Abstract
Effects of exposure of Swiss albino adult male mice to 17.6 mg NaF/L in their drinking water for up to 30 days on the NADPH diaphorase (NADPH-d) positive neurons in the forebrain were studied. Histochemical study by the method developed by Hope and Vincent for the distribution of NADPH-d positive neuron cell bodies was conducted in the cerebral cortex, hippocampus, amygdala, caudate putamen, and selected nuclei of the hypothalamus. Counting neuronal cell bodies, their dendritic intersections, and varicosities in the brain of the F-exposed mice showed significant increase in the neuron cell bodies. In the cerebral cortex, amygdala, and caudate putamen, the increase in the number of NADPH-d positive neurons and their dendritic intersections was highly significant (p<0.05), but no significant difference was seen in the dendritic branching. A significant increase in the number of varicosities was also observed in the brain of the F-treated mice. These results indicate that excessive F intake caused morphological changes in NADPH-d/NOS (nitric oxide synthase) positive neurons in the brain, thus increasing nitric oxide (NO) synthesis, which is implicated in F-induced neuron cell death. A possible mechanism of F neurotoxicity is thereby suggested.
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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Neuroprotective effects of methyl-3-O-methyl gallate against sodium fluoride-induced oxidative stress in the brain of rats
Methyl-3-O-methyl gallate (M3OMG) is a rare natural product that showed promising in vitro antioxidant activities. In this study, the protective role of synthetic M3OMG against sodium fluoride (NaF)-induced oxidative stress in rat brain was evaluated. Animals were treated with either M3OMG (10 and 20 mg/kg i.p.), vitamin C (10 mg/kg
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Activation of the AGE/RAGE system in the brains of rats and in SH-SY5Y cells exposed to high level of fluoride might connect to oxidative stress
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
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Effect of sodium fluoride on neuroimmunological parameters, oxidative stress and antioxidative defenses
Aims: This study was designed to evaluate the effect of sodium fluoride (NaF) in inducing neuroimmunological, oxidative and antioxidative damage. Methods: Twenty-four male Wistar rats broadly grouped into four groups containing six rats in each were fed with drinking water containing 20 ppm, 60 ppm, 100 ppm and 0.8 ppm (control)
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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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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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