synthesis of phospholipase C substrates
from PtdIns. |
Int J Dev
Neurosci 1999 Jul;17(4):357-67
Fluoride-induced depletion
of polyphosphoinositides in rat brain cortical slices: a rationale
for the inhibitory effects on phospholipase C.
Sarri E, Claro E.
Departament de Bioquimica i de Biologia Molecular, Facultat
de Medicina, Universitat Autonoma de Barcelona, Spain. |
Not cited
by ATSDR |
Not
cited by NRC |
1999 |
Intracellular
blockade of GABA receptors with fluoride reveals a novel component
of evoked GDPs |
J Neurophysiol
81: 2095-2102, 1999
Glutamate
Controls the Induction of GABA-Mediated Giant Depolarizing
Potentials Through AMPA Receptors in Neonatal Rat Hippocampal
Slices
Sonia Bolea (1), Elena Avignone (2), Nicola Berretta (2),
Juan V. Sanchez-Andres (1), Enrico Cherubini (2)
1. Departamento
de Fisiologia, Instituto de Bioingenieria, Universidad Miguel
Hernandez, Campus de San Juan, 03550 San Juan, Alicante,
Spain;
2. Neuroscience Program and Istituto Nazionale Fisica della
Materia Unit, International School for Advanced Studies, 34014 Trieste,
Italy |
Not cited
by ATSDR |
Not
cited by NRC |
1998
RAT
30 or
100 ppm F for 3, 5, and 7 months.
|
The
results demonstrate that the contents
of phospholipid and ubiquinone are modified in brains affected
by chronic fluorosis and these changes of membrane lipids could
be involved in the pathogenesis of this disease. |
Neurotoxicol
Teratol 1998 Sep-Oct;20(5):537-42
Influence of chronic fluorosis on
membrane lipids in rat brain.
Guan ZZ, Wang YN, Xiao KQ, Dai DY, Chen
YH, Liu JL, Sindelar P, Dallner G.
Dept. of Pathology, Guiyang Medical College, Guizhou, China.
jialiul@public.gy.gz.cn |
Not
cited
Cited
in References, but not in text of ATSDR's 2003 Tox Profile
on Fluoride |
CITED
BY NRC |
1998
RAT
pregnant
rats ingested ad libitum fluorinated drinking water (5, 15,
50 ppm F-) during gestation and
lactation |
It was
shown that the AChE activities of the
SPM and peripheral RBCs in maternal rats exposed 5-50 ppm F-
for 60 days were elevated significantly
by 30.0-67.6% and 12.5-31.9% in a dose-dependent manner,
respectively. The AChE activities of their
offspring 80 days after birth were also increased (8.7-28.7%
for SPM and 20.6-32.4% for RBC). |
Biomed
Environ Sci 1998 Mar;11(1):1-6
Actions of sodium fluoride on acetylcholinesterase
activities in rats.
Zhao XL, Wu JH.
Dept. of Environmental Toxicology, Chinese Academy of Preventive
Medicine, Beijing, China. |
Not cited
by ATSDR |
Not
cited by NRC |
1998
RAT
52-weeks
1 ppm F in doubly distilled, deionized
drinking water
|
•
a greater uptake of aluminum
into the brain
•
beta amyloid plaques
•
Authors specultate
that fluoride facilitates aluminum to cross the blood brain
barrier |
Brain
Res 1998 Feb 16;784(1-2):284-98
Chronic
administration of aluminum-fluoride or sodium-fluoride to
rats in drinking water: alterations in neuronal and cerebrovascular
integrity.
Varner JA, Jensen KF, Horvath W, Isaacson RL.
Psychology
Department, Binghamton University, Binghamton, NY, USA.
|
ATSDR
comment: "This study did not assess
neurofunction; thus, it is difficult to assess the toxicological
significance of these effects (page 111)." |
CITED
BY NRC |
1998
RAT |
We
herein demonstrate that sodium fluoride (NaF) acts as a stress
response inducer on HeLa and 9L rat brain tumor cells. |
JOURNAL
OF CELLULAR BIOCHEMISTRY; 69 (2). 1998. 221-231.
Induction
of stress response and differential expression of 70 kDa stress
proteins by sodium fluoride in HeLa and rat brain tumor 9L
cells.
