Abstract
To explore the mechanisms by which chronic fluorosis damages the brain, we determined the levels of the advanced glycation end-products (AGEs), the receptor for AGE (RAGE), NADPH oxidase-2 (NOX2), reactive oxygen species (ROS) and malondialdehyde (MDA) in the brains of rats /and or SH-SY5Y cells exposed to different levels of sodium fluoride (5 or 50ppm in the drinking water for 3 or 6 months and in the incubation medium for as long as 48hr, respectively). The levels of AGEs, RAGE and NOX2 protein and mRNA were measured by an Elisa assay, Western blotting and real-time PCR, respectively. The ROS content was assessed by fluorescein staining and MDA by thiobarbituric acid-reactive substance assay. In comparison to the unexposed controls, the protein and mRNA levels of AGEs, RAGE and NOX2 in the brains of rats after 6 months of exposure and in SH-SY5Y cells following high-dose exposure to fluoride were elevated. In contrast, no significant changes in these parameters were detected in the rats exposed for 3 months. In addition, the levels of ROS and MDA in the SH-SY5Y cells exposed to high-dose of fluoride were elevated in a manner that correlated positively with the levels of AGE/RAGE. In conclusion, our present results indicate that excessive fluoride can activate the AGE/RAGE pathway, which might in turn enhance oxidative stress.
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Sirt3-mediated mitochondrial dysfunction is involved in fluoride-induced cognitive deficits.
Highlights Fluoride induces cognitive deficits in mice. Fluoride exposure results in neural/synaptic injury in the hippocampus of mice. Mitochondrial dysfunction contributes to neural/synaptic alternations. Inhibition of Sirt3 is involved in the fluoride-evoked mitochondrial abnormalities. Abstract Excessive fluoride is capable of inducing cognitive deficits, but the mechanisms remain elusive. This study aimed
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AMPK/p38/Nrf2 activation as a protective feedback to restrain oxidative stress and inflammation in microglia stimulated with sodium fluoride.
Highlights NaF-stimulated redox imbalance and inflammation. NaF activated the Nrf2 signaling in BV-2 cells and primary cultured microglia. Nrf2 activation exerts a neuroprotective effect on NaF-stimulated redox imbalance and inflammation. ROS-AMPK-p38 signaling is the upstream signaling pathway involved in NaF-induced Nrf2 activation. Dysregulated activation of inflammation plays an important role in the
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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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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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Fluoride Induces Neuroinflammation and Alters Wnt Signaling Pathway in BV2 Microglial Cells.
Fluoride is a common element in nature and our daily life, and excessive intake of this element can cause fluorosis and irreversible brain damage. The toxic effects of fluoride on the central nervous system may be attributed to the release of inflammatory cytokines and ROS. GSK3B is a key protein
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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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Fluoride content in tea and its relationship with tea quality.
J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
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