- NaF induced damage of liver structure and function through the IL-17A pathway.
- NaF induced hepatocyte mitochondrial damage and mitophagy disorder.
- IL-17A addition aggravated NaF-induced hepatocyte mitochondrial damage and mitophagy.
- IL-17A knockout mitigated NaF-induced hepatocyte mitochondrial damage and mitophagy.
As an environmental toxicant, the damage of fluoride to the body has attracted global attention. Because liver is an essential organ for fluoride accumulation and damage. Our previous studies revealed fluoride-induced hepatic injury through interleukin 17A (IL-17A) pathway, but the underlying cellular mechanism remains unclear. Hence, this research explored the mechanism of IL-17A pathway and mitophagy in fluoride-induced liver injury through the use of the mice fluorosis model, IL-17A addition fluorosis cell model, IL-17A gene knockout mice fluorosis model, flow cytometry, immunohistochemistry, fluorescence double staining, ELISA, western blotting, and other techniques. The results showed that fluoride reduced the bodyweight and liver coefficient, increased the bone fluoride content, the aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamate dehydrogenase (GDH) levels, caspase 8 and caspase 9 activities, and induced liver morphology and ultrastructure damage. Furthermore, the protein expression levels of IL-17A pathway key proteins, IL-17A, IL-17R, and Act1 were increased, but I?B was decreased after fluoride exposure. In addition, fluoride exposure elevated the mitochondrial depolarization percent, the mitochondria damage, the fluorescent spots of mitophagy, and the LC3II/LC3I protein relative expression level. To further verify the role of the IL-17A pathway in fluoride-induced hepatocyte mitochondrial damage and mitophagy disorder, the IL-17A was added and knocked out in cells of animals. The results showed that the addition of IL-17A aggravated fluoride-induced liver morphology and functional damage, activation of the IL-17A pathway, mitochondrial injury, and mitophagy, but the IL-17A knockout mitigated fluoride-induced changes. These results suggested that fluoride exposure induced mitochondrial damage and mitophagy through the IL-17A pathway in hepatocytes.
*Original abstract online at https://www.sciencedirect.com/science/article/abs/pii/S004896972105261X?via%3Dihub
The effects of fluoridated water on rat urine and tissue cAMP levels
Male Wistar rats were fed a fluoride deficient diet (less than 0.5 parts/10(6) F), and either distilled water or fluoridated water (1.0 parts/10(6)). By week 3, the control group had urinary excretions of 106 +/- 5 nmol cAMP/day (mean +/- SEM) whereas the experimental group excreted 129 +/- 6 nmol
Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3F1 Mice (Drinking Water Studies)
CASRN: 7681-49-4 Chemical Formula: NaF Molecular Weight: 41.99 Report Date: December 1990 Sodium fluoride is a white, crystalline, water-soluble powder used in municipal water fluoridation systems, in various dental products, and in a variety of industrial applications. Toxicology and carcinogenesis studies were conducted with F344/N rats and B6C3F1 mice of each sex by incorporating
Epidemiologic health study of workers in an aluminum smelter in Kitimat, B.C. II. Effects on musculoskeletal and other systems
A health study was carried out on 2066 workers in an aluminum smelter in Kitimat, British Columbia to study the effects of exposure to fluoride and other air contaminants encountered on the potlines on the musculoskeletal system, hemopoietic tissue, liver, and renal function. Three hundred seventy-two railway repair workers from
The effect of dietary sodium fluoride on internal organs, breast muscle, and bones in captive American kestrels (Falco sparverius)
In 1982, 29 7-day-old American kestrel (Falco sparverius) chicks from captive stock were randomly assigned to one of three dietary regimens: (1) 10 birds were fed daily with cockerel mash (0 ppm of F-: control birds); (2) 10 birds were fed daily with cockerel mash containing 1,120 ppm of F-;
The Effects of Calcium, Magnesium, Phosphorus, Fluoride, and Lead on Bone Tissue.
Bones are metabolically active organs. Their reconstruction is crucial for the proper functioning of the skeletal system during bone growth and remodeling, fracture healing, and maintaining calcium-phosphorus homeostasis. The bone metabolism and tissue properties are influenced by trace elements that may act either indirectly through the regulation of macromineral metabolism,
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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.
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.
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