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This study is aimed at evaluating the neurotoxic effects of chronic exposure of sodium fluoride (NaF) in developmental stages in rat using prenatal models. NaF (100 ppm, orally) dosing via drinking water was given to pregnant rats in disease group. In the treatment groups, Metformin & Dehydrozingerone (DHZ) (200 mg/kg) were administered orally along with NaF, and the dosing was continued throughout the gestation and lactation periods to the pups until the end of experiment.

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Excessive fluoride exposure can lead to health problems, such as fluorosis and neurotoxicity. However, effective therapeutic strategies for neurofluorosis remain elusive due to a limited understanding of the underlying molecular mechanisms. This study aimed to investigate the effects of Tanshinone IIA on spinal cord injury induced by high-fluoride exposure.

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Background: Exposure to high levels of fluoride leads to brain developmental and functional damage. Motor performance deficits, learning and memory dysfunctions are related to fluoride neurotoxicity in human and rodent studies.

Materials And Methods: Here, we evaluated the effects of Quercetin treatment (25 mg/kg) against sodium fluoride-induced neurotoxicity (NaF, 200 ppm) in the medial prefrontal cortex (mPFC) of male adult rats based on oxidative markers, behavioral performances, mRNA expressions, and stereological parameters.

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Fluoride Product Inhibition: New Insight into the Degradation of Nerve Agents by Zr-MOFs.

ACS Appl Mater Interfaces

December 2024

State Key Laboratory of NBC Protection for Civilian, Beijing 102205, China.

Zirconium-based metal-organic frameworks (Zr-MOFs) have shown remarkable efficacy in catalytically degrading neurotoxic agents in recent years. However, the catalytic activity of Zr-MOFs can be inhibited due to the binding of phosphate degradation products to the Zr nodes. Here, we reported the inhibition effect of a nonphosphate substance, fluoride, which can deactivate Zr-MOF nodes for the degradation of GD and VX and simulate DEPPT.

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Excessive fluoride exposure beyond the tolerable limit may adversely impacts brain functionality. Betaine (BET), a trimethyl glycine, possesses antioxidant, anti-inflammatory and anti-apoptotic functions, although the underlying mechanisms of the role of BET on fluoride-induced neurotoxicity remain unelucidated. To assess the mechanism involved in the neuro-restorative role of BET on behavioural, neurochemical, and histological changes, we employed a rat model of sodium fluoride (NaF) exposure.

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