Abstract
Blood samples from 24 adult males, age 25 to 40, with endemic skeletal fluorosis, living in the Vaillapally village of the Nalgonda district, Andhra Pradesh, India, were examined and compared with samples from 15 matched controls for their antioxidant enzyme activity and lipid peroxidation. Elevated malondialdehyde (MDA) levels indicated an increase in lipid peroxidation products, and decreased activity levels of catalase (CAT) and glutathione-S-transferase (GST) reflected significant alterations in their antioxidant status. These results, in agreement with recent findings by others, demonstrate that chronic fluoride intoxication in adult males elicits increased lipid peroxidation associated with a significant decrease in the activities of CAT and GST.
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Fluoride-induced oxidative stress in three-dimensional culture of OS732 cells and rats.
Exposure to excessive fluoride poses a threat to human health, including increased susceptibility to developing the skeletal fluorosis. Despite its recognized importance as an endemic disease, little is known about how fluoride directly impacts on osteoblasts. We previously reported that fluoride-stimulating monolayer-cultured osteoblast proliferation or inhibiting cell viability depended on
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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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Distribution of Fluoride in Plasma, Brain, and Bones and Associated Oxidative Damage After Induced Chronic Fluorosis in Wistar Rats.
The study was aimed to determine fluoride levels in plasma, brain, and bones of Wistar rats following chronic administration of fluoride at different dose levels and the consequent oxidative damage inflicted in these tissues. Brain histomorphology and bone radiographs were also evaluated to assess the extent of damage in these
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Fluoride in Drinking Water and Skeletal Fluorosis: a Review of the Global Impact.
When safe and adequate exposure of an essential trace element is exceeded it becomes potentially toxic. Fluoride is one classic example of such a double edged sword which both plays a fundamental role in the normal growth and development of the body for example the consumption of levels between 0.5–1.0 ppm
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Effect of fluoride on oxidative stress and biochemical markers of bone turnover in postmenopausal women
The present study was conducted on 42 postmenopausal women subjects in Vailapally village, Nalgonda district, Andhra Pradesh, India, an endemic fluorotic area (water fluoride >4 ppm) and 34 postmenopausal women of nonfluorotic villages (water fluoride <0.4 ppm) of the Nalgonda area. The age group of the recruited subjects was 48–58
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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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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 & DISH (Diffuse Idiopathic Skeletal Hyperostosis)
Among individuals with skeletal fluorosis, the fluoride-induced changes to the spine, and the accompanying symptoms, can bear a close resemblance to DISH (Forestier's Disease). Some authors report that skeletal fluorosis can so closely resemble that DISH that the only way to distinguish the two would be to conduct an invasive bone biopsy. No studies have ever been conducted to determine what role, if any, fluoride plays in the development of DISH.
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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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