CHENG T-J , CHEN T-M, CHEN C-H LAI Y-K
Dep. Life Sci., Natl. Tsing Hua Univ., Hsinchu 30043, Taiwan.
|
Not cited
by ATSDR |
Not
cited by NRC |
1998
RAT
(adult female)
NaF 20
or 40 mg:kg dose
level daily for 60 days |
Spontaneous
motor activity and motor coordination were tested in adult female
rats after treating with sodium fluoride... A
suppression of spontaneous motor activity suggests that fluoride
has, by a central action, inhibited motivation of these animals
to exhibit locomotor behavior. A cholinergic mechanism
through a change in the activity of acetylcholinesterase may
not account for this effect, since sodium fluoride treatment
did not alter the activity this enzyme in brain regions. However,
an involvement of monoamines may be proposed
in view of previously reported finding that excessive fluoride
intake has decreased the concentrations of 5-hydroxyindoleacetic
acid and increased that of norepinephrine in rat brain. |
Environmental
Toxicology and Pharmacology 1998; 6: 187-191.
Effects of sodium fluoride on locomotor
behavior and a few biochemical
parameters in rats
Vanaja Paul, P. Ekambaram, A.R. Jayakumar
Department of Pharmacology and Environmental Toxicology, Dr
A.L.M.
Postgraduate Institute of Basic Medical Sciences, University
of Madras, Taramani Chennai 600 113, India |
Not cited
by ATSDR |
Not
cited by NRC |
1997
RAT
66.3
mg/L and 221 mg/L F-containing water for 3, 5, and 7months |
Coenzyme
Q content of brain tissue in rats fed with fluorine-containing
water decreased at early stage of fluorosis, but increased significantly
at late stage. It is speculated that changes
in content of coenzyme Q could correlate with changes in free
radical levels induced by fluorine. |
Zhonghua
Yu Fang Yi Xue Za Zhi 1997 Nov;31(6):330-3
[Changes of coenzyme Q content in brain tissues of rats with
fluorosis]
Wang Y, Guan Z, Xiao K.
Dept. of Scientific Research, Guiyang Medical College.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1997
RAT
Wistar
rats were fed with NaF until
chronic fluorosis was induced
|
CONCLUSION:
The metabolism of brain phospholipid might
be interfered by fluoride accumulated in brain tissue, which
is related with the degeneration of neuron.
The changes of brain phospholipid could be involved in the pathogenesis
of chronic fluorosis. |
Zhonghua
Yi Xue Za Zhi 1997 Aug;77(8):592-6
[Influence of experimental fluorosis
on phospholipid content and fatty acid composition in rat
brain]
Guan Z, Wang Y, Xiao K.
Guiyang Medical College.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
CITED
BY NRC |
1997
Female
MICE
Fluoride
(50 ppm F as NaF) in
dd water |
Sixty-four
CD-1 female mice were assigned to one of four water treatment
groups: Control (distilled, deionized water) (C); Fluoride
(50 ppm F as NaF) (F); Aluminum (100 ppm Al as AlCl3)
(Al); and Al & F (50 ppm F &
100 ppm Al) (AlF). One-half of the animals in each
group were mated. The study was terminated on the 5th days
after parturition.
brain
Al increased 168% in the F group, and 260% to 350% in the
remaining three groups. |
FASEB J
1997 Feb;11(3):A406
Effects of fluoride and aluminum exposure to dams prior to and
during gestation on mineral compositions of bone and selected
soft tissues of female mice dams and pups.
Koh ET, Clarke SL
Univ. of Oklahoma Health Sci. Center, Oklahoma City, OK. |
Not
cited.
ATSDR
lists this study in its References but does not cite it in
its text.
ATSDR
fails to correlate the accumulation of Al in the brain with
Varner et al. 1998 study., and Isaacson et al. 1997 study. |
Not
cited by NRC |
1997
RAT
NaF
2.1 ppm in drinking water for 45 weeks |
elevated
brain level of aluminum
Neuronal
abnormalities were observed in the NaF treated animals- especially
in the deeper cell layers.
Both
the AlF- and NaF-treated animals had substantial numbers of
argentophilic cells on Bielchowsky staining and these cells
showed condensed Nissl substance with hematoxylin and eosin
staining. The NaF treatment also produced distortions of cells
and, in some rats, cell losses could be demonstrated in particular
brain regions. Both AlF3 and NaF induced vascular inclusions,
although of a different character: the
AlF3 produced the Al-based particles and the NaF produced
the IgM inclusions. |
Annals
of the New York Academy of Sciences 825 152-166 1997
Toxin-induced
blood vessel inclusions caused by the chronic administration
of aluminum and sodium fluoride and their implications for
dementia.
Isaacson
RL, Varner JA, Jensen KF.
