Abstract
Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH-SY5Y cells were treated with high doses of NaF for 24?hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF-induced toxicity in SH-SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH-SY5Y cells. In addition, NaF exposure increased the protein expression of p-ERK1/2 and decreased the protein expressions of Nrf2 and HO-1, as well as facilitated increasing ROS, 4-hydroxynonenal (4-HNE), and 8-Hydroxy-2′-deoxyguanosine (8-OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.
*Original abstract online at https://onlinelibrary.wiley.com/doi/abs/10.1002/tox.22928
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The Effect of Chronic Fluorosis on Calcium Ions and CaMKIIa, and c-fos Expression in the Rat Hippocampus.
This study investigated neurotoxicity of chronic fluorosis in the rat hippocampus. Newly weaning, male, Sprague-Dawley (SD) rats were administered 15, 30, and 60 mg/L sodium fluoride (NaF) solution (fluorine ion concentration 8.25, 16.50, and 33.00 mg/L, respectively), and tap water, for 18 months. The neurotoxicological mechanism was examined with a focus on intracellular
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Rutin attenuates neurobehavioral deficits, oxidative stress, neuro-inflammation and apoptosis in fluoride treated rats.
Highlights The influence of rutin on fluoride – induced neurotoxicity in rat was studied. Rutin reversed the fluoride – induced neurobehavioral deficits in rats. Rutin reversed the fluoride – induced inhibition of acetylcholinesterase activity in rat cerebrum and striatum. Rutin enhanced antioxidant status and inhibited neuro-inflammation and apoptosis in fluoride
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Toxin-induced blood vessel inclusions caused by the chronic administration of Aluminum and Sodium fluoride and their implications for dementia
Until our knowledge of the etiology of Alzheimer's dementia, as well as related conditions involving mental impairments, is greatly extended, no line of investigation should be ignored. We believed that the possible contributions of aluminum exposure to neural impairments deserved further study. In coming to this opinion we were mindful
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Relationship between intracellular Ca²+ and ROS during fluoride-induced injury in SH-SY5Y cells.
The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca²? concentration ([Ca²?]i ) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH-SY5Y) cells were incubated with sodium fluoride (NaF, 20, 40, 80 mg/L) for 24 h, with 40
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Effect of fluoride exposure on anxiety- and depression-like behavior in mouse.
Highlights Anxiety-like behavior was significantly altered in the mice exposed to NaF for 120 days. Depression-like behavior was significantly altered in the 120 days NaF treated mice. NaF significantly altered mRNA expression levels of anxiety- and depression-like related genes in the hippocampus. Fluoride led to an imbalance between excitation and
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