Abstract
Fincoal type fluorosis has only been reported from China, but its pathogenesis is unclear. Many people believe that fluorosis is associated with oxidative stress. Oxidative stress can be reduced at higher selenium (Se) level. Heat shock protein (HSP70) is the most conserved and induced against different stressors. The aim of this study is to detect the expression of HSP70 in fluorosis patients and explore the role of Se in fluorosis protection. The subjects were divided into four groups: “High Se + F group” (n = 50), “High F group” (n = 50), “High Se group” (n = 20) and “Control group” (n = 46). Expression of HSP70 was evaluated by Western blotting and real-time PCR techniques. The concentration of fluoride, content of Se in hair, activity of antioxidant enzymes (GSH-Px, SOD, CAT) and content of malondialdehyde (MDA) were determined. The relative amount of HSP70 gene transcription was significantly higher in “High Se + F group” than the other groups. The same results were found for expression of HSP70 protein to beta-actin ratio. There was a significant difference between “High Se + F group” and “High F group” regarding MDA content and glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activity. These results suggest that oxidative stress plays an important role in the pathogenesis of the Fincoal type fluorosis and it can be reduced at higher Se level.
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Protective role of gallic acid on sodium fluoride induced oxidative stress in rat brain
Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C
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Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants
The objective of the present communication is to address the issues concerning reversal of fluoride induced cell injury and disease (i.e. fluorosis) through the elimination of fluoride and consumption of a diet containing essential nutrients and antioxidants. Humans afflicted with fluorosis, as a result of consuming fluoride contaminated water or
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Selenium Exerts Protective Effects Against Fluoride-Induced Apoptosis and Oxidative Stress and Altered the Expression of Bcl-2/Caspase Family.
Fluoride is widely distributed in nature, and at high concentrations, it targets the kidney and especially proximal tubule epithelial cells. Selenium is a typical trace element beneficial to humans, and the role of selenium in the prevention and treatment of fluoride-induced organ damage is an important research topic. The purpose
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Role of fish oil against physiological disturbances in rats brain induced by sodium fluoride and/or gamma rays
The impacts of environmental and occupational exposure to ionizing radiation and to long-term intake of high levels of fluoride have caused health problems and increasingly alarming in recent years. Fish oil omega-3 (polyunsaturated fatty acids essential fatty acids) is found in the highest concentrations in fish oil, claim a plethora
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[The primary study of antagonism of selenium on fluoride-induced reproductive toxicity of male rat].
The protective effect of ascorbic acid at dose level of 1.0 mg/L in drinking water against the fluoride-induced damage on reproductive system of rat was studied. 150 mg/L sodium fluoride (NaF) in drinking water of male rat can cause the significant decrease of sperm count and mobility, the increase of
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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 & 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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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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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