Effects of fluoride exposure on mitochondrial function: Energy metabolism, dynamics, biogenesis and mitophagy.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical and mechanistic evidence.
PubMed 35738460 · doi:10.1016/j.etap.2022.103916
What was done
The authors conducted a narrative literature review summarizing preclinical evidence regarding the impact of chronic fluoride exposure on mitochondrial function, specifically focusing on energy metabolism, mitochondrial dynamics, biogenesis, and mitophagy across various soft and hard tissues (including liver, reproductive organs, heart, brain, lung, kidney, bone, and tooth).
What was found
The abstract provides no quantitative data or specific effect estimates. It reports descriptively that while low fluoride levels support bone and tooth development, chronic exposure is associated with oxidative stress, inflammation, apoptosis, and disruptions in mitochondrial quality control mechanisms (dynamics, biogenesis, and mitophagy) leading to tissue-specific toxicity.
Why it matters
Understanding the cellular mechanisms of fluoride-induced mitochondrial dysfunction helps clarify the toxicological pathways underlying chronic fluorosis in multiple organs.
Limits
The abstract lacks quantitative metrics, search methodology, inclusion/exclusion criteria, and sample sizes. The summarized evidence relies primarily on preclinical mechanistic models rather than direct human clinical or epidemiological data.
Cited by
- supports Fluoride damages the myelin sheath of neurons and impairs mitochondrial integrity in the brain.