Abstract
Highlights
- We studied the toxic effects of different concentrations of NaF in H9c2 cells.
- NaF inhibited H9c2 cell proliferation and induced early apoptosis.
- Mitochondrial membrane potential decreased with increase in NaF.
- Caspase-3, caspase-9, and cytochrome c mRNA levels increased with increase in NaF.
- Fluoride induces apoptosis via activation of the mitochondrial pathway.
Numerous studies have shown that chronic excessive fluoride intake can adversely affect different organ systems. In particular, the cardiovascular system is susceptible to disruption by a high concentration of fluoride. The objectives of this study were to explore the mechanism of apoptosis by detecting the toxic effects of different concentrations of sodium fluoride (NaF) in H9c2 cells exposed for up to 96 h. NaF not only inhibited H9c2 cell proliferation but also induced apoptosis and morphological damage. With increasing NaF concentrations, early apoptosis of H9c2 cells was increased while the mitochondrial membrane potential was decreased. Compared with the control group, the mRNA levels of caspase-3, caspase-9, and cytochrome c all increased with increasing concentrations of NaF. In summary, these data suggest that apoptosis is involved in NaF-induced H9c2 cell toxicity and that activation of the mitochondrial pathway may occur.
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Preliminary screening of fluorine-stained osteoblastic apoptosis-related microRNA.
This article has been accepted for publication and undergone full peer review but has not been through the copy editing, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ar.24709. Endemic fluorosis is a chronic systemic
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The mitochondrial pathway is involved in sodium fluoride (NaF)-induced renal apoptosis in mice.
The objective of the present study was to explore the molecular mechanism of apoptosis induced by sodium fluoride (NaF) in the mouse kidney by using the methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4
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A deep insight into the transcriptome of midgut and fat body reveals the toxic mechanism of fluoride exposure in silkworm.
Highlights 200 mg/L fluoride soaked mulberry leaves exposure inhibits the growth of silkworm larvae. RNA-seq reveals the toxic mechanism of fluoride exposure in silkworm. Fluoride damages oxidative phosphorylation process and disturbs MAPK signaling pathway. The identification of potential transports for fluoride. Fluoride generally exists in the natural environment, and has
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Arsenic and fluoride co-exposure affects the expression of apoptotic and inflammatory genes and proteins in mononuclear cells from children
Humans may be exposed to arsenic (As) and fluoride (F) through water consumption. However, the interaction between these two elements and gene expression in apoptosis or inflammatory processes in children has not been thoroughly investigated. Herein, the expression of cIAP-1, XIAP, TNF-?, ENA-78, survivin, CD25, and CD40 was evaluated by
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The effect of vitamin E and selenium combination in repairing fluoride-induced DNA damage to NRK-52E cells.
Prolonged and excessive fluoride exposure can lead to fluorosis. The kidney is one of the organs that are injured mostly due to fluoride-induced damage. Fluoride can induce DNA damage at cytotoxic concentrations. This study aims to determine the extent of NaF-induced DNA damage and to investigate the effect of vitamin
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