Abstract
Male Wistar rats were fed a fluoride deficient diet (less than 0.5 parts/10(6) F), and either distilled water or fluoridated water (1.0 parts/10(6)). By week 3, the control group had urinary excretions of 106 +/- 5 nmol cAMP/day (mean +/- SEM) whereas the experimental group excreted 129 +/- 6 nmol cAMP/day. After 111 days, the control group excreted 270 +/- 26 nmol cAMP/day compared to 600 +/- 78 nmol cAMP/day for the experimental group. Body weight, food and water consumption, urine volume, and urinary creatinine and phosphate levels were not significantly different between the two groups. Tissue cAMP levels were determined after 4, 6 and 16 weeks. By week 4, the rats receiving the fluoridated water had significantly higher levels of cAMP in the liver (113 per cent) tibia (130 per cent), femur (89 per cent) and heart (35 per cent). At week 6, the liver (119 per cent), tibia (296 per cent), heart (168 per cent), kidney (73 per cent) and submandibular gland (27 per cent) had significantly higher levels of cAMP. By week 16, the liver, femur, kidney and submandibular gland continued to have elevated levels of cAMP. Liver glycolytic metabolites were determined after 6 weeks, and the results suggested a decrease in pyruvate kinase activity.
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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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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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Evaluation of serum lipoprotein and tissue antioxidant levels in sheep with fluorosis
The aim of this study was to evaluate serum lipoprotein and tissue antioxidant levels of sheep with and without fluorosis living in a volcanic area of Turkey. Fifteen Akkaraman sheep with fluorosis in the A?ri region north of Lake Van and 10 Akkaraman sheep without fluorosis in the Van region
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New data for the validation of the mean daily maximum permissible concentration of hydrogen fluoride in atmospheric air
1. Round-the-clock exposure to hydrogen fluoride concentrations of 0.10 and 0.03 mg/m3 causes inhibition in the central nervous system, decreases the activity of a number of enzymes, impairs the phosphorus-calcium metabolism, and causes the accumulation of fluorine in the body and damage to the internal organs and bone tissue. 2. A
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Effect of fluoride on enzymes from serum, liver, kidney, skeletal and heart muscles of mice.
White mice maintained on water containing 100 ppm NaF showed changes in the enzyme level in serum, liver, kidney, heart and skeletal muscles. Enzymes studies were alkaline phosphatase (ALP), acid phosphatase (AcP), glutamate-oxalacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH) and cholinesterase (CE). AcP was markedly
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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, Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et
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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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Fluoride & Electrocardiogram Abnormalities
An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems
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Fluoride & Myocardial Damage
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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