XXXVTH Conference of the International Society for Fluoride Research (35.ISFR-2022), Harbin, Çin, 28 - 31 Temmuz 2022, cilt.1, sa.1, ss.61-62
ABSTRACT: Background/objectives. Fluoride is a highly reactive element that is
excreted through the kidneys and metabolized in the liver. Prolonged and excessive
fluoride intake leads to a disease known as fluorosis. Cell structures of liver and kidney
tissues are damaged in fluorosis. IL-1B is a pro-inflammatory cytokine that plays a rolein pain, inflammation, and autoimmune conditions. Studies are carried out on the
molecular metabolism of fluoride in our laboratory. This study was carried out to
investigate the effects of fluoride on IL-1B in vitro and thus elucidate its potential role in
cell proliferation and inflammation. Methods. NaF was used as fluoride source in this study. NaF concentrations were
determined by MTT assay. NaF concentrations were determined as proliferative
concentration (10 µM) and cytotoxic concentrations (IC25 (2250 µM) and IC50 (4250 µM))
at 24 hours. The determined NaF concentrations were administered to the cells. The
IL-1B gene was considered the target gene. Total mRNA was isolated. mRNAs were
converted to cDNA. The expression level of the target gene was determined by
RT-qPCR method. Results. It was determined that it was expressed approximately 2.5 times in proliferative
concentration, 3.4 times in IC25 concentration and 40 times in IC50 concentration. Conclusion. In conclusion, it was thought that NaF had a limited effect on IL-1B at
proliferative and IC25 doses on kidney cells. At the same time, the IC50 was highly
effective at toxic doses and can therefore be considered an indicator of damage. High
expression of IL-1B gene in toxic concentration can be considered as an indicator of
the importance of the inflammation pathway in the pathogenesis of fluoride-induced
cell damage in the NRK-52E kidney cell