Department
of Psychology, Binghamton University, New York 13902-6000,
USA. isaacson@binghamton.edu |
Not cited
by ATSDR |
Not
cited by NRC |
1997 |
Small
doses of sodium fluoride accelerated
axonal transport (AT), and this correlated with a rise in
cAMP levels in ventral roots. High doses
of sodium fluoride decelerated AT more markedly in old rats.
Changes
in AT could be an important mechanism of disordering the growth
of neurons and innervated cells in old age. |
Exp Gerontol
1997 Jul-Oct;32(4-5):441-50
Age-related changes in axonal transport.
Frolkis VV, Tanin SA, Gorban YN.
Institute of Gerontology, Academy of Medical Sciences of Ukraine,
Ukraine. |
Not cited
by ATSDR |
Not
cited by NRC |
1998
RAT |
The activity
and regulatory properties of the adenylate cyclase system of
the rat striatum were studied. Agents
such as Gpp(NH)p, forskolin, and NaF were found to show classical
in vitro stimulation of adenylate cyclase activity in the striatum
membrane fraction. |
Neurosci
Behav Physiol. 1998 Jul-Aug;28(4):392-6.
Adenylate cyclase system of the rat striatum:
regulatory properties and the effects of gangliosides.
Plesneva SA, Nalivaeva NN, Zhuravin IA.
I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry,
Russian Academy of Sciences, St. Petersburg, Russia.
|
Not cited
by ATSDR |
Not
cited by NRC |
1996
|
Oxidative
stress appears to contribute to neuronal dysfunction in a
number of neurodegenerative conditions, notably including
Alzheimer's disease, in which cholinergic receptor-linked
signal transduction activity is severely impaired.
activation
with NaF of G-proteins coupled
to phospholipase C was concentration dependently inhibited
by H2O2, indicating impaired G-protein function. These effects
of H2O2 are similar to signaling impairments reported in Alzheimer's
disease brain, which involve deficits in receptor- and G-protein-stimulated
phosphoinositide hydrolysis, but not phospholipase C activity.
|
J Neurosci
1996 Oct 1;16(19):5914-22
Cholinergic stimulation of AP-1 and
NF kappa B transcription factors is differentially sensitive
to oxidative stress in SH-SY5Y neuroblastoma: relationship to
phosphoinositide hydrolysis.
Li X, Song L, Jope RS.
Department of Psychiatry and Behavioral Neurobiology, University
of Alabama at Birmingham 35294-0017, USA. |
Not cited
by ATSDR |
Not
cited by NRC |
1995
RAT
Behavior
was tested in a computer pattern recognition system |
Prenatal
weanling and adult exposures all caused
sex- and dose-specific behavioral deficits with a common pattern.
Males
were most sensitive to prenatal day 17-19 exposure, while
females were more sensitive to weanling and adult exposures.
After weanling and adult exposures the
severity of deficits increased with
increasing F levels found in plasma and specific brain
regions such as the hippocampus. |
Neurotoxicol
Teratol. 1995 Mar-Apr;17(2):169-77.
Neurotoxicity of sodium fluoride
in rats
Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. |
Cited
by ATSDR
in this way:
page 180:
"Alterations in spontaneous behavior were found in rats
orally exposed to sodium fluoride (Mullenix
et al. 1995a;
Paul et al. 1998); however, another study did
not find this effect (Whitford et al.
2003)..." [ATSDR notes that the Whitford paper
was "only available as an abstract" - page 111] |
CITED
BY NRC |
1995
NaF |
Calcium
currents in CA1 neurons from rat hippocampus were studied with
the whole-cell, patch-clamp technique. Under control conditions
high-voltage-activated (HVA) calcium currents activated from
membrane potentials of -80 mV and -40 mV underwent "run-down".
The rate of run-down of the current activated from -40 mV was
significantly attenuated by inclusion of the G-protein activator
NaF (1 mM) in the pipette and also irreversibly attenuated by
brief batch application of NaF (10 mM)... It is suggested
that activation of guanine nucleotide-binding proteins by NaF
leads to a long-lasting attenuation of HVA calcium current run-down
in hippocampal CA1 cells. |
Exp Brain
Res. 1995;106(3):505-8.
Attenuation of high-voltage-activated
Ca2+ current run-down in rat hippocampal CA1 pyramidal cells
by NaF.
Breakwell NA, Behnisch T, Publicover SJ, Reymann KG.
Department of Physiology, Trinity College Dublin, Ireland. |
Not
cited by ATSDR |
Not
cited by NRC |
1994
RABBIT
5, 10,
20, and 50 mg/kg body wt/day by subcutaneous injection for
100 days |
In
fluoride treated rabbits the brain showed
significant decline (P <0.001) in
soluble, basic total protein and free amino acid levels.
