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2001 Fluoride Abstracts. Part 1.
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http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11275672&dopt=Abstract
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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]
[Article in Chinese]
Zhang Z, Shen X, Xu X.
College of Life and Environmental Science, Zhejiang Normal University, Jinhua 321004, China.
Sodium fluoride added with or without sodium selenite in deionized water was administered to male mice for 8 weeks. The influences of fluoride on learning-memory behavior were tested on Y-maze, and the ultrastructure of Gray I synaptic interface in the CA3 area hippocampus was quantitatively analyzed by electron microscopy and computer image processing appliance. The main results showed that the learning capability of mice drinking higher concentration of fluoride presented remarkable deterioration. The thickness of post-synaptic density (PSD) was decreased. The width of the synaptic cleft was remarkably increased. It was found that combined administration of fluoride and proper concentration of selenium could decrease the toxic effect of fluoride. There were synergetic toxicities if the concentration of selenium was too high. The results suggested that selenium might antagonize the neurotoxicity of fluoride on behavior and morphology.
PMID: 12525083 [PubMed - in process]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11310568&dopt=Abstract
Biochem Cell Biol 2001;79(2):207-17
Effect of prevention and potentiation of diisopropyl phosphorofluoridate (DFP)-induced delayed neurotoxicity on the mRNA expression of neurofilament subunits in hen central nervous system.
Xie K, Gupta RP, Abou-Donia MB.
Neurotoxicology Laboratory, School of Life Science, University of Science and Technology of China, Hefei, Anhui, P.R. China.
Diisopropyl phosphorofluoridate (DFP) is an organophosphorus ester, which produces mild ataxia in 7-14 days and severe ataxia or paralysis in about 20 days (OPIDN) in hens. Previous studies in this laboratory have shown enhanced temporal expression of neurofilament (NF) subunit mRNAs in the spinal cord (SC) of DFP-treated hens. The main objective of this investigation was to study the effect of DFP administration on NF subunit mRNAs expression, when OPIDN is protected or potentiated by pre-treatment or post-treatment, respectively, with phenylmethylsulfonyl fluoride (PMSF). The hens were sacrificed 1, 5, 10, and 20 days after the last treatment. In contrast with enhanced mRNA expression of NF subunits reported in OPIDN, there was no alteration in the expression of NF subunits in the SC of PMSF-protected hens that did not develop OPIDN. PMSF post-treatment of DFP-treated hens, which enhanced delayed neurotoxicity produced by a low dose of DFP, exhibited decrease in the mRNA expression of NF subunits in SC at all time periods (1-20 days) of observation. The expression of NF subunits was also studied in the degeneration-resistant tissue cerebrum of treated hens. The results from protected hens suggested that temporal enhanced expression of NF subunit mRNAs in DFP-treated hens might be contributing to the development of OPIDN in hens. By contrast, PMSF post-treatment seemed to potentiate OPIDN by a mechanism different from that followed by DFP alone to produce OPIDN.
PMID: 11310568 [PubMed - indexed for MEDLINE]
Full report available at: http://www.fluoride-journal.com/01-34-3/343-165.pdfFluoride 2001; 34(3 ):165-173
Effect of fluoride on thyroid function and cerebellar development in mice
Mahmoud Trabelsi (a), Fadhel Guermazi (b), Najiba Zeghal (c)
(a) Synthesis and Physical-Organic Chemistry Laboratory, Faculty of Sciences-Sfax;
(b) Nuclear Medicine Service, CHU Habib Bourguiba-Sfax.
(c) For correspondence: Dr N Zeghal, Animal Physiology Laboratory, Department of Biology, FacultŽ des Sciences de Sfax-Route de la Soukra-Km 3.5, 3038 Sfax BP802, Tunisia. Email: Nejiba.Zghal@fss.rnu.tnSUMMARY: The effect of fluoride on murine thyroid function and cerebellar development was studied by administering 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 a control group, the NaF-treated pups, at age 14 days, showed a 35% decrease in body weight, a 75% decrease in plasma free T4, and 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 differenti-ated and arranged in a single layer at the surface of the internal granular layer, and with more apoptotic Purkinje cells being present.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11512573&dopt=AbstractJ Epidemiol 2001 Jul;11(4):170-9
Regression analysis of cancer incidence rates and water fluoride in the U.S.A. based on IACR/IARC (WHO) data (1978-1992). International Agency for Research on Cancer.
Takahashi K, Akiniwa K, Narita K.
Department of Physical Medicine, Faculty of Medicine, University of Tokyo, Japan.
Age-specific and age-standardized rates (ASR) of registered cancers for nine communities in the U.S.A. (21.8 million inhabitants, mainly white) were obtained from IARC data (1978-82, 1983-87, 1988-92). The percentage of people supplied with "optimally" fluoridated drinking water (FD) obtained from the Fluoridation Census 1985, U.S.A. were used for regression analysis of incidence rates of cancers at thirty six sites (ICD-WHO, 1957). About two-thirds of sites of the body (ICD) were associated positively with FD, but negative associations were noted for lip cancer, melanoma of the skin, and cancers of the prostate and thyroid gland. In digestive organs the stomach showed only limited and small intestine no significant link. However, cancers of the oral cavity and pharynx, colon and rectum, hepato-biliary and urinary organs were positively associated with FD. This was also the case for bone cancers in male, in line with results of rat experiments. Brain tumors and T-cell system Hodgkin's disease, Non-Hodgkin lymphoma, multiple myeloma, melanoma of the skin and monocytic leukaemia were also correlated with FD. Of the 36 sites, 23 were positively significant (63.9%), 9 not significant (25.0%) and 4 negatively significant (11.1%). This may indicate a complexity of mechanisms of action of fluoride in the body, especially in view of the coexising positive and negative correlations with the fluoridation index. The likelihood of fluoride acting as a genetic cause of cancer requires consideration.
