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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Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain
Fluoride induced oxidative stress through depletion in levels of various anti-oxidants such as glutathione, superoxide dismutase (SOD), fat soluble vitamins (D and E) with increased levels of lipid peroxidation (LPO) and fluoride aggravate the damage in rodents as well as in humans. Vitamins A, a fat soluble vitamin possess antioxidant
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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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[Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis].
OBJECTIVE: To study changes in content of lipid peroxide and composition of fatty acids in the brain of rats affiliated with chronic fluorosis after treatment with free radical inducer (ferric ion). METHODS: Thirty-six Wistar rats were divided into three groups, fed with similar fodder and varied concentrations of fluoride in drinking
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Ameliorative effects of oleanolic acid on fluoride induced metabolic and oxidative dysfunctions in rat brain: experimental and biochemical studies
Beneficial effects of oleanolic acid on fluoride-induced oxidative stress and certain metabolic dysfunctions were studied in four regions of rat brain. Male Wistar rats were treated with sodium fluoride at a dose of 20 mg/kg b.w./day (orally) for 30 days . Results indicate marked reduction in acidic, basic and neutral
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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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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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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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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
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