- NaF induced NETs formation.
- NaF caused imbalance between ROS and antioxidant system.
- NaF induced NETs formation via ROS, ERK, and p38 signaling pathways.
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.
Involvement of Bmal1 and circadian clock signaling in chondrogenic differentiation of ATDC5 cells by fluoride.
Highlights Fluoride inhibited chondrocyte viability and delayed chondrocyte differentiation. Fluoride disrupted the circadian clock signaling pathway in ATDC5 cells. Overexpression of Bmal1 reversed the delayed chondrogenic differentiation induced by fluoride. Skeletal fluorosis causes growth plate impairment and growth retardation during bone development. However, the mechanism of how fluoride impairs chondrocyte
The dose-time effects of fluoride on the expression and DNA methylation level of the promoter region of BMP-2 and BMP-7 in rats.
Highlights Fluoride has a dose-time effect on Bone Morphogenetic Protein-2 expression. Fluoride increases the expression of Bone Morphogenetic Protein-2 and 7. DNA methylation may be involved in fluoride regulation of target protein expression. Skeletal fluorosis is a chronic metabolic bone disease caused by excessive exposed to fluoride. Recent studies have
Fluoride promotes osteoblastic differentiation through canonical Wnt/B-catenin signaling pathway
Although fluoride is known to stimulate bone formation, the underlying mechanisms are not fully understood. Recent studies have implicated the Wnt/B-catenin pathway as a major signaling cascade in bone biology. Our earlier studies highlighted a probable role of canonical Wnt pathway in bone formation of chronic fluoride-exposed rats, but the
Bone quality in fluoride-exposed populations: A novel application of the ultrasonic method.
Highlights A novel ultrasonic bone quality biomarker was tested in a population with low to high exposure to F.- Negative associations were found between F- exposure and bone quality Decreased bone quality reflects net bone loss, abnormal mineralization and altered collagen. The finding highlights that F- exposure has complex
A Rat Experimental Study of the Relationship Between Fluoride Exposure and Sensitive Biomarkers.
Chronic excessive fluoride exposure impairs human health and damages not only the skeletal system and the teeth but also the soft tissues such as the brain, liver, kidneys, pancreas and spinal cord. However, there is limited research regarding the exposure levels and sensitive biomarkers. This study was aimed to establish
Related Studies :
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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