Fluoride toxicity, resulting from prolonged exposure to elevated fluoride levels leading to oxidative stress, poses significant health risks, affecting various bodily systems and cellular processes. It also upregulates hormonal mechanisms, causing hormonal disruption in exposed individuals. Extracellular matrix degradation and bone deformity are expected impacts of fluoride toxicity, which are executed by elevated levels of Cyt c, Beclin 1, calcium, and Nf-kB. Due to the excessive release of calcium ions in the cytosol, it was depleted from its natural reservoir in the body, like teeth and bone, which finally leads to dental fluorosis, enamel hypo mineralization, weakening tooth structure, and susceptibility to decay. Skeletal fluorosis was also found commonly in fluoride-exposed individuals, which finally leads to bone and joint abnormalities. Fluoride also hampers ATP formation by interfering with glycolysis pathways, and it alters metabolic and reproductive hormones, causing impaired spermatogenesis, reduced sperm quality, and infertility. Hepatic effects manifest as hepatocyte degeneration and necrosis, contributing to liver damage. Developmental effects include genetic damage to DNA, IQ deficits, and increased risk of developmental abnormalities. Neurological impacts involve structural changes in the brain, memory issues, and neuronal loss. In this way, it was evident that Fluoride toxicity affects cellular organelles, inducing oxidative stress, apoptosis, and disrupting hormonal balance, mediated through alterations in cellular signaling pathways, transcription factors, and protein synthesis. It alters different genes implicated in bone metabolism, hormone signaling, and immune function, which leads to harmful impacts of fluoride on human health.

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Molecular Mechanism of Fluoride-Induced Toxicity and Associated Health Hazards

  • Disha Chauhan,
  • Ranjit Kumar

摘要

Fluoride toxicity, resulting from prolonged exposure to elevated fluoride levels leading to oxidative stress, poses significant health risks, affecting various bodily systems and cellular processes. It also upregulates hormonal mechanisms, causing hormonal disruption in exposed individuals. Extracellular matrix degradation and bone deformity are expected impacts of fluoride toxicity, which are executed by elevated levels of Cyt c, Beclin 1, calcium, and Nf-kB. Due to the excessive release of calcium ions in the cytosol, it was depleted from its natural reservoir in the body, like teeth and bone, which finally leads to dental fluorosis, enamel hypo mineralization, weakening tooth structure, and susceptibility to decay. Skeletal fluorosis was also found commonly in fluoride-exposed individuals, which finally leads to bone and joint abnormalities. Fluoride also hampers ATP formation by interfering with glycolysis pathways, and it alters metabolic and reproductive hormones, causing impaired spermatogenesis, reduced sperm quality, and infertility. Hepatic effects manifest as hepatocyte degeneration and necrosis, contributing to liver damage. Developmental effects include genetic damage to DNA, IQ deficits, and increased risk of developmental abnormalities. Neurological impacts involve structural changes in the brain, memory issues, and neuronal loss. In this way, it was evident that Fluoride toxicity affects cellular organelles, inducing oxidative stress, apoptosis, and disrupting hormonal balance, mediated through alterations in cellular signaling pathways, transcription factors, and protein synthesis. It alters different genes implicated in bone metabolism, hormone signaling, and immune function, which leads to harmful impacts of fluoride on human health.