化学
氟化钠
过氧化氢酶
超氧化物歧化酶
活性氧
中性粒细胞胞外陷阱
氟化物
细胞外
中性粒细胞
超氧化物
MAPK/ERK通路
磷酸化
生物化学
细胞生物学
氧化应激
酶
免疫学
炎症
生物
体外
无机化学
作者
Jingjing Wang,Zhengkai Wei,Zhen Han,Ziyi Liu,Yong Zhang,Xingyi Zhu,Xiaowen Li,Kai Wang,Zhengtao Yang
标识
DOI:10.1016/j.envpol.2019.113583
摘要
In recent years, numerous studies paid more attention to the molecular mechanisms associated with fluoride toxicity. However, the detailed mechanisms of fluoride immunotoxicity in bovine neutrophils remain unclear. Neutrophil extracellular traps (NETs) is a novel immune mechanism of neutrophils. We hypothesized that sodium fluoride (NaF) can trigger NETs activation and release, and investigate the related molecular mechanisms during the process. We exposed peripheral blood neutrophils to 1 mM NaF for 120 min in bovine neutrophils. The results showed that NaF exposure triggered NET-like structures decorated with histones and granule proteins. Quantitative measurement of NETs content correlated positively with the concentration of NaF. Mechanistically, NaF exposure increased reactive oxygen species (ROS) levels and phosphorylation levels of ERK, p38, whereas inhibiting the activities of superoxide dismutase (SOD) and catalase (CAT) compared with control neutrophils. NETs formation is induced by NaF and this effect was inhibited by the inhibitors diphenyleneiodonium chloride (DPI), U0126 and SB202190. Our findings described the potential importance of NaF-triggered NETs related molecules, which might help to extend the current understanding of NaF immunotoxicity.
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