Abstract
To investigate the effects of fluoride on DNA damage as well as the effects of selenium and zinc against fluoride respectively or jointly in pallium neural cells of rats, single cell gel electrophoresis was used to detect the DNA damage of neural cells prepared in vitro. The results showed that the degree of DNA damage in the fluoride group and the selenium group were significantly greater than that in control group(P < 0.01). The damage in the fluoride group was even more serious. The damage in the fluoride + selenium group and fluoride + zinc group was slighter than that in the fluoride group but with no significant difference. The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group(P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively. Moreover, the joint antagonistic effect of selenium and zinc against fluoride was more obvious.
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[Study of the mechanism of neurone apoptosis in rats from the chronic fluorosis].
Objective: Study the mechanism of action chronic fluorosis in neurones. Methods: Terminal deoxyribo-nucleotide transferase-mediated dUTP-biotin nick end labeling (TUNEL) and flow cytometry (FCM) were used to observe changes of apoptosis in cerebral cells in chronic fluorosis in rats. Results: TUNEL results show non-random expression of DAB positive stain apoptosis cells which appear
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Genotoxicity of fluoride subacute exposure in rats and selenium intervention.
Highlights Subacute exposure of Wistar rats to fluoride and selenium. Fluoride at a dose of 150 ppm induced DNA damage in the liver, spleen and brain tissue cells, not in blood. Selenium supplementation reduces DNA damage in liver and spleen cells. Fluoride damage did not occur on a histological
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[Studies on DNA damage and apoptosis in rat brain induced by fluoride].
OBJECTIVE: To explore the DNA damage effects and apoptosis in brain cells of rats induced by sodium fluoride. METHODS: SD rats were divided into two groups, i.e. control group and fluoride treated group, which were injected intraperitoneally with distilled water and sodium fluoride (20 mg.kg(-1).d(-1)) respectively. On the hand, 5
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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-induced neuronal oxidative stress amelioration by antioxidants in developing rats
Premated 3-month-old albino rats received 200-ppm fluoride ion (F) in their drinking water; the pups born to them were separately administered, in groups of six, daily doses of clinoptilolite, zinc, selenium, vitamin C, vitamin D, and propolis. On post-partum day 45, the pups were sacrificed, brain regions separated, and oxidative
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Fluoride Affects Learning & Memory in Animals
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Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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Fluoride Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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