Fluoride Action Network


Excessive fluoride mainly causes skeletal lesions. Recently, it has been reported that an appropriate level of calcium can alleviate fluorosis. However, the appropriate concentration and mechanism of calcium addition is unclear. Hence, we evaluated the histopathology and ultrastructure, DNA fragmentation, hormonal imbalances, biomechanical levels and the expression of apoptosis-related genes, after treating the rats with 150 mg/L NaF and different concentrations of CaCO3. Our results suggested that NaF induced the histopathological and ultrastructural injury, with a concomitant increase in the DNA fragmentation (P<0.05), and serum OC (17.4899±0.8907 pmoL/L) at 120 d. In addition, the qRT-PCR and western blotting results indicated that NaF exposure up-regulated the mRNA and protein expression of Bax, Calpain, Caspase 12, Caspase 9, Caspase 7, Caspase 3, CAD, PARP and AIF while down-regulated the Bcl-2 (P<0.01), decreased the bone ultimate load by 27.15 %, the ultimate stress by 10.07 %, and the ultimate deformity by 23.27 % at 120 d. However, 1 % CaCO3 supplementation decreased the serum OC (14.6559±0.6478 pmoL/L), bone F content (P<0.01), fracture and breakage of collagen fibers, and changed the expression of endoplasmic reticulum pathway related genes and proteins at 120 d. Further 1 % CaCO3 supplementation increased the bone ultimate load by 20.86 %, the ultimate stress by 4.89 %, and the ultimate deformity by 21.57 %. In summary, we conclude that 1 % CaCO3 supplementation alleviated fluoride-induced bone damage by inhibiting endoplasmic reticulum stress and mitochondrial dysfunction.