Abstract

Fluoride generated the attention of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. This study focused on examining the adverse effects of inorganic fluoride (NaF) on human lymphocyte cells in vitro. Mitochondrial function, oxidative stress, cell cycle progression and mode of cell death were combined with genotoxic endpoints. Data demonstrated that NaF at lower concentrations though not significantly cytotoxic and genotoxic, induced oxidative stress leading to apoptotic cell death. The results also suggested that at low concentrations (<1 µg/ml), NaF may affect cell cycle progression. Taken together our finding confirms earlier reports on mechanisms involved in NaF induced apoptosis.

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  • Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats.

    OBJECTIVE: To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. METHODS: Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups

  • Fluoride increases the susceptibility of developmental dysplasia of the hip via increasing capsular laxity triggered by cell apoptosis and oxidative stress in vivo and in vitro.

    Highlights Fluoride does not cause DDH directly but increases its susceptibility by increasing hip capsular laxity. Hip laxity results from apoptosis occurring in capsular fibroblast after fluoride exposure. Fluoride-induced fibroblast apoptosis was triggered by oxidative stress via mitochondrial pathway. The etiology of developmental dysplasia of the hip (DDH) is multifactorial,

  • The morphological changes and molecular biomarker responses in the liver of fluoride-exposed Bufo gargarizans larvae

    Highlights Fluoride triggered marked histological changes in the liver of Bufo gargarizans [the Asiatic toad or Chusan Island toad] Fluoride caused disruption of lipid metabolism. Fluoride resulted in impairing of antioxidant capacity. Fluoride induced alterations of mRNA expression of genes involved in apoptosis. The goal of the current study was to

  • Effects of chronic fluorosis on the brain.

    Highlights Reviewing the mechanism of brain injury caused by chronic fluorosis is of great significance for protecting residents in fluorosis endemic areas. Abstract This article reviews the effects of chronic fluorosis on the brain and possible mechanisms. We used PubMed, Medline and Cochraine databases to collect data on fluorosis, brain injury,

  • Sodium fluoride promotes apoptosis by generation of reactive oxygen species in human lymphocytes

    Fluoride generated the attention of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and with in vivo experimental models. Interest in its undesirable effects has resurfaced due to the awarenessFluoride generated the attention of toxicologists due to its deleterious effects at high concentrations

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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

  • 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 & 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