PMID: 11512573 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11405255&dopt=AbstractNeurotoxicology 2001 Apr;22(2):233-48
Acute neurobehavioral effects in rats from exposure to HFC 134a or CFC 12.
Ritchie GD, Kimmel EC, Bowen LE, Reboulet JE, Rossi J 3rd.
Geo-Centers, Inc., Wright-Patterson Air Force Base (WPAFB), OH 45433-7903, USA. glenn.ritchie@wpafb.af.mil
1,1,1,2-Tetrafluoroethane (HFC 134a), a chlorine-free hydrofluoroalkane, is internationally replacing billions of pounds of dichlorodifluoromethane (CFC 12) for coolant, refrigerant and aerosol propellant applications. The ALC50 for HFC 134a in rats is 567,000 ppm for 4 h; its potential for cardiac epinephrine sensitization in beagle dogs is acceptable (75,000 ppm); and its capacity to induce carcinogenicity or developmental disorders in animals is minimal. HFC 134a, with a serum half life estimated at 4-11 min, has been accepted for use as a propellant in metered-dose inhalant products, implying a low human toxicity risk from periodic brief exposures. There has been little published human or animal research evaluating possible neurobehavioral toxicity from longer HFC 134a exposures, as may be expected to occur in operational scenarios. In this study, male Wistar rats were exposed to various concentrations of HFC 134a or CFC 12 for up to 30 min while performing in either a rotarod/motorized running wheel apparatus or in an operant chamber The relative neurobehavioral toxicity of CFC 12 and its ozone-depleting substance replacement HFC 134a was assessed by comparing both gross motor system incapacitation and more subtle changes in ability to perform an operant discrimination task. It was shown that exposure to HFC 134a or CFC 12 concentrations from 40,000 to 470,000 ppm, for up to 30 min, induced neurobehavioral deficits in every subject, ranging from reduced operant efficiency to apparent anesthesia. For neurobehavioral endpoints examined in these experiments, HFC 134a inhalation was shown to induce deficits more rapidly, and at lower concentrations when compared to CFC 12 exposure.
PMID: 11405255 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11299208&dopt=AbstractAm J Physiol Heart Circ Physiol 2001 May;280(5):H2069-75
Pregnancy enhances G protein activation and nitric oxide release from uterine arteries.
Thompson LP, Weiner CP.
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
We hypothesized that pregnancy modulates receptor-mediated responses of the uterine artery (UA) by altering G protein activation or coupling. Relaxation and contraction to NaF (0.5-11.5 mM), acetylcholine (10(-9)-10(-5) M), and bradykinin (10(-12)-3 x 10(-5) M) were measured in isolated UA of pregnant and nonpregnant guinea pigs. Responses were measured in the presence and absence of either cholera toxin (2 microg/ml) or pertussis toxin (Galpha(s) and Galpha(i) inhibitors, respectively). NaF relaxation was endothelium dependent and nitro-L-arginine sensitive (a nitric oxide synthase inhibitor). Relaxation to NaF, acetylcholine, and bradykinin were potentiated by pregnancy. Cholera but not pertussis toxin increased relaxation to acetylcholine and bradykinin in UA from nonpregnant animals, had no effect in UA from pregnant animals, and abolished the pregnancy-induced differences in acetylcholine relaxation. Cholera toxin potentiated the bradykinin-induced contraction of UA of both pregnant and nonpregnant animals, whereas pertussis toxin inhibited contraction of UA from pregnant animals only. Therefore, pregnancy may enhance agonist-stimulated endothelium-dependent relaxation and bradykinin-induced contraction of UA by inhibiting GTPase activity or enhancing Galpha(s) but not Galpha(i) activation in pregnant animals. Thus the diverse effects of pregnancy on UA responsiveness may result from hormonal modulation of G proteins coupled to their specific receptors.
PMID: 11299208 [PubMed - indexed for MEDLINE]
Full report available at http://www.fluoride-journal.com/01-34-1/341-9.pdfFluoride 2001; 34(1):9-20
Effects of sodium fluoride and aluminum chloride on ovary and uterus of mice and their reversal by some antidotes
NJ Chinoy * and TN Patel
* For correspondence: Reproductive Endocrinology and Toxicology Unit, Department of Zoology, School of Sciences, Gujarat University, Ahmedabad, India. E-mail: zooldeptgu@satyam.net.in
SUMMARY: A study was made of the effects on ovary and uterus of adminis-tering sodium fluoride (10 mg/kg body weight) or aluminium chloride (200 mg/kg body weight) alone and in combination to female albino mice (Mus musculus) for 30 days. The reversibility of the induced effects by withdrawal of NaF + AlCl3 treatment and by administering ascorbic acid (AA), calcium (Ca), or vitamin E alone and in combination were also investigated. All treat-ments (NaF, AlCl3, and NaF + AlCl3) resulted in a significant decline of ovarian protein and 3 ¥ - and 17 ¥ -hydroxysteroid dehydrogenase activities which could be related to increased cholesterol levels in the ovary suggesting altered steroidogenesis. The treatment also caused a hypercholesterolemic effect in serum. Accumulation of glycogen in uterus could be related to inhibition of phosphorylase activity affecting carbohydrate metabolism. The withdrawal of combined treatment for 30 days brought about an incomplete recovery. However, AA, Ca, or vitamin E supplementation alone and in combination produced an additive effect for recovery of most of the parameters almost to con-trol levels. Hence the effects of NaF and/or AlCl3 are transient and reversible.
