Abstract

Fluorine is one of the trace elements necessary for health. It has many physiological functions, and participates in normal metabolism. However, fluorine has paradoxical effects on the body. Many studies have shown that tissues and organs of humans and animals appear to suffer different degrees of damage after long-term direct or indirect exposure to more fluoride than required to meet the physiological demand. Although the aetiology of endemic fluorosis is clear, its specific pathogenesis is inconclusive. In the past 5 years, many researchers have conducted in-depth studies into the pathogenesis of endemic fluorosis. Research in the areas of fluoride-induced stress pathways, signalling pathways and apoptosis has provided further extensive knowledge at the molecular and genetic level. In this article, we summarize the main results.

Figure 2
PowerPoint
Common alterations in fluorosis?apoptosis. Caspases, a family of cysteine proteases, are the central regulators of apoptosis. FasL can activate initiator caspases (Pro-caspase 8 and 10), then cleave and activate the effector caspases 3, 6 and 7, leading to apoptosis. Fluoride exposure can activate these signalling pathways and induce apoptosis. In addition, excessive fluoride induces stress pathways such as oxidative stress and endoplasmic reticulum stress, thus promoting apoptosis. Many signalling pathways such as Erk1/2 and PI3K/Akt induce anti-apoptotic Bcl-2 family members. These Bcl-2 family members protect the integrity of mitochondria, preventing Cytochrome C release and the subsequent activation of caspase-9. TNF-a may activate both pro-apoptotic and anti-apoptotic pathways. TNF-a can induce apoptosis by activating caspase 8 and 10, but can also inhibit apoptosis via NF-kB. Fluoride exposure can inhibit these survival signalling pathways

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