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Bromuconazole exposure induces cardiac dysfunction by upregulating the expression LEF1.
Yilin Huang1, Weijie Gu1, Zhen Qin1
1College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
The Science of the Total Environment
|May 12, 2024
Summary
Bromuconazole (BRO) fungicide exposure harms zebrafish hearts, reducing body length and altering cardiac energy metabolism. This fungicide interferes with heart function by abnormally activating the LEF1 gene, posing risks to aquatic organisms.
Area of Science:
- Environmental toxicology
- Cardiovascular research
- Molecular biology
Background:
- Bromuconazole (BRO) is a widely used triazole fungicide.
- Environmental concerns regarding BRO contamination are increasing.
- Understanding BRO's impact on aquatic organisms is crucial.
Purpose of the Study:
- To investigate the cardiotoxic effects of environmental concentrations of BRO in zebrafish.
- To elucidate the molecular mechanisms underlying BRO-induced cardiotoxicity.
- To assess the role of LEF1 in BRO's cardiac effects.
Main Methods:
- Adult male zebrafish were exposed to BRO (0.50 ng/L and 7.5 mg/L) for 7 days.
- Physiological parameters, heart morphology, and cardiac gene expression were analyzed.
- Transcriptome analysis identified affected pathways in heart tissues.
- Rat cardiomyocytes (H9C2) were used to validate findings.
- Doxorubicin-induced heart failure model was employed to study LEF1's role.
Main Results:
- BRO exposure led to reduced body length, increased fatness, enlarged heart ventricles, and thinner heart walls in zebrafish.
- Cardiac energy metabolism pathways were significantly affected, with reduced ATP levels.
- Gene expression related to ion balance and myosin synthesis was altered.
- Similar effects on energy metabolism and heart function genes were observed in H9C2 cells.
- LEF1 expression was significantly increased in BRO-exposed fish and cardiomyocytes.
Conclusions:
- Bromuconazole exposure induces cardiotoxicity in zebrafish by disrupting cardiac energy metabolism and function.
- The Wnt/β-catenin signaling pathway, mediated by LEF1, appears to play a critical role in BRO-induced cardiotoxicity.
- Findings suggest a potential universal mechanism of BRO cardiotoxicity across species.
- Urgent monitoring and regulation of BRO are needed to protect aquatic organisms.
