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Some studies suggest sodium fluoride can disrupt hormone levels, impair reproductive and thyroid function, and cause oxidative stress and tissue damage, while other studies indicate it may increase bone mineral density but also skeletal fragility and is not effective in treating spinal osteoporosis.
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Sodium fluoride (NaF) has been shown to significantly disrupt testosterone biosynthesis by affecting the steroidogenic pathway in Leydig cells. Exposure to varying concentrations of NaF resulted in decreased cell viability, increased cytotoxicity, and reduced levels of testosterone and cyclic adenosine monophosphate (cAMP) in a dose-dependent manner. This disruption is linked to the suppression of steroidogenic genes and proteins, including steroidogenic acute regulatory protein and cholesterol side-chain cleavage enzyme, among others.
While sodium fluoride treatment can increase bone mineral density, it may also lead to reduced bone strength. In a four-year clinical trial involving postmenopausal women with osteoporosis, NaF treatment increased bone mineral density in the lumbar spine and femoral neck but decreased it in the cortical bone of the radius. This resulted in a higher incidence of nonvertebral fractures and significant side effects such as gastrointestinal symptoms and lower-extremity pain .
Sodium fluoride exposure has been associated with increased thyroid-stimulating hormone (TSH) levels and decreased concentrations of thyroid hormones T3 and T4. Additionally, NaF has been linked to increased secretion of parathyroid hormone (PTH), potentially affecting calcium metabolism. These endocrine disruptions can impair fertility and disrupt puberty.
Fluoride exposure may adversely affect pancreatic function, leading to abnormal glucose tolerance and potentially contributing to diabetes. Observations include decreased insulin levels and impaired glucose metabolism.
High doses of sodium fluoride can induce significant liver and kidney damage. This is evidenced by altered levels of liver enzymes (ALT, ALP, AST) and kidney function parameters (urea, creatinine). NaF exposure also increases oxidative stress markers and inflammatory markers in these tissues, leading to cellular damage and apoptosis.
Sodium fluoride has been shown to induce hypertension and cardiovascular complications through the generation of reactive oxygen species (ROS) and activation of nuclear factor kappa B (NF-κB). This results in increased blood pressure, oxidative stress, and damage to cardiac and renal tissues, as well as histopathological changes in these organs .
In female rats, sodium fluoride exposure leads to significant decreases in estrogen and progesterone levels, as well as abnormalities in receptor protein expression. This results in impaired fertility and disrupted ovarian development. Similar effects have been observed in Drosophila melanogaster, where NaF exposure reduced fecundity, altered ovarian morphology, and increased apoptosis .
Sodium fluoride, while beneficial for dental health, poses significant risks to various bodily systems when exposure levels are high. These include disruptions in testosterone biosynthesis, increased bone fragility, endocrine dysfunction, liver and kidney toxicity, cardiovascular complications, and impaired reproductive health. These findings underscore the importance of monitoring and regulating fluoride exposure to mitigate its adverse health effects.
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