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Fluoride-Induced Mitochondrial Dysfunction and Approaches for Its Intervention.

Sachindra Kumar1, Smita Shenoy2, Ravindra Shantakumar Swamy3

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Prolonged fluoride exposure harms human health by inducing mitochondrial dysfunction, oxidative stress, and inflammation. This review explores fluoride

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Area of Science:

  • Environmental toxicology
  • Cell biology
  • Mitochondrial research

Background:

  • Fluoride is ubiquitous, with drinking water as the primary exposure route.
  • Low fluoride levels benefit bone and tooth health, but prolonged exposure is detrimental.
  • Preclinical studies link fluoride toxicity to oxidative stress, inflammation, and apoptosis.

Purpose of the Study:

  • To review fluoride's impact on mitochondrial dynamics, mitophagy, and biogenesis.
  • To elucidate pathways of fluoride-induced mitochondrial toxicity and dysfunction.
  • To discuss therapeutic strategies against fluoride toxicity.

Main Methods:

  • Literature review of preclinical studies on fluoride toxicity.
  • Analysis of molecular mechanisms underlying fluoride's effects on mitochondria.
  • Examination of therapeutic interventions targeting fluoride-induced cellular damage.

Main Results:

  • Fluoride toxicity is associated with mitochondrial dysfunction, including altered dynamics and impaired mitophagy.
  • Mitochondria's role in reactive oxygen species (ROS) production is central to fluoride-induced cellular damage.
  • Mitochondrial DNA purification and regulated mitochondrial dynamics are crucial for cellular survival.

Conclusions:

  • Fluoride exposure induces significant mitochondrial toxicity and cellular dysfunction.
  • Understanding these mechanisms is key to developing effective treatments for fluoride poisoning.
  • Phytochemicals and pharmacological agents show promise in mitigating fluoride's adverse effects by managing ROS and cellular processes.