- 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
Investigations of soft tissue funtions in fluorotic Individuals of north Gujarat
The present study was undertaken to investigate the various health problems caused by water-borne fluoride in endemic villages of Mehsana and Banaskantha districts of Gujarat. The study revealed high levels of fluoride in serum samples of the villagers. Mottling of teeth and skeletal complications were common. Intake of fluoride caused
High levels of fluoride in groundwater from Northern parts of Indo-Gangetic plains reveals detrimental fluorosis health risks.
Highlights This study provides an overview of fluoride distribution and health risks in the fluoride endemic region of Northern Indo-Gangetic Plain. Groundwater fluorides concentration exceeded the safe drinking water limit in 98% of sampling locations. Health hazard index (HQFluoride) exceeded the unitary value in all the individual groups signifying that
Study on blood biochemical diagnostic indices for hepatic function biomarkers in endemic skeletal fluorosis
The aim of the study was to determine the relationship of fluoride in drinking water to liver function in individuals living in normal and seven endemic fluorosis areas of Punjab, India. The concentration of fluoride in drinking water of different areas varied from 5.9 to 24.5 mg/L. Study group consisted
Safety of osteoporosis treatment with sodium fluoride, calcium phosphate and vitamin D.
During an 8-year period, 163 consecutive patients with spinal crush fracture osteoporosis started a 5-year treatment with a combination of sodium fluoride (60 mg/day), calcium phosphate (45 mmol/day) and vitamin D2 (18,000 IU/day), and were followed in the outpatient clinic every 3 months. Fourty-three patients completed the 5-year treatment. Mean
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
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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.
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.
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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