Abstract
A study was made of the effect of fluoride on oxidative stress in rats during their early stages in life. Wistar albino rats were exposed to 30 ppm and 100 ppm fluoride (from sodium fluoride) in drinking water during the last one week of intrauterine life and then up to ten weeks after birth. Oxidative stress was evaluated by the assays of malondialdehyde and antioxidants in brain homogenates. Malondialdehyde (MDA), the marker of extent of lipid peroxidation, was elevated in the brain of rats treated with 100 ppm fluoride but was without change in rats treated with 30 ppm fluoride. Levels of total glutathione, reduced glutathione (GSH), and ascorbic acid (vitamin C) were elevated in 30 ppm fluoride-treated rats, while these levels decreased in 100 ppm fluoride-treated rats. The activity of glutathione peroxidase (GSH-Px) was elevated significantly in both 30 ppm and 100 ppm fluoride-treated rats. Glutathione S-transferase (GST) activitiy in the brain increased with 30 ppm and 100 ppm fluoride, and greater elevation occurred at 30 ppm. These results suggest that fluoride enhances oxidative stress in the brain, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of fluoride toxicity in the brain.
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Fluoride exposure during pregnancy and lactation triggers oxidative stress and molecular changes in hippocampus of offspring rats.
Highlights Fluoride exposure indirectly increased the levels of F in the offspring's plasma. Fluorine exposure promoted biochemical imbalance in the offspring's hippocampus. The 10 mgF/L and 50 mgF/L groups showed an overexpression of the neurotrophin BDNF. In exposed groups modulation of the proteomic profile of the offspring. Proteins associated
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Effects of sodium fluoride on lipid peroxidation and PARP, XBP-1 expression in PC12 cell
This study aims to clarify the molecular mechanism of fluorine exposure that leads to nerve injury. PC12 cells were treated with fluorine at different concentrations (0.5, 1.0, 1.5, and 2.0 mM). Cytoactivity was detected at different time points (2, 4, 6, 8, 12, 24, and 48 h). After 2 h, DCF was used
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Neurobehavioral and neurochemical effects in rats offspring co-exposed to arsenic and fluoride during development.
Highlights Arsenic/Fluoride co-exposure during development causes neurobehavioral alterations in offspring. iAs/F causes delayed development of sensorimotor reflexes and produces less nociceptive response. iAs/F co-exposure increase locomotor activity. Antioxidant enzymes and neurotransmitter level are altered in the striatum area. Arsenic (iAs) and fluoride (F) are ubiquitous in the environment. All over
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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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Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity in rats
Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity were studied in rats. A total of 28 Wistar albino male rats were used. Four study groups were randomly formed with seven animals in each. The groups were treated for 21 days with distilled water (control group), with
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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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Fluoride Affects Learning & Memory in Animals
An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out
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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 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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