RNA content rapidly decreased (P <0.001)
in the brains of experimental animals compared to the controls.
However, in male animals treated with 5 and 10 mg fluoride no
statistically significant differences in RNA content of brain
were observed. The depletion of
proteins produced degenerative changes in purkinje cells of
the cerebellar cortex. |
Fluoride
1994; 27(3):155-159
Effect of long-term administration
of fluoride on levels of protein, free amino acids and RNA
in rabbit brain
Shashi A, Singh JP, Thapar SP
Department
of Zoology, Punjabi University, Patiala 14702, India |
Not cited
by ATSDR |
CITED
BY NRC |
1994
RAT |
Effects
of NaF on Ca2+Mg(2+)-ATPase activity
of synaptic membrane in rat brain were studied with in vitro
or in vivo methods. Concentrations of
NaF of 0.3, 1.6, 8.0, 20.0 and 40.0 mmol/L can significantly
inhibit the activity of the enzyme with proportions of
6.6%, 18.0%, 41.0%, 55.5% and 63.1%, respectively, and with
a half inhibitory concentration of 14.8 mmol/L reflecting an
obvious dose-effect and time effect relationship.
Analysis of enzyme substrate kinetics showed the effect that
NaFhad was a non competitive inhibition.
Activity of Ca2+Mg(2+)-ATPase on synaptic
membrane in female rat brain showed a decreasing tendency
after feeding with water fluorinated with 5, 15 and 50 mg/L
of fluoride during their gestation
and lactation for 50 days, and that in
their newborn offsprings with 5 and 50 mg/L of fluoride was
inhibited by 11.3 and 32.1%, respectively. |
Zhonghua
Yu Fang Yi Xue Za Zhi 1994 Sep;28(5):264-6
[Effects of sodium fluoride on the
activity of Ca2+Mg(2+)-ATPase in synaptic membrane in rat
brain]
Zhao XL, Gao WH, Zhao ZL.
Department of Environment Health Ningxia Medical College,
Yinchuan.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1994 |
(3)
Excessive fluoride intake decreased 5-hydroxy indole acetic
acid and increased norepinephrine in rat brain |
Hua
Hsi I Ko Ta Hsueh Hsueh Pao. 25(2):188-91.1994
[Effect
of excessive fluoride intake on mental work capacity of children
and a preliminary study of its mechanism]
Li Y,
et al. 1994
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1992
15
aborted fetuses
at 5-8th gestation month from an endemic fluorosis area compared
with those from a non-endemic area |
Stereological
study of the brains showed that the numerical density of volume
of the neurons and the undifferentiated neuroblasts as well
as the nucleus-cytoplasm ratio of the neurons were increased.
The mean volume of the neurons was reduced. The numerical density
of volume, the volume density and the surface density of the
mitochondria were significantly reduced. The
results showed that chronic fluorosis in the course of intrauterine
fetal life may produce certain harmful effects on the developing
brain of the fetus. |
Zhonghua
Bing Li Xue Za Zhi 1992 Aug;21(4):218-20
[The
effect of fluorine on the developing human brain]
Du L.
Department of Pathology, Guiyang Medical College.
Article
in Chinese. Suggest NRC translate |
Not
cited by ATSDR |
Not
cited by NRC |
1992
RABBIT
NaF
at 5, 10, 20 and 50 mg/kg BW/day was injected subcutaneously
for 100 days |
Biochemical
studies showed hyperlipidemia,
hyperphospholipidemia, and hypertriglyceridemia in the brain
of treated animals of both sexes.
Fluoride
exerts an inhibitory effect on
the free fatty acids in brain of both
sexes. The relevance of these results in experimental fluorosis
is discussed. |
Fluoride
1992; 25(2):77-84
Studies
on alterations in brain lipid metabolism following experimental
fluorosis
A Shashi
Department of Zoology, Punjabi University, Patala 147002,
India |
Not cited
by ATSDR |
CITED
BY NRC |
1992
RAT
streptozotocin
induced diabetic rats after 5 weeks of induction of diabetes |
The
net NaF stimulated AC activity in diabetic rats (109.5 +/-
11.4) was significantly lower than the control rats (154.3
+/- 16.3) (P less than 0.05).
It is
concluded that diabetes mellitus in rats is associated with
reduced post receptor activation of adenylate cyclase in cerebral
microvessels |
Res 1992
Jun 26;583(1-2):155-60
Beta-adrenergic receptor activity of cerebral microvessels in
experimental diabetes mellitus.
Mooradian AD, Scarpace PJ.