Full report available at http://www.fluoride-journal.com/01-34-2/342-108.pdfFluoride 2001; 34(2):108-113
Effect of fluoride intoxication on lipid peroxidation and antitoxidant systems in rats
YM Shivarajashankara (a), AR Shivashankara (a), P Gopalakrishna Bhat (b), S Hanumanth Rao (c)
(a) YM Shivarajashankara, Dept. of Biochemistry, MR Medical Col-lege, Gulbarga-585 105, Karnataka, India; E-mail: shivrajsym@yahoo.com;
(b) Dept. of Biochemistry, Kasturba Medical College, Manipal-576 119, Karnataka, India;
(c) Dept. of Biochemistry, KBN Institute of Medical Sciences, Gulbarga-585 104, Karnataka, India.SUMMARY: The effect of fluoride intoxication on lipid peroxidation and anti-oxidant systems in the blood, brain, and liver of rats was studied. Twelve one-month-old albino rats were administered 100-ppm fluoride (as NaF) in their drinking water for four months. In the red blood cells the levels of malondial-dehyde (MDA) and glutathione (GSH) increased, along with the activity of glutathione peroxidase (GSH-Px), but the activity of superoxide dismutase (SOD) decreased. In the plasma the level of ascorbic acid increased while that of uric acid decreased. 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 available at http://www.fluoride-journal.com/01-34-2/342-132.pdfFluoride 2001; 34(2):132-138
Glutathione metabolism in rats exposed to high-fluoride water and effect of spirulina treatment
Toshi Kaushik (a), Radhey Shyam (b), Praveen Vats (b), Shoba Suri (b), MML Kumria (b), PC Sharma (a), Som Nath Singh (b)
(a) Dept. of Biotechnology, Chaudhary Charan Singh University, Meerut-250 004, India.
(b) For correspondence: Dr Som Nath Singh, Nutrition Division, Defence Institute of Physiology and Allied Sciences, Timarpur, Delhi-110 054, India. Email: dipnut@rediffmail.comSUMMARY: Effects of high fluoride intake through water on glutathione and related enzymatic activities in blood and liver of albino rats were studied. Twenty four rats were divided into three groups of 8 each. Group I was given normal municipal supply water (fluoride content 0.55 ppm), Groups II and III were exposed to 12 ppm fluoride in water for 15 days. Group III was treated orally with Spirulina ¨ (200 mg/kg bwt), a functional food rich in protein, vitamins and minerals, for study of protective effects. After 15 days of exposure reduced and oxidised glutathione (GSH and GSSG), lipid peroxidation and enzymes, i.e. glutathione reductase (GR), glutathione peroxidase (GPx), gluta-thione S-transferase (GST), and y-glutamyl transpeptidase (y-GT) activities were measured in blood/erythrocytes and liver. There was a significant rise in blood GSSG level and a decrease in GSH/GSSG ratio, with increased lipid peroxidation in fluoride-exposed animals. A marked decrease in GR and GST activities and an increase in y-glutamyl transpeptidase activity were also noted in blood of fluoride exposed animals. In the liver no significant changes in these variables were observed. Results indicate oxidative stress during fluoride exposure. Spirulina treatment was beneficial to some extent as a rich source of the antioxidant vitamin y carotene.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11383119&dopt=AbstractLaryngorhinootologie 2001 Apr;80(4):187-90
[Cytotoxicity and genotoxicity of fluorides in human mucosa and lymphocytes]
[Article in German]
Kleinsasser NH, Weissacher H, Wallner BC, Kastenbauer ER, Harreus UA.
Klinisch experimentelle Onkologie der Klinik und Poliklinik fur Hals-, Nasen- und Ohrenkranke der Ludwig-Maximilians-Universitat Munchen. norbert.kleinsasser@hno.med.uni-muenchen.de
BACKGROUND: Fluorides are widely used in dental health products and drinking water, due to their beneficial effects in caries-prophylaxis and -treatment. Nevertheless, irritation of the gingiva and oropharyngeal mucosa as well as in gastric mucosa is observed since neither local nor systemic application is restricted to the teeth. These effects may partly be attributed to a known cytotoxicity of fluorides. Whether fluorides also have genotoxic effects on human mucosa or lymphocytes as a possible factor in tumor initiation was investigated in this study.
MATERIAL AND METHODS: Human oropharyngeal epithelial cells and peripheral lymphocytes were incubated after single cell preparation with the aminefluoride Olaflur at concentrations of 2 ppm, 21 ppm, 35 ppm, 71 ppm and 213 ppm. The extent of cytotoxicity was investigated using the trypan blue exclusion test. Following incubation, electrophoresis for migration of DNA fragments, fluorescence staining and digital image analysis according to a standard protocol of the single cell microgel electrophoresis assay (Comet assay) followed. DNA damage was characterized using the Olive Tail Moment (OTM).
RESULTS: For fluoride concentrations of 2 ppm to 35 ppm, non vital cells of less than 10% could be shown. After incubation with 71 ppm and 213 ppm Olaflur, there were 15% and 43% of damaged cells, respectively. Weak genotoxic effects on mucosal cells as well as on lymphocytes could be demonstrated at all concentrations tested. In fluoride concentrations of 213 ppm genotoxicity increased to max. OTM-levels of 23.
CONCLUSIONS: Beside the cytotoxic effect of fluorides, also a minor genotoxic impact on human mucosa and on peripheral lymphocytes could be demonstrated using the Comet assay. Further investigations are warranted to examine fluorides in a model allowing for repeated or long term incubations on structurally intact human mucosa in vitro. Such a model will help to distinguish between DNA damage that may be repaired successfully and other impairments that may show an additive character in repetitive or chronic exposure in vivo.
PMID: 11383119 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11372831&dopt=AbstractChemosphere. 2001 May-Jun;43(4-7):493-5.
Synthesis and S(N)Ar reactions of new dioxins and predioxins. Litvak VV, Korshunova OA, Saikovich EG.
Institute of Bioorganic Chemistry, Siberian Branch of Russian Academy of Sciences, Novosibirsk, Russian Federation. litvak@niboch.nsc.ru
A method for two-step synthesis of dioxin derivatives containing the perfluoropyridine ring has been suggested. It consists of the preparation of corresponding predioxin in the first stage and its cyclization in the next stage. A number of new predioxins have been synthesized using the interaction of polyhalogenpyridines with pyrocatechin and its 4,5-dihaloid derivatives. Formation of dioxins on the basis of not very active arenes occurs smoothly without the necessity for the isolation of predioxin intermediates. For the first time, an interaction of polyhalogenpyridine-containing dioxins and predioxins with nucleophiles of various types (alkyl and arylamines, propylenediamine, hydroxyl anion, and ammonia) has been studied. It was shown that the pyridine fragment does not change the fundamental rules of orientation influence of substituents detemined for non-heterocyclic polyfluorinated arenes. The presence of the labile fluorine atoms reveals a possibility for various modifications of dioxins and predioxins.
