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Mitochondrial translation impairment-triggered neuroinflammation mediates fluoride-induced cognitive deficits

Wenhui Liu1, Chenxi Wang1, Huayang Tang1

  • 1Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China; Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, State Key Laboratory of Environmental Health (incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.

Ecotoxicology and Environmental Safety
|October 11, 2025
PubMed

Insights

Fluoride exposure disrupts mitochondrial translation, causing neuroinflammation and cognitive deficits. The natural compound curcumin (CUR) reversed these effects by targeting mitochondrial dysfunction and inflammation.

Area of Science:

  • Environmental Health
  • Neuroscience
  • Toxicology

Background:

  • Fluoride exposure causes multi-organ toxicity, including neuroinflammation and cognitive deficits.
  • Fluoride-induced neurotoxicity is linked to mitochondrial dysfunction, specifically disrupted mitochondrial translation.
  • The precise mechanisms linking translational impairment, neuroinflammation, and cognitive decline are not well understood.

Purpose of the Study:

  • To elucidate the mechanistic interplay between fluoride exposure, mitochondrial translation, neuroinflammation, and cognitive deficits.
  • To identify key molecular players in fluoride-induced neurotoxicity.
  • To evaluate the therapeutic potential of curcumin (CUR) against fluoride neurotoxicity.

Main Methods:

  • Integrated proteomic and functional analyses were performed in vivo and in vitro.
  • Mitochondrial ribosomal protein L15 (MRPL15) and CCAAT/enhancer-binding protein-α (C/EBPα) levels were assessed.
  • Mitochondrial reactive oxygen species (mtROS) production, NLRP3 inflammasome activation, pyroptosis, and cognitive function were evaluated.
  • The effects of curcumin (CUR) on these pathways were investigated.

Main Results:

  • Fluoride exposure upregulated MRPL15 via C/EBPα, disrupting mitochondrial translation fidelity.
  • This disruption led to increased mitochondrial reactive oxygen species (mtROS) overproduction.
  • Elevated mtROS activated the NLRP3 inflammasome, causing pyroptotic cell death and cognitive impairment.
  • Curcumin (CUR) treatment attenuated fluoride neurotoxicity by improving mitochondrial bioenergetics and suppressing the mtROS/NLRP3-pyroptosis axis.

Conclusions:

  • Mitochondrial translation disruption is a novel mechanism underlying fluoride-induced neuroinflammation and cognitive deficits.
  • The mtROS/NLRP3 inflammasome pathway is critical in mediating fluoride's neurotoxic effects.
  • Curcumin (CUR) shows therapeutic potential for mitigating fluoride neurotoxicity.
  • Findings necessitate re-evaluation of fluoride safety thresholds in environmental health policies.
Keywords:
Cognitive impairmentFluorideMitochondrial translationPyroptosis

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