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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Decreased learning ability and low hippocampus glutamate in offspring rats exposed to fluoride and lead.
Fluoride (F) and lead (Pb) are two common environmental pollutants which are linked to the lowered intelligence, especially for children. Glutamate, a major excitatory neurotransmitter in the central nervous system, plays an important role in the process of learning and memory. However, the impact of F and Pb alone or
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Fluoride exposure regulates the elongation phase of protein synthesis in cultured Bergmann glia cells
Fluoride is an environmental pollutant present in dental products, food, pesticides and water. The latter, is the greatest source of exposure to this contaminant. Structural and functional damages to the central nervous system are present in exposed population. An established consequence of the neuronal is the release of a substantial
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Effects of fluoride on synapse morphology and myelin damage in mouse hippocampus
Highlights Fluoride induced myelin damage in mouse hippocampus. Fluoride shortened the synaptic cleft and thickened the postsynaptic density. Fluoride altered the expressions of CREB, BDNF, and NCAM in hippocampus. To investigate the fluoride-induced neurotoxicity on mice hippocampus, healthy adult mice were exposed to 25, 50, and 100 mg NaF/L for 60 days.
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Histological effects of fluoride on cerebrum of adult albino rats.
The pilot study was conducted on 10 adult albino rats of either sex 150 - 200gm each. Two equal groups of control and experimental was made. The control group received food and water ad libitum whereas experimental group received 30 ppm of NaF for 8 weeks. The macroscopic features like
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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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