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Fluoride ion toxicity in rabbit kidney thick ascending limb cells
M L Cittanova1, L Estepa, R Bourbouze
1Département d'Anesthésie-Réanimation, Hĵpital Pitié-Salpêtrière, Paris, France. marie-laure.cittanova@psl.ap-hop-paris.fr
European Journal of Anaesthesiology
|July 4, 2002
Summary
Fluoride toxicity impairs kidney function by damaging the Na-K-ATPase pump in Henle
Area of Science:
- Nephrology
- Cell Biology
- Toxicology
Background:
- Methoxyflurane and other halogenated agents can cause kidney concentrating defects.
- This defect is linked to increased fluoride production and potential damage to the renal ascending limb.
Purpose of the Study:
- To investigate the cellular mechanisms of fluoride toxicity.
- To determine the impact of fluoride on kidney cells, specifically focusing on the ascending limb.
Main Methods:
- Immortalized kidney cell lines were exposed to varying concentrations of fluoride for different durations.
- Toxicity was assessed through cell counts, protein content, metabolic activity assays (leucine incorporation), and enzyme release (LDH, NAG).
- Key ion transport activities (Na-K-ATPase, Na-K-2Cl) and mitochondrial crystal formation were analyzed.
Main Results:
- Fluoride exposure significantly reduced cell viability, protein content, and leucine incorporation.
- Key ion transporters, particularly Na-K-ATPase, were highly sensitive to fluoride, showing impairment at low concentrations and short exposure times.
- Crystal formation within mitochondria was observed, composed of sodium, phosphate, and fluoride.
Conclusions:
- The Na-K-ATPase pump is identified as a primary target of fluoride toxicity in the kidney.
- These findings provide cellular evidence for the mechanism behind fluoride-induced renal concentrating defects.