Abstract

Prolonged exposure to high doses of fluoride causes chronic poisoning called fluorosis, which affects many tissues and causes serious health problems. This study was planned to investigate the apoptotic, autophagic, and necrotic molecular pathways of fluoride. Sodium fluoride (NaF) was administered to normal rat kidney epithelial (NRK-52E) cells. The NaF IC50 value was determined using the MTT assay. The expression of the genes in the autophagic, apoptotic, and necrotic pathways was determined by real-time PCR. It was determined that there were significant changes in NaF-induced molecular pathways depending on the time. There were no increases in apoptotic and necrotic pathway markers except for Atg3, an autophagy gene, at the 3rd and the 12th hours. However, there was an induction in all cell death signaling pathways at 24 h. The molecular mechanisms demonstrated NaF-induced cellular death in the NRK-52E cell line. It was concluded that these molecular mechanisms were activated with NaF, and different mechanisms accelerated the cellular death at the 24th hour.

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