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Note: The following is a limited selection of abstracts from 1994
Due to length, we present this as a separate section
• Click here to return to the 4-part Kidney
for fluorine & organofluorine pesticides.
When time allows more information will be added.
Wei Sheng Yan
Jiu. 2005 May;34(3):287-8.
[The dose-effect relationship of water fluoride levels and
renal damage in children]
JL, Xia T, Yu YY, Sun XZ, Zhu Q, He W, Zhang M, Wang A.
Medical College, Huazhong University of Science and Technology,
Wuhan 430030, China.
explore the dose-effect relationship of water fluoride levels and
renal damage in children and observe the difference of renal function
between high-loaded fluoride people and dental fluorosis people
in the same water fluoride level region.
METHODS: 210 children were divided into seven groups in term of
drinking water fluoride levels and whether they suffered from dental
fluorosis. Fluoride concentrations in urine and serum and activities
of urine NAG and gamma-GT were determined.
RESULTS: The urine and serum fluoride of high-loaded fluoride people
and dental fluorosis people increased compared with control, moreover
fluoride contents in urine and serum increased gradually with the
increase of fluoride level in drinking water. Urine NAG and gamma-GT
activities significantly increased in dental fluorosis people from
area of 2.58 mg/L fluoride in drinking water and in those two groups
from area of 4.51 mg/L fluoride in drinking water. Moreover, there
existed an obvious dose-effect relationship between the drinking
water fluoride concentration and NAG and gamma-GT activity.
CONCLUSION: Over 2.0 mg/L fluoride in drinking
water can cause renal damage in children, and the damage degree
increases with the dinking water fluoride content. Renal damage
degree is not related to whether the children suffered from dental
fluorosis and mainly due to water fluoride concentration.
[PubMed - in process]
Toxicol Lett. 2005 Jul 22; [Epub ahead
Proteomic analysis of kidney in fluoride-treated
Xu H, Hu LS, Chang M, Jing L, Zhang XY, Li
Institute of Endemic Disease, Jilin University, Changchun 130021,
The recent development of proteomic techniques has enabled investigators
to directly examine the population of proteins present in biological
systems. We first report here the proteomic changes of renal protein
induced by fluoride. To investigate molecular mechanisms of renal
injury induced by fluoride, proteins were isolated from rat kidney
and profiled by two-dimensional gel electrophoresis (2DE). With
the analysis of Image-Master 2D Elite software, 141 up-regulated
and eight down-regulated protein spots in 2DE gels of fluoride-treated
group were gained by comparison to the control group, 13 of which
were identified by matrix-assisted laser desorption ionization-time
of flight mass spectrometry (MALDI-TOF MS). The
identified proteins are mainly related with cell proliferation,
metabolism and oxidative stress, and provide a valuable clue to
explore the mechanism of renal fluorosis. This study also
shows that the proteomic techniques were powerful in fluoride toxical
PMID: 16043314 [PubMed - as supplied by publisher]
Research, 1998 Feb 16;784(1-2):284-98.
administration of aluminum-fluoride and sodium-fluoride to rats
in drinking water: alterations in neuronal and cerebrovascular integrity.
JA, Jensen KF, Horvath W, Isaacson RL.
Psychology Department, Binghamton University,
Binghamton, NY, USA..
This low-dose (1 ppm
fluoride in deionized distilled drinking water) and long-term (52
weeks) rat study reported histological evidence of glomerular
distortions and other signs of kidney disorders in animals
in both the AlF3 and NaF groups. The Al levels in samples of brain
and kidney were higher in both the AlF3 and NaF groups relative
Inorg Biochem 2003 Jan 15;93(3-4):243-6.
inhibition of rat liver and kidney arginase with fluoride
Department of Chemistry, Central Michigan University, Mount Pleasant,
MI 48858, USA. firstname.lastname@example.org
Fluoride is an uncompetitive inhibitor of rat liver arginase.
This study has shown that fluoride caused substrate inhibition of
rat liver arginase at substrate concentrations above 4 mM.
Rat kidney arginase was more sensitive to inhibition by fluoride
than liver arginase. For both liver and kidney arginase preincubation
with fluoride had no effect on the inhibition. When assayed with
various concentrations of L-arginine, rat kidney arginase did not
have Michaelis-Menten kinetics. Lineweaver-Burk and Eadie-Hofstee
plots were nonlinear. Kidney arginase showed strong substrate activation
at concentrations of L-arginine above 4 mM. Within narrow concentrations
of L-arginine, the inhibition of kidney arginase by fluoride was
uncompetitive. Fluoride caused substrate inhibition of kidney arginase
at L-arginine concentrations above 1 mM. The
presence of fluoride prevented the substrate activation of rat kidney
PMID: 12576287 [PubMed - indexed
effects of fluoride on rabbit kidney
JP Singh, SP Thapar.
