Abstract
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 years and their years since menopause (YSM) was <10 years. Serum levels of fluoride (F), total alkaline phosphatase (ALP), tartarate resistant acid phosphatase-5b (TRAP-5b), catalase (CAT), glutathione-S-transferase (GST) and malondialdehyde (MDA) were estimated for bone mineral antioxidant and lipid peroxidation status. Significantly increased bone turnover markers ALP, TRAP-5b (p<0.01), and oxidative stress were observed with decreased levels of CAT and GST (p<0.01) activity in postmenopausal women residing in the fluorotic village. Significantly elevated levels of MDA (p<0.01) in these women compared to those in the nonfluorotic village indicated an increase in lipid peroxidation under fluoride stress.
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The toxic effect of fluoride on MG-63 osteoblast cells is also dependent on the production of nitric oxide
Some soda-lime-phospho-silicate glasses, such as Hench's Bioglass(®) 45S5, form bone-like apatite on their surface when bound to living bone. To improve their osteointegration for clinical purposes, the fluoride insertion in their structure has been proposed, but we recently showed that fluoride causes oxidative damage in human MG-63 osteoblasts, via inhibition
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[Experimental studies of pathogenesis of chronic fluoride intoxication].
The article presents the results of studies of occupational fluorosis pathogenesis on experimental model of chronic fluoride intoxication (CFI). In early fluoride intoxication, fluoride and calcium in the body are in compensatory relations. Later, they are disturbed. High reaction ability of fluoride in CFI is associated with hypocalciemia which triggers
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Role of oxidative stress in osteoblasts exposed to sodium fluoride
We investigated the relationship between oxidative stress and osteoblasts viability in osteoblasts exposed to various concentrations of fluoride in this study. Primary calvarial osteoblasts from neonatal Kunming mice were cultured and subcultured to the third generation. Osteoblasts were incubated with sodium fluoride (0, 0.5, 1, 2, 4, 8, 12, and
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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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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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"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 & 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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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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Fluoride content in tea and its relationship with tea quality.
J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected
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