Abstract

The purpose of this study was to investigate whether fluoride (F) induces cardiotoxicity in rats and to discuss its underlying mechanisms by detecting morphological change, enzyme activity of oxidative stress, and the expression of Bcl-2 family protein. With increasing dosages of F, obvious pathological changes occurred in the myocardial tissue of rats with a trend to increased expression in the cardiomyocytes of Bax and a trend to decreased expression of Bcl-2. Excessive fluoride caused peroxidation damage with inhibition of the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in myocardial tissue leading to a rise of malonaldehyde (MDA) content. These results indicate that a molecular basis for the cardiac damage by fluoride involves the Bax/ Bcl-2 signalling pathway.

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