St. Louis DVA Medical Center, MO. |
Not cited
by ATSDR |
Not
cited by NRC |
1992
Rat hippocampal
slices were exposed briefly (12-15 min) to AlF4- (10 mmol/l
NaF, 10 mumol/l AlCl3). |
The
effect on synaptic transmission in area CAl was measured using
extracellular electrodes placed in the stratum pyramidale
and stratum radiatum. During fluoride
exposure, both spike and EPSP amplitude fell to very low levels.
It
is concluded that NaF/ACl3 exposure induces an LTP-like process
by G-protein activation, |
Exp Brain
Res 1991;84(3):680-4
Brief exposure to the G-protein
activator NaF/AlCl3 induces prolonged enhancement of synaptic
transmission in area CAl of rat hippocampal slices.
Publicover SJ.
School of Biological Sciences, University of Birmingham, Edgbaston,
UK. |
Not cited
by ATSDR |
Not
cited by NRC |
1991
RAT
(Lactating) |
2) During
chronic fluorosis serum PRL level was decreased, however, PRL
content in pituitary was increased. Electronmicroscopic examination
showed accumulation of large
mature secretory granules and appearance of extremely large
abnormal secretory granules in lactotroph cytoplasma. These
finding indicate that
hormone release of pituitary lactotrophs is obstructed in lactating
rats with fluorosis, and the toxic effect
of fluoride is mediated by an enhanced function of dopaminergic
system in hypothalamus. |
ACTA
PHYSIOL SIN; 43 (5). 1991. 512-517.
An
experimental study of inhibition on lactation in fluorosis
rats.
YUAN S-D, SON K-Q, XIE Q-W, LU F-Y
Neuroendocrine Res. Lab., China Med. Univ., Shenyang 110001.
|
Cited
by ATSDR, but only relating to reproductive effects |
Not
cited by NRC |
1991
HUMAN |
160 cases
of acute sodium silicofluoride poisoning due to accidental intake
are reported in this paper... The cardiovascular findings were
notable. Ninety-six cases had abnormal electrocardiographic
findings. Abnormal heart rhythm and S-T segment changes were
the main findings. These changes were
positively correlated with the toxin amount of fluoride.
Two cases died from sudden arrest of heart beat. Lung, kidney,
liver, and brain functions were also impaired.
|
CHIN
J PREV MED; 25 (5). 1991. 269-271.
The
clinical features of 160 cases of acute sodium silico fluoride
poisoning.
Dong Y et al.
First People's Hosp., Wenling County, Zhejiang 317500 |
Not
cited by ATSDR |
Not
cited by NRC |
1990 |
It
is concluded that fluoride ions inhibit
agonist-stimulated inositol phospholipid breakdown via actions
not only on G-proteins but also on phosphoinositide-specific
phospholipase C substrate availability. |
Brain Res
1990 Dec 24;537(1-2):93-101
Multiple actions of fluoride
ions upon the phosphoinositide cycle in the rat brain.
Tiger G, Bjorklund PE, Brannstrom G, Fowler
CJ.
Dept. of Pharmacology, University of Umea, Sweden.
|
Not cited
by ATSDR |
Not
cited by NRC |
1990 |
Evidence
is presented to suggest that NaF affects the dephosphorylation
of the formed [3H]inositol polyphosphates. |
Eur J Pharmacol
1990 Jan 23;188(1):51-62
Effect of monovalent ions upon G proteins coupling muscarinic
receptors to phosphoinositide hydrolysis in the rat cerebral
cortex.
Tiger G, Bjorklund PE, Cowburn RF, Garlind
A, O'Neill C, Wiehager B, Fowler CJ.
Dept. of Pharmacology, University of Umea, Sweden. |
Not cited
by ATSDR |
Not
cited by NRC |
1990
membranes
from rat brain cortex |
under conditions
where breakdown of polyphosphoinositides by phospholipase C
was dependent on PtdIns kinase activity, fluoride
inhibited activation by GTP[S] plus carbachol of phospholipase
C. When conditions allowed direct breakdown
of PtdIns and precluded PtdIns kinase activity, the stimulatory
effects of fluoride and GTP[S] plus carbachol on phospholipase
C activity were additive. |
Biochem
J 1990 Jun 15;268(3):733-7
Dual effect of fluoride on phosphoinositide
metabolism in rat brain cortex.
Stimulation of phospholipase C and inhibition of polyphosphoinositide
synthesis.
Claro E, Wallace MA, Fain JN.