PMID: 11372831 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11738173&dopt=AbstractCurr Opin Chem Biol 2001 Dec;5(6):643-9
Dissection of nucleophilic and acid-base catalysis in glycosidases.
Zechel DL, Withers SG.
Protein Engineering Network of Centres of Excellence of Canada and Department of Chemistry, University of British Columbia, Vancouver, Canada.
A startling array of added anions have been observed to function as replacement catalytic nucleophiles in mutant glycosidases, including formate, azide, fluoride and other halides. Likewise, the mechanism of acid-base catalysis is somewhat plastic. The carboxylic acids can be substituted by a sulfenic acid or by ascorbate, and the effective acid strength enhanced by the introduction of strong hydrogen bonds. These studies provide an interesting bridge between enzymes and models thereof.
Publication Types:
- Review
- Review, Tutorial
PMID: 11738173 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11885920&dopt=AbstractInt J Occup Med Environ Health 2001;14(4):369-73
The effect of sodium fluoride on the adenine nucleotide pool in erythrocytes of Wistar rats.
Suska M.
Department of Biochemistry, Institute of Life Sciences, University of Szczecin, Poland. biochem@univ.szczecin.pl
The effect of sodium fluoride on the content of adenine nucleotides, adenine nucleotide pool and energy potential of erythrocytes was studied in male Wistar rats, depending on the dose and time of exposure. Sodium fluoride was administered for 4 and 8 weeks at 4 or 16 ppm through a gastric tube. The concentration of fluorine in serum, ATP, ADP and AMP content in blood and erythrocytes, adenine nucleotide pool and energy potential of erythrocytes were calculated. The results were expressed in SI units and compared statistically with Student's t-test (Statgraphics v. 5.0 software). A significant reduction in the content of ATP and ADP and an increase in the content of AMP in erythrocytes was found after 4 weeks of exposure to 4 or 16 ppm NaF. The adenine nucleotide pool and energy potential were reduced with the smaller dose. After 8 weeks, the ADP content remained significantly reduced with the smaller dose, while the greater dose was associated with a higher energy potential of the cells. Correlations between serum concentration of fluorine, content of adenine nucleotides and adenine nucleotide pool in erythrocytes were noted in all study groups.
PMID: 11885920 [PubMed - indexed for MEDLINE]
Full report available at: http://www.fluoride-journal.com/01-34-3/343-174.pdfFluoride 2001; 34(3):174-180
Influence of fluoride ions on Na+-H+ exchanger actvity in human red blood cells
J Bober (a,b), D Chlubek (a), E Kwiatkowska (c), K K ¥ dziersk (c), E Stachowska (a), P Wieczorek (a) E Byra (d), Z Machoy (a), E Herdzik (c)
(a) Department of Biochemistry and Chemistry. Pomeranian Academy of Medicine (PAM).
(b) For correspondence: Dept. of Biochem. and Chem., PAM, 70- 111 Szczecin, Al. Pow-stancow Wlkp.72, Poland.; E-mail: jbober@sci.pam.szczecin.pl,
(c) Chair and Dept. of In-ternal Medicine,
(d) Main Laboratory, Clinical Hospital of PAM.Summary: The influence of fluoride ion (F - ) at concentrations of 0.25 and 2.5 mM on intracellular pH and Na + -H + exchanger (NHE) activity in human red blood cells was investigated. Erythrocytes from 15 healthy individuals were examined. We found that F - caused a decrease in NHE activity and an in-crease in intracellular H + ion concentration (decrease of intracellular pH). marrow haematopoietic cells.3
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11724534&dopt=AbstractJ Mol Biol 2001 Nov 16;314(1):83-92
The phosphoryl-transfer mechanism of Escherichia coli phosphoenolpyruvate carboxykinase from the use of AlF(3).
Sudom AM, Prasad L, Goldie H, Delbaere LT.
Department of Biochemistry, University of Saskatchewan, Saskatoon, Canada.
The mechanism of reversible transfer of the gamma-phosphate group of ATP by Escherichia coli phosphoenolpyruvate carboxykinase (PCK) on to its substrate is of great interest. It is known that metallofluorides are accurate analogs of the transition state in the context of kinase mechanisms. Therefore, two complexes of PCK, one with AlF(3), Mg(2+) and ADP (complex I), the other with AlF(3), Mg(2+), ADP and pyruvate (complex II) were crystallized. The X-ray crystal structures of these two complexes were determined at 2.0 A resolution. The Al atom has trigonal bipyramidal geometry that mimics the transition state of phosphoryl transfer. The Al atom is at a distance of 2.8 A and 2.9 A from an oxygen atom of the beta-phosphoryl group of ADP in complex I and II, respectively. A water molecule in complex I and an oxygen atom of the pyruvate in complex II are located along the axis of the trigonal bipyramid on the side opposite to the beta-phosphoryl oxygen with respect to the equatorial plane, suggesting that the complexes are close mimics of the transition state. Along with the presence of positively charged species around the AlF(3) moiety, these results indicate that phosphoryl transfer occurs via a direct displacement mechanism with associative qualities. Copyright 2001 Academic Press.
PMID: 11724534 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11855746&dopt=AbstractMol Cell Biochem 2001 Dec;228(1-2):91-8
Differential effects of bacterial toxins on mitogenic actions of sodium fluoride and those of aluminum fluoride in human TE85 osteosarcoma cells.
Hashimoto H, Lau KH.
Department of Medicine, Loma Linda University, Jerry L. Pettis Memorial VA Medical Center, CA 92357, USA.
