Effect of High Fluorine on the Cell Cycle and Apoptosis of Renal Cells in Chickens

Bai, Chenglian; Chen, Tao; Cui, Yun; Gong, Tao; Peng, Xi; Cui, Hengmin

doi:10.1007/s12011-009-8599-z

Cited by 38 publications

(18 citation statements)

References 11 publications

(13 reference statements)

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“…Many of these cellular events ultimately lead to cell death. NaFinduced apoptosis was demonstrated in the cells from different organs and tissues including lungs [25,26], kidneys [27,28], liver [29][30][31], brain [32][33][34], pancreas [35,36], thymus [37], endometrium [38,39], bone marrow [40], hair follicles [41], erythrocytes [42][43][44], as well as leukemic cells [45][46][47].…”

Section: Fluoride-induced Toxicity and Cell Deathmentioning

confidence: 99%

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

2012

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Fluoride (F) is ubiquitous natural substance and widespread industrial pollutant. Although low fluoride concentrations are beneficial for normal tooth and bone development, acute or chronic exposure to high fluoride doses results in adverse health effects. The molecular mechanisms underlying fluoride toxicity are different by nature. Fluoride is able to stimulate G-proteins with subsequent activation of downstream signal transduction pathways such as PKA-, PKC-, PI3-kinase-, Ca 2+ -, and MAPK-dependent systems. G-protein-independent routes include tyrosine phosphorylation and protein phosphatase inhibition. Along with other toxic effects, fluoride was shown to induce oxidative stress leading to excessive generation of ROS, lipid peroxidation, decrease in the GSH/GSSH ratio, and alterations in activities of antioxidant enzymes, as well as to inhibit glycolysis thus causing the depletion of cellular ATP and disturbances in cellular metabolism. Fluoride triggers the disruption of mitochondria outer membrane and release of cytochrome c into cytosol, what activates caspases-9 and -3 (intrinsic) apoptotic pathway. Extrinsic (death receptor) Fas/FasL-caspase-8 and -3 pathway was also described to be implicated in fluoride-induced apoptosis. Fluoride decreases the ratio of antiapoptotic/proapoptotic Bcl-2 family proteins and upregulates the expression of p53 protein. Finally, fluoride changes the expression profile of apoptosis-related genes and causes endoplasmic reticulum stress leading to inhibition of protein synthesis.

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Section: Fluoride-induced Toxicity and Cell Deathmentioning

confidence: 99%

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

2012

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“…Fluoride toxicity targets to not only bone and teeth, but also soft tissues [6]. Previous studies have proved that fluorine can induce genotoxicity, cytotoxicity, immunotoxicity, oxidative damage, apoptosis and lesions in the broiler peripheral blood [7–10], liver [11, 12], kidney [13–15], thymus [16], spleen [17–19], bursa of Fabricius [20], cecal tonsil [21–25], and intestine [26–30], and in the mouse spleen and kidney [31–35]. …”

Section: Introductionmentioning

confidence: 99%

Sodium fluoride causes oxidative stress and apoptosis in the mouse liver

Luo

Cui

et al. 2017

Aging

108

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The current study was conducted to investigate the effect of sodium fluoride (NaF) on the oxidative stress and apoptosis as well as their relationship in the mouse liver by using methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blot, biochemistry and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4 groups and exposed to different concentration of NaF (0 mg/kg, 12 mg/kg, 24 mg/kg and 48 mg/kg) for a period of 42 days. The results showed that NaF caused oxidative stress and apoptosis. NaF-caused oxidative stress was accompanied by increasing reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and decreasing mRNA expression levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-PX) and glutathione-s-transferase (GST). NaF induced apoptosis via tumor necrosis factor recpter-1 (TNF-R1) signaling pathway, which was characterized by significantly increasing mRNA and protein expression levels of TNF-R1, Fas associated death domain (FADD), TNFR-associated death domain (TRADD), cysteine aspartate specific protease-8 (caspase-8) and cysteine aspartate specific protease-3 (caspase-3) in dose- and time-dependent manner. Oxidative stress is involved in the process of apoptotic occurrence, and can be triggered by promoting ROS production and reducing antioxidant function. NaF-caused oxidative stress and apoptosis finally impaired hepatic function, which was strongly supported by the histopathological lesions and increased serum alanine amino transferase (ALT), aspartic acid transferase (AST), alkaline phosphatase (AKP) activities and TBIL contents.

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“…In an earlier study, Zhang et al (2008) demonstrated that F (40 or 80 ppm) induced S-phase cell cycle arrest and DNA damage in primary cultured rat hippocampal neurons. Bai et al (2010) reported G0/G1 arrest in chicken renal cells at high F concentrations. In agreement with Barbier et al (2010), F arrested the cell cycle at various phases of the cell cycle progression depending upon the concentrations and cell types tested.…”

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confidence: 99%

Sodium Fluoride Promotes Apoptosis by Generation of Reactive Oxygen Species in Human Lymphocytes

Jothiramajayam¹,

Sinha²,

Ghosh³

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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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 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, although 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 findings confirm earlier reports on mechanisms involved in NaF-induced apoptosis.

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Effect of High Fluorine on the Cell Cycle and Apoptosis of Renal Cells in Chickens

Cited by 38 publications

References 11 publications

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

Sodium fluoride causes oxidative stress and apoptosis in the mouse liver

Sodium Fluoride Promotes Apoptosis by Generation of Reactive Oxygen Species in Human Lymphocytes

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