Department of Biochemistry, University of Tennessee, Memphis
38163. |
Not cited
by ATSDR |
Not
cited by NRC |
1990 |
NaF
and guanosine 5'-O-thiotriphosphate [GTP(S)] stimulated the
accumulation of [3H]inositol monophosphate ([3H]InsP) in rat
brain cortical membranes, with half-maximal
stimulation at 2 mM and 1 microM, respectively.
Our findings of different characteristics of GTP(S) and fluoride
activation of polyphosphoinositide (PPI) hydrolysis suggest
that separate regulatory mechanisms are involved in these
two modes of stimulation in brain membranes. Activation
of PPI hydrolysis by fluoride may be mediated by a direct
stimulation of PPI phosphodiesterase or by activating a putative
guanine nucleotide regulatory protein at a location distinct
from the GTP-binding site. |
J Neurochem
1990 Apr;54(4):1426-32
Guanosine 5'-O-thiotriphosphate
and sodium fluoride activate polyphosphoinositide hydrolysis
in rat cortical membranes by distinct mechanisms.
Li PP, Sibony D, Warsh JJ.
Section of Biochemical Psychiatry, Clarke Institute of Psychiatry,
Toronto, Ontario, Canada.
|
Not cited
by ATSDR |
Not
cited by NRC |
1990 |
In
this study we have used fluoride as a tool to investigate
the involvement of G protein-coupled effector systems in the
regulation of the depolarization-induced release of gamma-aminobutyric
acid (GABA) from rat cerebral cortex.
From these
studies, it is concluded that GABA release in cerebral cortex
is subject to regulation by G protein-linked effector systems
that are distinct from those affecting the release of [3H]ACh
in cerebral cortex. |
J Neurochem
1990 Apr;54(4):1130-5
Modulation of gamma-aminobutyric
acid release in cerebral cortex by fluoride, phorbol ester,
and phosphodiesterase inhibitors: differential sensitivity of
acetylcholine release to fluoride and K+ channel blockers.
Gardiner IM, de Belleroche J.
Dept. of Biochemistry, Charing Cross and Westminster Medical
School, London, England. |
Not cited
by ATSDR |
Not
cited by NRC |
1989
RAT
33-42-day
old rat pups generated by three groups of female Wistar rats,
which were given distilled water containing 0, 30 and 60 ppm
NaF respectively beforehand as drinking water for 85 days |
The
results of behavior test showed that the latent
period of pain reaction and that of conditioned reflex in the
30 ppm F and 60 ppm F groups were longer than that in the control
group (P less than 0.05 or P less than 0.01). morphological
examination of the pup brains showed that
the nerve cell density of the 60 ppm F group was higher than
that of the control group (P less than 0.05). Electronmicroscopically,
mild degeneration of organelles of the
nerve cells was observed in those brains of the 60 ppm F group.
|
Zhonghua
Bing Li Xue Za Zhi 1989 Dec;18(4):290-2
[Experimental study of behavior
and cerebral morphology of rat pups generated by fluorotic
female rat]
Liu WX.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1989
RABBIT |
The
mechanism of sodium fluoride (NaF) induced hypothermia was
investigated on relations between the monoamine synthesis
and metabolism in the rabbit brain.
Administration
of NaF made a significant decrease in norepinephrine levels
in the rabbit hypothalamus, but had no effect on 5-HT levels. |
Shikwa
Gakuho 1989 Mar;89(3):607-26
[The rabbit thermo-regulatory
system. Effects of high dose of sodium fluoride]
Machida H.
Article
in Japanese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1988
RAT |
Since
fluoride ions are known to activate G-proteins in the concentrations
used in this study, these results may indicate the existence
of a novel G-protein linked to receptor inhibition of phospholipase
C. |
Biochem
Biophys Res Commun 1988: Sep 15;155(2):664-9
Fluoride inhibits agonist-induced
formation of inositol phosphates in rat cortex.
Godfrey PP, Watson SP.
Dept. of Clinical Pharmacology, Radcliffe Infirmary, Oxford,
United Kingdom. |
Not cited
by ATSDR |
Not
cited by NRC |
1987
RAT |
results
indicate that, in cerebral-cortical membranes, activation of
phospholipase C by guanine nucleotides or fluoride directly
increases a phospholipase C activity which specifically hydrolyses
PIP2. |
Biochem
J 1987 May 15;244(1):35-40
Guanine nucleotide and NaF stimulation
of phospholipase C activity in rat cerebral-cortical membranes.
Studies on substrate specificity.
Litosch I.
Department of Pharmacology, University of Miami School of Medicine,
FL 33101. |
Not cited
by ATSDR |
Not
cited by NRC |
1986
RAT |
The
blood-brain barrier fails to exclude the fluoride ion from
nerve tissue.
