Open AccessFluoride resistance in fibroblasts is conferred via reduced susceptibility to oxidative stress and apoptosis
Author(s) -
Ni Jing,
Zhong Zhe,
Zhang Wu,
Liu Bin,
Shu Rong,
Li Yiming
Publication year - 2020
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12786
Subject(s) - apoptosis , reactive oxygen species , sodium fluoride , oxidative stress , downregulation and upregulation , fluoride , chemistry , caspase 9 , mitochondrion , caspase 3 , microbiology and biotechnology , caspase , programmed cell death , biology , biochemistry , gene , inorganic chemistry
Chronic fluoride exposure from drinking water may result in endemic fluorosis. To better understand the mechanisms by which some people are resistant to fluorosis, here we investigated the effect of treatment with NaF (sodium fluoride) on production of reactive oxygen species (ROS), morphological changes in mitochondria, the mRNA expression of Fas ligand (Fas‐L), and the protein expression of cleaved caspase‐3 in regular L‐929 cells and fluoride‐resistant (FR) L‐929 cells. While morphological changes indicative of apoptosis and a network of fragmented mitochondria were observed in regular L‐929 cells after NaF treatment, there were no morphological changes in FR L‐929 cells after NaF treatment. Treatment with 10 m m NaF induced a significant difference in the production of ROS, triggered the expression of cleaved caspase‐3, and upregulated the mRNA expression of Fas‐L in regular L‐929 cells. However, there was no significant production of ROS in FR L‐929 cells. Additionally, cleaved caspase‐3 and upregulated Fas‐L were not detected in FR L‐929 cells. These results suggest that FR fibroblasts are resistant to oxidative stress and apoptosis induced by fluoride.