This study compared the effects of cholera toxin (CTX) and pertussis toxin (PTX) on the actions of sodium fluoride (NaF) and those of aluminum fluoride (AlF3) on cell proliferation and differentiation, as well as tyrosine phosphorylation level of mitogen activated protein kinase (MAPK) in human bone cells. NaF and AlF3 each significantly stimulated the proliferation of human TE85 osteosarcoma cells, increased cellular alkaline phosphatase (ALP) activity, and increased MAPK tyrosine phosphorylation level. CTX completely blocked the bone cell anabolic activities of both NaF and AlF3. While PTX (2 ng/ml) inhibited the bone cell actions of NaF, it had no significant effect on those of AlF3. Both CTX and PTX completely blocked the stimulatory action of AlF3 on MAPK tyrosine phosphorylation, but neither toxin had an effect on the action of NaF on MAPK tyrosine phosphorylation. In conclusion, PTX and CTX had contrasting effects on the anabolic bone cell actions of NaF and AlF3 actions. These findings argue against the hypothesis that the osteogenic activity of NaF is mediated via the formation of AlF3 in human TE85 osteosarcoma cells.
PMID: 11855746 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11704544&dopt=AbstractAm J Physiol Lung Cell Mol Physiol 2001 Dec;281(6):L1472-83
Mechanisms of sodium fluoride-induced endothelial cell barrier dysfunction: role of MLC phosphorylation.
Wang P, Verin AD, Birukova A, Gilbert-McClain LI, Jacobs K, Garcia JG.
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224-6801, USA.
NaF, a potent G protein activator and Ser/Thr phosphatase inhibitor, significantly increased albumin permeability and decreased transcellular electrical resistance (TER), indicating endothelial cell (EC) barrier impairment. EC barrier dysfunction induced by NaF was accompanied by the development of actin stress fibers, intercellular gap formation, and significant time-dependent increases in myosin light chain (MLC) phosphorylation. However, despite rapid, albeit transient, activation of Ca(2+)/calmodulin-dependent MLC kinase (MLCK), the specific MLCK inhibitor ML-7 failed to affect NaF-induced MLC phosphorylation, actin cytoskeletal rearrangement, and reductions in TER, suggesting a limited role of MLCK in NaF-induced EC activation. In contrast, strategies to reduce Rho (C3 exoenzyme or toxin B) or to inhibit Rho-associated kinase (Y-27632 or dominant/negative RhoK) dramatically reduced MLC phosphorylation and actin stress fiber formation and significantly attenuated NaF-induced EC barrier dysfunction. Consistent with this role for RhoK activity, NaF selectively inhibited myosin-specific phosphatase activity, whereas the total Ser/Thr phosphatase activity remained unchanged. These data strongly suggest that MLC phosphorylation, mediated primarily by RhoK, and not MLCK, participates in NaF-induced EC actin cytoskeletal changes and barrier dysfunction.
PMID: 11704544 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11697895&dopt=AbstractExp Cell Res 2001 Nov 15;271(1):189-99
Involvement of heterotrimeric G proteins in phagocytosis and recycling from the phagosomal compartment.
Damiani MT, Colombo MI.
Instituto de Histologia y Embriologia, Universidad Nacional de Cuyo-CONICET, Mendoza, 5500, Argentina.
Phagocytosis is a receptor-mediated process by which specialized cell types engulf large extracellular particles. Phagosome maturation involves a series of intracellular membrane fusion and budding events resulting in the delivery of particles to compartments enriched in lysosomal hydrolases where they are digested. Substantial amounts of plasma membrane and many phagosomal proteins, such as receptors, rapidly recycle to the plasma membrane following phagosome formation. Despite the importance of this recycling pathway in phagosome maturation and in the retrieval of immunogenic peptides from phagosomes, the molecular machinery involved is largely unknown. To assess the participation of GTPases in phagocytosis and recycling from phagosomes we used aluminum fluoride (AIF(-)(4)), which activates the GDP-bound form of stimulatory and inhibitory trimeric G proteins. AlF(-)(4) inhibited both the uptake to and the recycling from the phagosomal compartment. Cholera toxin, which activates Galphas, and pertussis toxin, which uncouples Gi and Go from receptors, were effective inhibitors of phagocytosis. However, both toxins stimulated recycling from phagosomes. These results suggest that more than one GTP-binding protein participates either directly or indirectly not only in phagocytosis, but also in maturation and recycling from phagosomes, and thereby assign a role for heterotrimeric G proteins in controlling traffic through the phagocytic pathway. Copyright 2001 Academic Press.
PMID: 11697895 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11567778&dopt=AbstractToxicology 2001 Oct 15;167(2):145-58
Mechanisms in fluoride-induced interleukin-8 synthesis in human lung epithelial cells.
Refsnes M, Thrane EV, Lag M, Hege Thoresen G, Schwarze PE.
Department of Environmental Medicine, National Institute of Public Health, PO Box 4404, Nydalen, N-0403, Oslo, Norway. magne.refnes@folkhelsa.no
Sodium fluoride (NaF) has previously been reported to induce a strong IL-8 response in human epithelial lung cells (A549) via mechanisms that seem to involve the activation of G proteins. In the present study the signal pathways downstream of the G proteins have been examined. NaF induced a weak, but sustained increase in PKC activity. In contrast, the PKC activator TPA induced a relatively strong, but transient effect and augmented the NaF-induced PKC activity. TPA induced a marked IL-8 response compared to NaF. PDB, another PKC activator, was less effective, but augmented the IL-8 response to NaF. Pretreatment with TPA for 20 h, or the PKC inhibitor GF109203X for 1 h, abolished the basal and NaF-induced PKC activities and partially prevented the NaF-induced IL-8 response. Inhibition of the MAP kinase p38 by SB202190 partially reduced the IL-8 response to NaF, whereas a reduction in ERK activity by PD98059 led to an increased response. The NaF-induced IL-8 response was weakly augmented by the PKA stimulator forskolin and the G(i) inhibitor pertussis toxin. The PKA inhibitor H89 seemed to reduce the NaF-induced IL-8 response, but the measured effect was not statistically significant. BAPTA-AM, KN93 and W7, that inhibit Ca(2+)-linked effects, did not affect the IL-8 response. Furthermore, the tyrosine kinase inhibitor genestein, the PI-3 kinase inhibitor wortmannin and phosphatase inhibition were without effects. In conclusion, the data suggest that NaF-induced increase of IL-8 in A549 cells involved PKC- and p38-linked pathways, whereas an ERK-dependent pathway counteracted the response. Tyrosine kinases, Ca(2+)-linked pathways, PI-3 kinase, PKA and phosphatase inhibition seem to play no or minor roles in the fluoride-induced IL-8 response.
