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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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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Effects of fluoride exposure on mitochondrial function: Energy metabolism, dynamics, biogenesis and mitophagy.
Fluoride is ubiquitous in the environment. Furthermore, drinking water represents the main source of exposure to fluoride for humans. Interestingly, low fluoride concentrations have beneficial effects on bone and teeth development; however, chronic fluoride exposure has harmful effects on human health. Besides, preclinical studies associate fluoride toxicity with oxidative stress,
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Evaluation of multi-endpoint assay to detect genotoxicity and oxidative stress in mice exposed to sodium fluoride
Fluoride compounds are naturally present in soil, water and food. The objective of this study was to investigate the genotoxic and oxidative damage induced by chronic fluoride exposure on mammalian cells in vivo. For this purpose, the genotoxic potential was investigated in bone marrow cells by the micronucleus test, chromosome
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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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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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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 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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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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