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Sodium Fluoride Exposure Induces Developmental Toxicity and Cardiotoxicity in Zebrafish Embryos.
Feiqing Wang1,2, Fa Chen1, Wen Song1
1Clinical Research Center, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, No. 71 Bao Shan North Road, Yunyan District, Guiyang, 550001, Guizhou Province, China.
Biological Trace Element Research
|September 17, 2024
Summary
Fluoride exposure harms embryonic zebrafish hearts, causing developmental defects and reduced heart function. Molecular analysis revealed activated cardiac pathways, offering insights into fluorosis prevention and treatment.
Area of Science:
- Developmental toxicology
- Cardiovascular research
- Environmental health
Background:
- Fluorosis is a global health issue with cardiac implications.
- Limited understanding of fluoride's toxicological mechanisms during embryonic development.
Purpose of the Study:
- To assess sodium fluoride (NaF) toxicity in zebrafish embryos.
- To investigate the molecular mechanisms underlying fluoride-induced cardiac abnormalities.
Main Methods:
- Zebrafish embryos exposed to varying NaF concentrations.
- Evaluated mortality, hatching rates, and phenotypic malformations.
- Assessed heart function, morphology, and gene expression (qRT-PCR, RNA sequencing).
Main Results:
- LC50 of NaF was 335.75 mg/L at 96 hours post-fertilization.
- NaF exposure (≥200 mg/L) caused severe deformities and dose-dependent cardiac dysfunction (reduced heart rate, stroke volume, cardiac output).
- Transcriptome analysis identified 1354 differentially expressed genes and activated cardiac-related pathways (e.g., actin cytoskeleton, Jak-Stat).
Conclusions:
- Fluoride exposure induces significant cardiac morphological and functional abnormalities in zebrafish embryos.
- Molecular pathways involved in heart development are disrupted by NaF.
- Findings provide insights into fluorosis pathogenesis and potential clinical interventions.
