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Published on: February 15, 2021
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.
Abstract:
Fluorosis is a worldwide public health problem, in which the heart is an important target organ. However, studies on its toxicological mechanism in embryonic development are limited. This study assessed the toxicity of sodium fluoride (NaF) toward zebrafish embryos. We determined the mortality, hatching rate, phenotypic malformation, heart function, and morphology of zebrafish embryos after exposure to NaF. Subsequently, the molecular mechanism was revealed using high-throughput RNA sequencing analysis. The expression levels of key genes for heart development were detected using quantitative real-time reverse transcription PCR. The 50% lethal concentration (LC50) value of NaF toward zebrafish embryos at 96 h post-fertilization was 335.75 mg/L. When the concentration of NaF was higher than 200 mg/L, severe deformities, such as pericardial edema, yolk sac edema, spine curvature, shortened body length, reduced head area, and eye area, were observed. The heart rate of the embryos exposed to NaF decreased in a dose-dependent fashion. The distance between the sinus venosus and bulbus arteriosus was significantly increased in the NaF-exposed group compared with that in the control group. The stroke volume and cardiac output decreased significantly in the NaF groups. Compared with the control group, the expression levels of Gata4, Tbx5a, Hand2, Tnnt2c, Nppa, and Myh6 were significantly increased in the NaF-treated group. Through transcriptome sequencing, 1354 differentially expressed genes (DEGs) were detected in the NaF (200 mg/L) treated groups, including 1253 upregulated genes and 101 downregulated genes. Gene ontology functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway analyses of the DEGs showed that cardiac-related pathways, such as actin cytoskeleton regulation, Jak-Stat, PI3k-Akt, and Ras, were activated in the NaF-exposed group. This study revealed the underlying mechanism of fluoride-induced cardiac morphological and functional abnormalities and provides clues for the clinical prevention and treatment of fluorosis.
Insights
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.
