Abstract
Fluoride is found in the atmosphere, water, soil, coal, food, dental and industrial uses. There were some case reports concerning acute fluoride poisoning in workplaces and laboratories. However, there is limited information concerning the mechanism of fluoride-induced cell death. To study the cytotoxicity of fluoride, the effect of sodium fluoride (NaF) on rat thymocytes has been examined by using a flow cytometer with appropriate fluorescence probes for membrane and cellular parameters. The cytotoxicity of NaF under nominal Ca2+-free condition was significantly lower than that under control condition. NaF also increased intracellular Ca2+ concentration. NaF significantly increased the population of shrunken cells and the cells positive to annexin V. Both are known to be parameters for early stage of apoptosis. However, NaF decreased the population of cells with hypodiploidal DNA, indicating that NaF apparently attenuated spontaneous apoptosis in rat thymocytes. It may be suggested that NaF induces necrosis, associated with some apoptotic characteristics.
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Analysis of the roles of dietary protein and calcium in fluoride-induced changes in T-lymphocyte subsets in rat
The roles of dietary protein (Pr) and calcium (Ca) levels on the changes in T-lymphocyte subsets induced by excessive fluoride (F) intake were assessed using rats that were malnourished for 120 days as a model. The CD4+ and CD8+ T-lymphocytes in the spleen tissue were determined by flow cytometry and
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Effects of dietary protein and calcium on thymus apoptosis induced by fluoride in female rats (Wistar rats)
Our previous studies showed that excessive fluoride (F) ingestion seriously damaged the nonspecific immune function in rabbits. However, the underlying mechanisms of the F-induced damage to the immune system are unclear. The purpose of this study was to investigate whether F induces thymus apoptosis in female rats and its underlying
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Mitigating effects of some antidotes on fluoride and arsenic induced free radical toxicity in mice ovary
The effects of oral administration of sodium fluoride (NaF) and/or arsenic trioxide (As(2)O(3)) (5 mg and 0.5 mg/kg body weight, respectively) for 30 days were investigated on free radical induced toxicity in the mouse ovary. The reversibility of the induced effects after withdrawal of NaF+As(2)O(3) treatment and by administration of
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Effects of malnutrition and supplemented nutrition on nonspecific immune function changes induced by fluoride in rabbits
This study was designed to investigate the protective role of protein (Pr) and calcium (Ca) on effects of fluoride (F) induced in nonspecific immunological function in New Zealand rabbits fed a Pr and a Ca nutritionally deficient (malnutrition) diet. Eighty healthy 30-day-old rabbits (1.07±0.25 kg) were divided randomly into four equal groups of twenty
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Selenium may suppress peripheral blood mononuclear cell apoptosis by modulating HSP70 and regulate levels of SIRT1 through reproductive hormone secretion and oxidant stress in women suffering fluorosis.
Excessive taking fluoride (F) causes severe damage to reproductive system through stimulation of apoptosis and oxidant stress. Selenium (Se) may promote anti-oxidant enzymes and invert cell apoptosis. The aim of this study was to investigate the effect of Se on peripheral blood mononuclear cell (PBMC) apoptosis and oxidant stress in
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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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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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