Abstract
The aim of this work was to evaluate the effect of fluoride (F) on oxygen consumption (VO2) in rats and how it might affect the respiratory chain and the levels of reactive oxygen species (ROS). Eighteen Sprague-Dawley rats were divided into three groups: Control, NaF20, and NaF40, which received 0, 20, and 40 ?mol F/100 g bw/day for 30 days, respectively. In vivo, VO2 decreased 90 min after treatment with F, whereas TBARS, CAT, and GPx were higher. In vitro, F decreased VO2 in liver and in mitochondria. These results support the hypothesis that the bone inflammatory foci observed in treatments with NaF could involve an inhibition of the respiratory chain that would cause increase in reactive oxygen species (ROS).
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Environmental Fluoride 1977 by Rose & Marier
The Associate Committee on Scientific Criteria for Environmental Quality was established by the National Research Council of Canada in response to a mandate provided by the Federal Government to develop scientific guidelines for defining the quality of the environment. The concern of the NRC Associate Committee is strictly with scientific
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Fluoride in Drinking Water: A Scientific Review of EPA’s Standards.
Excerpts: Summary Under the Safe Drinking Water Act, the U.S. Environmental Protection Agency (EPA) is required to establish exposure standards for contaminants in public drinking-water systems that might cause any adverse effects on human health. These standards include the maximum contaminant level goal (MCLG), the maximum contaminant level (MCL), and the secondary
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Effects of melatonin and epiphyseal proteins on fluoride-induced adverse changes in antioxidant status of heart, liver, and kidney of rats
Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart,
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The effect of antioxidative vitamins A and E and coenzyme Q on the morphological picture of the lungs and pancreata of rats intoxicated with sodium fluoride
Fluorides, when taken in amounts exceeding the standard therapeutic dosage, are regarded as toxic substances. Recent studies show that fluorides may affect the oxidoreductive processes of cells. The aim of the following study is to investigate the effect of antioxidative vitamins A and E and coenzyme Q on the morphological
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Effect of long term fluoride exposure on lipid composition in rat liver
Chronic fluorosis can severely damage many systems of human body, but its pathogenesis is unclear. Normal composition and structure of cellular membrane lipids are a basic factor to maintain cell function. In this investigation, cellular membrane lipids of the liver were analysed after a long term fluoride treatment for rats
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Fluoride Enhances Toxicity of Beryllium
Occupational exposure to beryllium is well-documented to put workers' health at risk. The two principal targets of beryllium poisoning are the respiratory system and the skin. Of all beryllium compounds, beryllium fluoride complexes (including beryllium fluoride and beryllium oxyfluoride) appear to be the most toxic. As shown below, studies dating back
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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Respiratory Risks from Occupational Fluoride Exposure
Starting in the 1930s, scientists have observed that workers exposed to airborne fluorides suffer from an elevated rate of respiratory disorders. For over 50 years, however, US government and industry scientists made repeated assurances that the allowable level of fluoride dusts and gases in industrial workplaces would not cause any
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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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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