PMID: 11567778 [PubMed - indexed for MEDLINE]
Full report available free at http://toxsci.oupjournals.org/cgi/content/full/61/1/83?ijkey=afjKDnA8vjjNUToxicological Sciences 61, 83-91 (2001)
Fluoride-Induced Apoptosis in Epithelial Lung Cells Involves Activation of MAP Kinases p38 and Possibly JNK
E. V. Thrane* ,M. Refsnes* ,G. H. Thoresen ,M. Låg* andP. E. Sch warze*,1 * Department of Environmental Medicine, National Institute of Public Health, Oslo, Norway; and Department of Pharmacology, Faculty of Medicine, University of Oslo, Oslo, Norway.
1 To whom correspondence should be addressed at the Department of Environmental Health, NIPH, 4404 Torshov, 0403-Oslo, Norway. Fax: + 47 22 04 22 43. E-mail: per.schwarze@folkehelsa.no.
Exposure to fluorides can induce inflammatory reactions, cell cycle arrest, and apoptosis in different experimental systems. Fluorides are known G-protein activators, but less is known about fluoride effects downstream of G-protein activation. The aim of this study was to elucidate whether the induction of apoptosis by fluorides and inhibition of proliferation is mediated by MAP kinases in primary rat lung, alveolar type 2 cells and the human epithelial lung cell line A549. Sodium fluoride (NaF) induced apoptosis in both cell types but at different concentrations, with the primary cells being more sensitive to NaF. Proliferation of the type 2 cells and A549 cells was inhibited in the presence of NaF. NaF induced a prolonged activation of MAP kinase ERK. NaF also activated p38 and JNK in A549 cells for several hours (maximally 6-fold and 3-fold increase, respectively). Inhibition of ERK with the MEK1,2 inhibitor PD98059 increased apoptosis 2-fold, whereas the inhibitor of p38, SB202190, decreased the level of apoptotic cells by approximately 40%. SB202190 also inhibited apoptosis by almost 40% when ERK activity was reduced in the presence of PD98059. Neither PD98059 nor SB202190 did affect the NaF-induced inhibition of proliferation. These observations indicate that activation of MAP kinases p38 and possibly JNK are involved in NaF-induced apoptosis of epithelial lung cells, whereas ERK activation seems to counteract apoptosis in epithelial lung cells. In contrast, activation of ERK and p38 are not involved in NaF-induced inhibition of cell proliferation.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11797833&dopt=AbstractJ Environ Pathol Toxicol Oncol 2001;20(3):237-43
Low levels of p53 mutations in Indian patients with osteosarcoma and the correlation with fluoride levels in bone.
Ramesh N, Vuayaraghavan AS, Desai BS, Natarajan M, Murthy PB, Pillai KS.
Frederick Institute of Plant Protection and Toxicology, Padappai, Tamil Nadu, India.
The pathogenesis of osteogenic sarcoma is not known. Recently, chronic fluoride exposure has been incriminated as having a possible etiologic role by causing a nonspecific osteoblast proliferation. We were interested in exploring the possible relationship between fluoride bone content and p53 mutations. We analyzed p53 mutations in various exons in tissue of osteosarcoma, and correlated the findings with the bone fluoride levels in Indian patients. We analyzed tissue samples from 20 osteosarcoma patients for possible genetic alterations including mutations, and we assessed the extent of fluoride accumulation in bone. Fragments displaying an altered electrophoretic mobility were confirmed as having mutated sequences. Mutation was observed in samples of two cases (10% incidence). Eighteen samples showed bone fluoride levels between 1000 and 27,000 ppm, whereas the 2 mutated samples showed fluoride levels of 64,000 and 89,000 ppm, respectively. The high levels of bone fluoride levels and the similarity of the mechanisms of action between fluoride-induced DNA damage and chemically-induced p53 mutations lead us to propose that high fluoride bone content might have been one of the major factors causing osteosarcoma.
PMID: 11797833 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11461774&dopt=AbstractFree Radic Biol Med 2001 Aug 1;31(3):367-73
Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells.
Anuradha CD, Kanno S, Hirano S.
Regional Environment Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305 8506, Japan.
It has been suggested that oxidative stress plays a major role in various forms of cell death, including necrosis and apoptosis. We have previously reported that fluoride (NaF) induces apoptosis in HL-60 cells by caspase-3 activation. The main focus of this investigation was to arrive at a possible pathway of the apoptosis induced by NaF upstream of caspase-3, because the mechanism is still unknown. The present study showed that after exposure to NaF, there was an increase in MDA and 4-HNE and a loss of mitochondrial membrane potential (deltaPsi(m)) was also observed in NaF-treated cells.There was a significant increase in cytosolic cytochrome c, which is released from the mitochondria. We have reported a downregulation of Bcl-2 protein in NaF-treated cells. The antioxidants N-acetyl cysteine (NAC), glutathione (GSH) protected the cells from loss of deltaPsi(m), and there was no cytochrome c exit or Bcl-2 downregulation, and we suggest that these antioxidants prevent apoptosis induced by NaF. These results suggested that perhaps NaF induced apoptosis by oxidative stress-induced lipid peroxidation, causing loss of deltaPsi(m), and thereby releasing cytochrome c into the cytosol and further triggering the caspase cascade leading to apoptotic cell death in HL-60 cells.