Fluoride
levels in brain reach a maximum approximately two hours after
it has been administered. |
Fluoride
1986; V 19, No 3: 108-112
Kenetics
of fluoride penetration in liver and brain
Geeraerts
F, Gijs G, Finne E, Crokaert R
Department
of Biochemistry and Pharmacology, Vrije Universiteit, Laarbeeklaan,
Brussels, Belgium. |
Not
cited
ATSDR
lists this study in its References but does not cite it in
its text. |
Not
cited by NRC |
1986
RAT |
No Abstract
available |
Zhonghua
Bing Li Xue Za Zhi 1986 Dec;15(4):297-9
[Morphology of the brain of the offspring
of rats with chronic fluorosis]
Guan ZZ.
Article
in Chinese. Suggest NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1986 |
We have
attempted to suppress voltage-dependent conductances in hippocampal
neurons by introducing various intracellular agents. Voltage-clamp
studies were carried out using acutely dissociated hippocampal
neurons from adult guinea pigs. Synaptic events were examined
using intracellular recordings in the slice preparation... We
also found that the anion fluoride could affect calcium conductance
by an intracellular action. When anions other than fluoride
were used for intracellular recordings, the voltage-dependent
calcium current inactivated slowly and showed persistent activation
at membrane potentials between -40 and -10 mV. In
contrast, when fluoride was present intracellularly, the inactivation
kinetics of the calcium current were accelerated and the persistent
component of the current was largely suppressed. Intracellular
recordings in the hippocampal slice showed that when electrodes
contained cesium, QX 314, and fluoride, the spiking and nonlinear
responses of the neuronal membrane to depolarization were blocked. |
J Neurosci.
1986 Oct;6(10):2915-20.
Intracellular fluoride alters the kinetic
properties of calcium currents
facilitating the investigation of synaptic events in hippocampal
neurons.
Kay AR, Miles R, Wong RK. |
Not cited
by ATSDR |
Not
cited by NRC |
1984
RAT |
The
influence was studied in vitro of certain agents (adenosine,
ADP, ATP, theophylline, together with
F- ions) on the cAMP concentrations in the nuclear
(N) and mitochondrial (M) fractions from different areas of
rat brain. F- ions caused a slight decrease
of the cAMP concentrations in nuclear fractions of the thalamus
with hypothalamus and a marked decrease of this cyclic nucleotide
in M fractions from the cerebral cortex. |
Acta Physiol
Pol 1984 May-Jun;35(3):199-206
Effect of certain agents on subcellular
cAMP level in different areas of rat brain.
Janiszewska G, Lachowicz L, Wojtkowiak
R. |
Not cited
by ATSDR |
Not
cited by NRC |
1982
CHILD
Accidental
ingestion of NaF tablets |
...
a 3-year-old boy who swallowed 200 sodium fluoride tablets
(1 mg fluoride each) for a dose of 16 mg fluoride/kg body
weight (Eichler et al. 1982).
... The boy died 7 hours after fluoride ingestion. Upon autopsy,
hemorrhagic edema of the lungs, hemorrhagic gastritis, and
massive cerebral edema were observed.
As
cited by ATSDR (2003), page 74 |
Int J Clin
Pharmacol Ther Toxicol. 1982 Jul;20(7):334-8.
Accidental ingestion of NaF tablets by
children--report of a poison control center and one case.
Eichler HG, Lenz K, Fuhrmann M, Hruby K. |
Cited
by ATSDR |
Not
cited by NRC |
1981
RAT |
The
effects of fluoride (F-) administration were studied on 2
groups of weanling male Wistar rats, a control fed a basal
diet containing 0.09 mg% F- and the other fed a diet containing
50 mg% F- for 30 days.
The
amount of F- accumulated in brain, heart, thymus, kidney,
testes, adrenal and femur of the F--fed group was significantly
higher than those of controls. |
J TOKYO
MED COLL; 39 (3). 1981. 441-460.
Hygienic
study on fluoride: 4. Physiological effects of fluoride on
rat.
Tomomatsu T
Dep. Biochem., Tokyo Med. Coll.
Toxline
abstract available at Toxnet |
Not cited
by ATSDR |
Not
cited by NRC |
1980
HUMAN |
Case
reports are presented of 8 patients with end stage renal disease
who while undergoing dialysis received IV, excessive amounts
of fluoride due to an unreported spill of hydrofluosilicic
acid into the public water supply caused by cross connections
in a treatment plant...
One
patient upon autopsy was found to have high fluoride levels
in lung tissue (5.6 ppm), kidney (7.0
ppm), brain (0.9 ppm) and blood
(4.9 ppm). |
Morb.
