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Published on: January 22, 2017
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Sirt3-mediated mitochondrial dysfunction is involved in fluoride-induced cognitive deficits
Dongmei Wang1, Luyang Cao1, Shunji Pan1
1School of Basic Medical Sciences, Henan University of Science and Technology, Henan, Luoyang, 471003, China.
Summary
Excessive fluoride exposure causes cognitive deficits and neural injury by impairing mitochondrial function and increasing oxidative stress. Sirt3 inhibition plays a key role in these fluoride-induced neurotoxic effects.
Area of Science:
- Neuroscience
- Toxicology
- Mitochondrial Biology
Background:
- Excessive fluoride intake is linked to cognitive deficits, but the underlying mechanisms are not fully understood.
- Mitochondrial dysfunction and oxidative stress are implicated in neurodegenerative processes.
Purpose of the Study:
- To investigate the impact of chronic fluoride exposure on cognitive function, neural integrity, and mitochondrial health.
- To elucidate the role of Sirt3 in fluoride-induced neurotoxicity.
Main Methods:
- Mice were administered varying doses of sodium fluoride (NaF) for 90 days.
- Human neuroblastoma cells (SH-SY5Y) were exposed to NaF with or without Sirt3 overexpression.
- Evaluated cognitive function, neural/synaptic injury, mitochondrial antioxidant enzyme activity, SOD2 and FoxO3A acetylation, and mtDNA transcription.
Main Results:
- Chronic fluoride exposure led to cognitive deficits and neural/synaptic injury in mice.
- Fluoride exposure downregulated Sirt3, increasing SOD2 and FoxO3A acetylation, and impairing mitochondrial function and mtDNA transcription.
- Sirt3 overexpression mitigated fluoride's adverse effects on mitochondrial function and oxidative stress in cells.
Conclusions:
- Chronic fluoride exposure induces cognitive impairment and neural injury via mitochondrial dysfunction and oxidative stress.
- Sirt3 inhibition is a significant factor in fluoride-induced neurotoxicity.
