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INTRODUCTION
Although many studies have been made of the various effects of chronic fluorosis on the different organ systems, only a few have been on the cardiovascular system. Fluorine is a lively nonmetal element, and the fluoride ion (F) combines avidly with blood calcium and magnesium with resultant metabolic disorder and cardiovascular system damage.1 F toxicity can cause atherosclerosis at the molecular level and aortic stiffness and disturbed ventricular distensibility clinically.2-5 The mechanism of F toxicity on the cardiovascular system is complex. Our investigations have previously demonstrated that F is a cytotoxic agent inducing damage in myocardial tissues by oxidative stress through the Bcl-2/Bax signal pathway, which also contributes to atherosclerosis, vascular stiffness, inflammatory mechanisms, and myocardial cell damage.6-8 Using in vitro cultured cardiomyocytes to study the toxic effects of F allows a direct evaluation to be made of the effect of F on the heart. In this study, we investigated the effect of F on cell viability, the cardiac arrest rate, and apoptosis of cardiomyocytes, to provide basic data for further elucidation of the molecular mechanisms of damage induced by F in cardiomyocytes.
MATERIALS AND METHODS
Cardiomyocyte culture: Cardiomyocytes were collected and purified from cardiac tissue of neonatal rats (The Experimental Animal Center of Shanxi Medical University) which was digested with pancreatin (Sigma Aldrich, St. Louis, MO, USA). The cardiomyocytes were cultured in the Dulbecco's modified Eagle medium (DMEM; Gibco, Grand Island, NY, USA) with 10% fetal bovine serum (FBS; Sijiqing, Hangzhou, China) at 37°C in a humid atmosphere with 5% CO2 for 72 hr. The cells were treated with NaF (guaranteed reagent; China Pharmaceutical Group, Shanghai Chemical Reagent Company, China) solution which was used in final concentrations of...