PMID: 11461774 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11434994&dopt=AbstractFood Chem Toxicol 2001 Aug;39(8):867-76
Developmental toxicity of sodium fluoride measured during multiple generations.
Collins TF, Sprando RL, Black TN, Shackelford ME, Olejnik N, Ames MJ, Rorie JI, Ruggles DI.
Center for Food Safety and Applied Nutrition, US Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA. tcoll60504@aol.com
Sodium fluoride (NaF) has been used to fluoridate drinking water in the United States since the mid 1940s. Because of the lack of reliable studies on the multigeneration effects of the compound, NaF (0, 25, 100, 175 or 250 ppm in drinking water) was given to rats continuously during three generations. Parental (F0) generation rats were treated for 10 weeks and mated within groups. At gestation day 20, caesarean sections were performed and eight F0 females per group and their litters (F1) were observed for implant status, fetal weight and length, sex and morphological development. The remaining F0 females (29-32 per group) were allowed to litter. F1 offspring (36 of each sex per group) were mated within groups, and caesarean sections were performed at gestation day 20. The F1 females and their litters (F2) were observed for implant status, fetal weight and length, sex and morphological development. In addition, F2 fetuses were evaluated for internal (soft-tissue) and skeletal development. Decreased fluid consumption for F0 and F1 dams at 175 and 250 ppm was attributed to decreased palatability of the solution. No dose-related effects in feed consumption or mean body weight gain were observed in either F0 or F1 females. Numbers of corpora lutea, implants, viable fetuses and fetal morphological development were similar in all groups. No dose-related anomalies in internal organs were observed in F2 fetuses. Ossification of the hyoid bone of F2 fetuses was significantly decreased at 250 ppm. Because of the decreased ossification of the hyoid bone, 250 ppm is considered the effect level.
PMID: 11434994 [PubMed - indexed for MEDLINE][Note from FAN:
Definition of Hyoid bone: a U-shaped bone lying between the mandible and the larynx, suspended from the styloid processes by slender stylohyoid ligaments. Ref: Steadman's Concise Medical Dictionary for the Health Professions. Illustrated 4th Edition. Ed: JH Dirckx, M.D. 2001.Lippincott Williams & Wilkins.
The chemical used to fluoridate over 90% of U.S. public drinking water is not sodium fluoride. The "chemical" used is hydrofluosilicic acid which is a toxic waste product from the phosphate fertilizer industry. The sodium fluoride that is used in less than 10% of fluoridation schemes is also a waste product, primarily from the aluminum industry. No tests have been published using these toxic waste products.- EC.]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11346491&dopt=AbstractFood Chem Toxicol 2001 Jun;39(6):601-13
Multigenerational evaluation of sodium fluoride in rats.
Collins TF, Sprando RL, Black TN, Shackelford ME, Bryant MA, Olejnik N, Ames MJ, Rorie JI, Ruggles DI.
Center for Food Safety and Applied Nutrition, US Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA. tfc@cfsan.fda.gov
Since the mid 1940s, fluoride has been added to tap water in American communities in an effort to reduce the incidence of dental caries in the population. When the levels of fluoride in drinking water were tested and set, water was the only measurable source of fluoride for most communities. Now, adults and children ingest fluoride with foods and beverages prepared with fluoridated water, and they are exposed to fluoride-containing dental products. As a result, exposure to fluoride is greater than had been anticipated. In the early 1990s, the existing reproductive studies were reviewed in several reports and were considered to be inadequate to determine potential reproductive or developmental hazards. The effects of sodium fluoride ingestion at 0, 25, 100, 175 or 250 ppm in drinking water measured in rats throughout three generations are reported here. Feed and fluid consumption, body weights and clinical signs were recorded at regular intervals. Decreased fluid consumption observed at 175 and 250 ppm was attributed to decreased palatability and did not affect reproduction. No cumulative effects were observed in the three generations. Mating, fertility and survival indices were not affected. Organ-to-body-weight ratios and organ-to-brain weight ratios were not affected. Sodium fluoride up to 250 ppm did not affect reproduction in rats.
PMID: 11346491 [PubMed - indexed for MEDLINE][Note from FAN:
The chemical used to fluoridate over 90% of U.S. public drinking water is not sodium fluoride. The "chemical" used is hydrofluosilicic acid which is a toxic waste product from the phosphate fertilizer industry. The sodium fluoride that is used in less than 10% of fluoridation schemes is also a waste product, primarily from the aluminum industry. No tests have been published using these toxic waste products.- EC.]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156568&dopt=AbstractBr J Pharmacol 2001 Jan;132(1):119-26
Effects of tyrosine kinase inhibitors on cell death induced by sodium fluoride and pertussis toxin in the pancreatic beta-cell line, RINm5F.
Elliott J, Scarpello JH, Morgan NG.
Cellular Pharmacology Group, School of Life Sciences, Keele University, Keele, Staffs ST5 5BG.
1. Sodium fluoride causes apoptosis of pancreatic beta-cells and this response is enhanced by pre-treatment with pertussis toxin. In the present study, tyrosine kinase inhibitors were used to investigate the mechanisms of action of NaF and pertussis toxin in the beta-cell line, RINm5F.
2. Exposure of RINm5F cells to low concentrations of genistein or tyrphostin A25 resulted in significant inhibition of cell death induced by 5 mM NaF. Higher concentrations (>25 microM) were cytotoxic in the absence of NaF but, paradoxically, the combination of genistein and NaF induced less cell death than when each agent was used alone.
3. The increase in cell death induced by 100 microM genistein was markedly inhibited by ciprofloxacin, a drug which binds to topoisomerase II. Etoposide (which inhibits topoisomerase II but has no effect on tyrosine kinase activity) also caused an increase in RINm5F cell death. Neither etoposide nor ciprofloxacin altered the response to 5 mM NaF.