Mortal. Wkly. Rep.; VOL 29 ISS Mar 28 1980, P134-136
Fluoride
intoxication in a dialysis unit--Maryland
Anderson R, Beard JH, Sorley D
Bureau
of State Services, and the Chronic Diseases Div., Field Services
Div., Bureau of Epidemiology, Cent. for Disease Control, Atlanta,
GA 30333 |
Not
cited
ATSDR
lists this study in its References but does not cite it in
its text. |
Not
cited by NRC |
1978 |
A wide
variety of symptoms are encountered in chronic (human, animal)
fluorosis. The soft tissue organs affected by F- are named
in the following order: aorta, thyroid gland, lungs, kidneys,
heart, pancreas, brain, spleen
and liver. With advancing age their F- content increases.
Inhalation
of fluoride produces foci of demyelinization in the cortex
and in subcortical areas and a decrease in the number of Purkinje
cells in the cerebellum. |
FLUORIDE;
12 (3). 1978 111-114
Nonskeletal
fluorosis.
Anon
|
Not
cited by ATSDR |
Not
cited by NRC |
1978
CHICKEN
NaF
150 ppm |
The
fluoride treatment decreased ascorbic acid concentration in
the
heart, spleen, brain, gizzard,
pancreas and pectoralis, while it elevated levels in lung
and kidney.
Excerpt:
"The sharp decrease in the vitaimin
level shown in the brain of the experimental birds could indicate
depletion of the vitamin arising from stresses caused by fluoride
treatment." |
FLUORIDE;
11 (2). 1978 60-67
The
effects of fluoride on the growth and L-ascorbic acid levels
of tissues from the domestic chicken (Gallus domesticus).
Yu MH, Driver CJ
Huxley Coll. Environ. Stud., West. Wash. Univ., Bellingham,
Wash. 98225, USA.
|
Not
cited by ATSDR |
Not
cited by NRC |
1974
GUINEA
PIG |
The
effect of prolonged administration of NaF on the metabolism
of (guinea pig) Purkinje cells in the cerebellar cortex was
studied by histochemical methods. Experimentation showed an
intensification of the metabolic activity of the mitochondria
and probably of the membrane system of the endoplasmic reticulum,
activation of the complex of enzymes connected with active
transport through membrane structures of cells and the absence
of perceptible changes in the process of protein synthesis
in experimental animals as compared with controls. |
Folia
Histochem Cytochem (Krakow) 1974;12(1):37-44
Histochemical studies on the
effect of sodium fluoride on metabolism in Purkinje's cells.
Czechowicz K, Osada A, Slesak B.
Toxline
abstract available at Toxnet
Suggest
NRC translate |
Not cited
by ATSDR |
Not
cited by NRC |
1974
Fluorosis
patients |
Neurological
symptomatology in the form of the syndrome of vegetative-vascular
dysfunction, or the asthenovegetative syndrome with polyneuritic
(sensory and vegetative) disorders was detected in 78.8% of
patients with occupational fluorosis in preosteal and osteal
stages. Clinical and physiological investigations of the nervous
system (psycho-physiological procedures, EEG, chronaximetry)
showed patients with fluorosis to exhibit
disturbed higher nervous activity and dysfunction of subcorticalaxial
nonspecific structures of the brain. |
GIG
TR PROF ZABOL; (5). 1974 25-27
Aspects
of nervous system affections in occupational fluorosis.
POPOV LI, FILATOVA RI, SHERSHEVER AS
Suggest
NRC translate |
Not
cited by ATSDR |
Not
cited by NRC |
1972 |
No
abstract available |
JAP
J PHARMACOL; 22 (SUPPL). 1972 82
EFFECTS
OF FLUORIDE AND ATP ON MEMBRANE STRUCTURE AND ADENYL CYCLASE
ACTIVITY IN BRAIN MICROSOMES
ASAKAWA T, YOSHIDA H |
Not
cited by ATSDR |
Not
cited by NRC |
1971 |
Sodium
fluoride activates adenyl cyclase at a rate that is dependent
on temperature and the concentration of NaF. The activation
is not readily reversed by dilution, extensive washing of the
membrane-bound enzyme, or dialysis. Activation occurs in the
absence of added Mg++, but the rate of activation is increased
2-fold by 5 mg Mg++... |
J Biol
Chem 1971 Jan 10;246(1):62-8
Adenyl cyclase of rat cerebral cortex. Activation of sodium
fluoride and detergents.
Perkins JP, Moore MM. |
Not cited
by ATSDR |
Not
cited by NRC |