Journal
BIOLOGICAL TRACE ELEMENT RESEARCH
Volume 166, Issue 2, Pages 210-215Publisher
HUMANA PRESS INC
DOI: 10.1007/s12011-015-0273-z
Keywords
H9c2 cells; Sodium fluoride; ROS; Apoptosis; Mitochondrial membrane potential
Funding
- China National Natural Science Foundation [31240009, 31302158]
- Shanxi Scholarship Council of China [2012-079]
- Shanxi Province Science and Technology Bureau Program [2011021030-1, 2013011059-1]
- Shanxi Province Soft Science [2013041084-03]
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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 the cell viability, intracellular reactive oxygen species (ROS) level, the changes of mitochondrial membrane potential (Delta Im), and the cell apoptosis. Sodium fluoride (NaF) at concentrations of 0, 2, 4, 8, and 16 mg/L was administered to cultured H9c2 cells for up to 48 h. After the treatment, H9c2 cells were collected and the associated parameters were measured by flow cytometry. Our study found that fluoride not only inhibited H9c2 cell proliferation but also induced cell apoptosis. With the increment of NaF concentration, the apoptotic rates and ROS generation were increased, while the Delta Im was decreased. In summary, these data suggested that NaF-induced H9c2 cell apoptosis is mediated by direct increased intracellular ROS and downregulated Delta Im.
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