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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Acetylcholinesterase activity in fluorosis adversely affects mental well-being: an experimental study in rural Rajasthan
Fluoride toxicity is a burgeoning problem worldwide and also in Rajasthan in India. In the state of Rajasthan, almost all districts have high fluoride (up to 18.0 ppm) in their drinking/ground water sources and about 11 million of the population [is] at risk. Several clinical and experimental studies have reported
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Influence of chronic fluorosis on membrane lipids in rat brain
Brain membrane lipid in rats were analyzed after being fed either 30 or 100 ppm fluoride for 3, 5, and 7 months. The protein content of brain with fluorosis decreased, whereas the DNA content remained stable during the entire period of investigation. After 7 months of fluoride treatment, the total
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ERK1/2-mediated disruption of BDNF–TrkB signaling causes synaptic impairment contributing to fluoride–induced developmental neurotoxicity
Highlights Rats were long–term chronic exposed to environmentally relevant doses of fluoride. Fluoride exposure results in synaptic alterations both in vivo and in vitro. Fluoride–induced cognitive failures correlates with synaptic deficits. BDNF–TrkB axis disruption contributes to fluoride–elicited impaired synaptogenesis. ERK1/2 plays a vital role in fluoride–induced BDNF–TrkB signaling disruption. Excessive
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Conceivable amelioration of NaF-induced toxicity in liver, kidney and brain of chicken by black tea extract: an in vitro study.
Sodium fluoride (NaF) toxicity on enzymatic and non-enzymatic oxidative stress markers of chicken liver, kidney and brain homogenate in in vitro condition where studied in present investigation. We studied alteration in the activity of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO) and glutathione (GSH) content to study oxidative stress.
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Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain.
We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes
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Fluoride: Developmental Neurotoxicity.
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Fluoride & IQ: 76 Studies
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