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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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-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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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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Sodium fluoride suppress proliferation and induce apoptosis through decreased insulin-like growth factor-I expression and oxidative stress in primary cultured mouse osteoblasts
It has been reported that sodium fluoride suppressed proliferation and induced apoptosis in osteoblasts. However, the details about the mechanism at work in bone metabolism are limited. In this study, we further investigated the mechanisms of NaF on proliferation and apoptosis in the primary cultured mouse osteoblasts, which were exposed
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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 & 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 Reduces Bone Strength Prior to Onset of Skeletal Fluorosis
The majority of animal studies investigating fluoride's impact on bone strength have found that fluoride has either no effect, or a detrimental effect, on bone strength. Importantly, several of the animal studies that have found fluoride reductes bone strength have reported that this reduction in strength occurs before signs of skeletal fluorosis
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Gastrointestinal Problems Among Individuals with Skeletal Fluorosis
Humans suffering from skeletal fluorosis are known to suffer from an increased occurrence of gastrointestinal disorders. When fluoride intake is reduced, these gastrointestinal problems are among the first symptoms to disappear. The following are some of the studies that have examined this issue: "It is clear from the observations presented in this article
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