Abstract: Summary: The
purpose of this study was to assess renal damage in experimental
fluorosis. Young albino rabbits were injected with 5, 10, 20, and
50 mg NaF/kg body weight/day for fifteen
weeks and then sacrificed. No significant clinical signs of toxicity
were found in animals exposed to the lowest dose. At the higher
doses, however, the cytoachitecture of the kidneys exhibited increasing
amounts of cloudy swellings, degeneration
of tubular epithelia, tissue necrosis, extensive vacuolization in
renal tubules, hypertrophy and atrophy of glomeruli, exudation,
interstitial oedema, and interstitial nephritis. These changes
in the kidneys result in impaired renal function in chronic fluoride
J Anaesthesiol 2002 May;19(5):341-9.
ion toxicity in rabbit kidney thick
ascending limb cells
Cittanova ML, Estepa L, Bourbouze R, Blanc
O, Verpont MC, Wahbe E, Coriat P, Daudon M, Ronco PM.
Departement d'Anesthesie-Reanimation, Hjpital Pitie-Salpetriere,
Paris, France. email@example.com
BACKGROUND AND OBJECTIVE: Some halogenated agents, especially methoxyflurane,
because of a higher level of fluoride production, induce a renal
concentrating defect that could be related to an ascending limb
impairment. We investigated the mechanisms of fluoride toxicity
on an immortalized cell line.
METHODS: Cells were cultured for 2, 6 or 24 h in the presence of
fluoride. Toxicity evaluation was based on: cell numbers, protein
content, leucine-incorporation, lactate dehydrogenase (LDH) and
N-acetyl-beta-glucosaminidase (NAG) releases, Na-K-ATPase and Na-K-2Cl
activities, electron microscope studies. Infrared analysis and fluoride
microdetermination allowed crystal components.
RESULTS: At 5 mmol after 24 h, fluoride decreased cell numbers (-14%,
*P < 0.05), protein content (-16%*), leucine incorporation (-54%*),
Na-K-2Cl activity (-84%*), increased LDH (+145%*) and NAG release
(+190%*). Na-K-ATPase was more sensitive and impaired from 1 mmol
for 24h and after 2 h at 5 mmol. Crystal formation in mitochondria
occurred after 6 h at 5 mmol. Infra-red analysis and fluoride microdetermination
established that crystals contained sodium, phosphate and fluoride.
CONCLUSIONS: The results suggest that the
Na-K-ATPase pump is a major target for fluoride toxicity in Henle's
Zealand MAF Biosecurity Authority, Ministry of Agriculture and Forestry
Impact of a Volcanic Eruption on Agriculture and Forestry
in New Zealand (2001)
... Experimental trials
involving NaF intoxication showed that the principal signs of acute
fluorosis were depression, salivation, hyperpnoea, nasal secretions,
inappetance, blindness, ataxia, coma
and death(6). The rumen, reticulum and abomasum showed epithelial
necrosis and hyperaemia, oedema and haemorrhage in the lamina propria
and submucosa. The kidneys showed necrosis
of epithelial cells in the proximal convoluted tubules.
renal damage dose response in rats to intravenous infustion of sodium
Tomotaro Dote, Koichi Kono, Kan Usuda, Hiroyuki Nishiura, Teruaki
Abstract: SUMMARY: Rapid
acute renal injury in Wistar rats from fluoride
(F) following single-dose NaF
infusions of 0 mg F (control), 1 mg F (Group 1), 2 mg F (Group 2),
and 3 mg F (Group 1) was assessed by examining three collections
of bladder urine at 2-h intervals for six hours after the infusions.
The urinary parameters investigated were: urine volume, excretion
of F, creatinine, and -glutathione
S-transferase (-GST), and the activity of N-acetyl- -D-glucosa-midase
(NAG). Compared with the control, the urine volume increased (polyuria)
in Group 1 but decreased in groups 2 and 3. F
excretion increased in groups 1 and 2 but was lower in Group 3 than
in Group 1. In Group 3, creatinine excretion decreased compared
with the control, but the activities of -GST and NAG steadily increased
in Group 3. The decreases in F and
creatinine excretion in Group 3 are attributable to glomerular dysfunction,
and the increases in -GST and NAG activities in Group 3 indicate
acute proximal renal tube injury. The kidney
toxicity of intravenous administration of NaF to laboratory rats
was thus dose related, and an infusion of 3 mg F was sufficient
to cause acute renal dysfunction.