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.

• Related Studies :

  • 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

  • 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

  • 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

  • Effect of dietary protein or calcium supplement on the expression of collagen I and dentine phosphoprotein of rats with dental fluorosis.

    This study aims to assess the roles of dietary protein (Pr) and calcium (Ca) levels associated with excessive fluoride (F) intake and the impact of Pr, Ca, and F on expression of collagen I (COL I) and dentine phosphoprotein (DPP) in rat incisors. Seventy-two rats were randomly allotted to six

  • Selenium Exerts Protective Effects Against Fluoride-Induced Apoptosis and Oxidative Stress and Altered the Expression of Bcl-2/Caspase Family.

    Fluoride is widely distributed in nature, and at high concentrations, it targets the kidney and especially proximal tubule epithelial cells. Selenium is a typical trace element beneficial to humans, and the role of selenium in the prevention and treatment of fluoride-induced organ damage is an important research topic. The purpose

• Related FAN Content :

  • 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,

  • Fluoride & Rickets

    One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride

  • 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.

  • Fluoride Is Not an Essential Nutrient

    In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can

  • Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients

    Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,