Abstract

Fluoride (F) causes not only chronic but also short-term toxic effects, such as apoptosis, in several kinds of human cells. Although human gingival epithelial cells (HGECs) are frequently exposed to topical applications of F to teeth, the apoptosis effects of F on HGECs does not appear to have been assessed. In this study we determined the extent of F-induced apoptosis in HGECs after 24-hr incubation in the presence of various concentrations of NaF. Lactate dehydrogenase activities and reactive oxygen species increased in some of the groups depending on the F concentration. Early apoptosis and caspase-3 activity were significantly increased at 150 and 200 mg/L NaF. An increment of DNA fragmentation was found at 150 mg/L NaF. At 150 and 200 mg/L NaF, caspase-3, -8, and -9 activities, mitochondrial membrane depolarization, and release of cytochrome c were significantly increased, but the expression of Bcl-2 was not suppressed. It was concluded that 150 to 200 mg/L NaF caused apoptosis in HGECs through both mitochondrial-mediated and death ligand–receptor pathways.

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