- 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.
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
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
Low-to-moderate fluoride exposure, relative mitochondrial DNA levels, and dental fluorosis in Chinese children.
Highlights Circulating mtDNA content is negatively related to low-to-moderate fluoride exposure. Dental fluorosis (DF) prevalence is positively related to fluoride exposure. Circulating mtDNA content is negatively associated with the DF prevalence. Gender modifies the associations of DF prevalence with mtDNA and fluoride exposure. mtDNA content partly mediates association of
Sodium fluoride induces apoptosis in H9c2 cardiomyocytes by altering mitochondrial membrane potential and intracellular ROS level
Chronic excessive fluoride intake is known to be toxic, and effects of long-term fluorosis on different organ systems have been examined. However, there are few studies about the effects of fluorosis on cardiovascular systems. Here, we studied the fluoride-induced apoptosis in H9c2 cells and determined the underlying molecular mechanisms including
Genes associated with sodium fluoride-induced human osteoblast apoptosis
This study aims to explore the potential pathways and molecular characteristics of fluorine-induced osteoblast apoptosis. In vitro fluorine-induced model was established with an osteogenesis sarcoma cell line Saos-2. Then flow cytometry was used to determine the mitochondrial membrane potential at 24 h after the intervention. 84 apoptosis-related genes in the
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