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

摘要: 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 cardiovascular systems. Here, we studied fluoride-induced apoptosis in H9c2 cells determined underlying molecular mechanisms including cell viability, intracellular reactive oxygen species (ROS) level, changes mitochondrial membrane potential (ΔΨm), apoptosis. Sodium (NaF) at concentrations 0, 2, 4, 8, 16 mg/L was administered cultured for up 48 h. After treatment, were collected associated parameters measured by flow cytometry. Our study found that not only inhibited proliferation but also induced With increment NaF concentration, apoptotic rates ROS generation increased, while ΔΨm decreased. In summary, these data suggested NaF-induced mediated direct increased downregulated ΔΨm.