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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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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Maize purple plant pigment protects against fluoride-induced oxidative damage of liver and kidney in rats
Anthocyanins are polyphenols and well known for their biological antioxidative benefits. Maize purple plant pigment (MPPP) extracted and separated from maize purple plant is rich in anthocyanins. In the present study, MPPP was used to alleviate the adverse effects generated by fluoride on liver and kidney in rats. The results
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Protective effects of blackberry and quercetin on sodium fluoride-induced oxidative stress and histological changes in the hepatic, renal, testis and brain tissue of male rat
BACKGROUND: Sodium fluoride (NaF) intoxication is associated with oxidative stress and altered antioxidant defense mechanism. The present study was carried out to evaluate the potential protective role of blackberry and quercetin (Q) against NaF-induced oxidative stress and histological changes in liver, kidney, testis and brain tissues of rats. METHODS: The rats
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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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Sub-acute deltamethrin and fluoride toxicity induced hepatic oxidative stress and biochemical alterations in rats
The current study investigated the effects of deltamethrin, fluoride (F(-)) and their combination on the hepatic oxidative stress and consequent alterations in blood biochemical markers of hepatic damage in rats. Significant hepatic oxidative stress and hepatic damage were observed in the toxicant exposed groups. These changes were higher in the
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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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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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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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