Sodium Fluoride Induces Apoptosis in H9c2 Cardiomyocytes by Altering Mitochondrial Membrane Potential and Intracellular ROS Level

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• 作者：Xiaoyan Yan ; Xia Yang ; Xianhui Hao ; Qiurong Ren…
• 关键词：H9c2 cells ; Sodium fluoride ; ROS ; Apoptosis ; Mitochondrial membrane potential
• 刊名：Biological Trace Element Research
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：166
• 期：2
• 页码：210-215
• 全文大小：816 KB
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• 作者单位：Xiaoyan Yan (1) (2)
  Xia Yang (2)
  Xianhui Hao (1)
  Qiurong Ren (1)
  Jiping Gao (2)
  Yu Wang (2)
  Na Chang (1)
  Yulan Qiu (2)
  Guohua Song (2)
  
  1. Department of Biology, Taiyuan Normal University, (TYNU), Taiyuan, 030031, People’s Republic of China
  2. Shanxi Key Laboratory of Experimental Animal Science and Animal Model of Human Disease, Health Toxicology Department, School of Public Health, Shanxi Medical University, Taiyuan, 030001, People’s Republic of China
  
• 刊物主题：Biochemistry, general; Biotechnology; Nutrition; Oncology;
• 出版者：Springer US
• ISSN：1559-0720

文摘

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 (ΔΨm), 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 ΔΨm was decreased. In summary, these data suggested that NaF-induced H9c2 cell apoptosis is mediated by direct increased intracellular ROS and downregulated ΔΨm.