4. Pertussis toxin markedly enhanced the extent of RINm5F cell death induced by NaF and this effect was completely prevented by 25 microM genistein. The inhibition caused by genistein was not affected by ciprofloxacin but was reproduced by a structurally dissimilar tyrosine kinase inhibitor, herbimycin A.
5. The results demonstrate that RINm5F beta-cells express a pertussis toxin sensitive pathway that is anti-apoptotic. The activity of this pathway is most evident in cells exposed to pro-apoptotic stimuli where the effects of pertussis toxin can be blocked by inhibitors of tyrosine kinase enzymes. A genistein-sensitive tyrosine kinase does not appear to be involved in RINm5F cell survival under basal conditions.
PMID: 11156568 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11900377&dopt=AbstractAdv Exp Med Biol 2001;498:263-71
Alterations in g-protein-linked signal transduction in vascular smooth muscle in diabetes.
Anand-Srivastava MB, Wang R, Liu YY.
Department of Physiology, Faculty of Medicine, University of Montreal, Quebec, Canada.
The present studies were undertaken to determine the levels of stimulatory and inhibitory guanine nucleotide regulatory proteins (Gs and Gi respectively) and their relationship with adenylyl cyclase activity in aorta from 5-day streptozotocin-induced diabetic (STZ) rats. The levels of Gi alpha-2 as determined by immunoblotting techniques using AS/7 antibody were significantly decreased by about 60% in STZ as compared to control rats, whereas the levels of Gs alpha were not altered. In addition, the stimulatory effect of cholera toxin (CT) on GTP-sensitive adenylyl cyclase was not different in STZ as compared to control rats. On the other hand, the stimulatory effects of GTPgammaS, isoproterenol, glucagon, forskolin (FSK) and sodium fluoride on adenylyl cyclase were enhanced in STZ-rats. Furthermore, GTPgammaS inhibited FSK-stimulated adenylyl cyclase activity in a concentration-dependent manner (receptor independent functions of Gi) in control rats which was almost completely abolished in STZ rats. In addition, receptor-mediated inhibition of adenylyl cyclase by angiotensin II (AII), oxotremorine and atrial natriuretic peptide (ANP) was attenuated in STZ rats. These results suggest that the decreased expression of Gi alpha, but not of Gs alpha, may be responsible for the observed altered responsiveness of adenylyl cyclase to hormonal stimulation and inhibition in STZ-rats. It may thus be suggested that the decreased Gi activity may be one of the possible mechanisms responsible for the impaired vascular functions in diabetes.
PMID: 11900377 [PubMed - indexed for MEDLINE]
Full report available at http://www.fluoride-journal.com/01-34-1/341-34.pdfFluoride 2001; 34(1):34-42
Histopathology of fluoride-induced hepatoxicity in rabbits
A Shashi * and SP Thapar **
* For Correspondence: Dr Aggarwal, Shashi, Department of Zoology, Punjabi University, Patiala - 147 002, Punjab, India. E-mail: shashi@pbi.ernet.in;
** Department of Anatomy, Dayanand Medical College and Hospital, Ludhiana, India.SUMMARY: The effect of chronic and acute exposure to sodium fluoride (5, 10, 20, and 50 mg/kg body weight/day) for fifteen weeks on hepatic damage in young albino rabbits was evaluated. Histopathological examination revealed increasing degrees of hepatocellular necrosis, degenerative changes, hepatic hyperplasia, extensive vacuolization in hepatocytes, and centrilobular necrosis in the liver of the exposed animals. The central vein and sinusoids of the liver were dilated and engorged with blood and were associated with small areas of haemorrhages. These effects were not observed in the control group.
Full report available at http://www.fluoride-journal.com/01-34-1/341-43.pdfFluoride 2001; 34(1):43-50
Histopathology of myocardial damage in experimental fluorosis in rabbits
A Shashi * and SP Thapar **
* For Correspondence: Dr Aggarwal, Shashi, Department of Zoology, Punjabi University, Patiala - 147 002, Punjab, India. E-mail: shashi@pbi.ernet.in;
** Department of Anatomy, Dayanand Medical College and Hospital, Ludhiana, India.SUMMARY: Young albino rabbits were administered 5, 10, 20, and 50 mg of sodium fluoride/kg body weight/day subcutaneously for 3.5 months. The control animals were given 1 mL of double distilled water/kg body weight/day. In the fluoridated rabbits, the myocardium showed cloudy swellings, sarcoplasmic vacuolization, and small hemorrhages followed by fibrous necrosis. The degenerative changes were most pronounced in animals treated with 50 mg of sodium fluoride/kg body weight/day. The myocardium exhibited fibrous necrosis, dissolution of nuclei, fibrillolysis, extensive vacuole formation and interstitial cells in the connective tissue. The degree of myocardial damage seemed to be directly proportional to the dosage of fluoride administered. In the control animals, the myocardium showed normal structure without any of the changes mentioned above.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11797379&dopt=AbstractRinsho Byori 2001 Nov;Suppl 116:45-51
[Pseudocholinesterase (ChE)]
[Article in Japanese]
Yanai M, Hoshino T.
Department of Clinical Pathology, Nihon University School of Medicine.
In order to establish a recommendation for the measurement of serum pseudocholinesterase (ChE), the Japan Society of Clinical Chemistry has been deribesating for several years. However, they have not yet reached a conclusion. A decrease in serum ChE is clinically meaningful and serum ChE sensitively reflects a degree of chronic diffuse liver damage. ChE isozyme is analyzed not for the estimation of origin of the enzyme, but for the evaluation of familial ChE variants. Electrophoresis or blocking by dibucaine or fluoride are employed for the detection of ChE isozyme. Familial ChE variants are related to succinylcholine apnea in cases of very low serum ChE activities.
Publication Types:
- Review
- Review, Tutorial
PMID: 11797379 [PubMed - indexed for MEDLINE]