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Antioxidant Astaxanthin Co-Treatment Protects Zebrafish from Dimethomorph-Induced Cardiovascular Toxicity
Chia-Chen Wu1,2, Ferry Saputra3, Ross D Vasquez4,5
1Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung 84001, Taiwan.
International Journal of Molecular Sciences
|April 14, 2026
Summary
Dimethomorph fungicide causes cardiac and metabolic issues in zebrafish. Astaxanthin shows potential to counteract these toxic effects, highlighting environmental risks of pesticides.
Area of Science:
- Environmental Toxicology
- Cardiovascular Toxicology
- Ecotoxicology
Background:
- Dimethomorph (DIM) is a widely used morpholine fungicide.
- Concerns exist regarding its toxicity to non-target organisms.
- Cardiovascular impacts of DIM are not fully understood.
Purpose of the Study:
- To investigate the cardiovascular and metabolic toxicity of DIM in zebrafish embryos.
- To explore the molecular mechanisms underlying DIM's toxic effects.
- To evaluate the potential protective role of Astaxanthin (AST) against DIM toxicity.
Main Methods:
- Zebrafish embryos were exposed to varying DIM concentrations for 48 hours.
- Cardiac and vascular performance was assessed.
- Gene expression analysis using qRT-PCR was performed.
- A rescue experiment with Astaxanthin was conducted.
Main Results:
- DIM exposure led to cardiac hypertrophy and reduced heart rate in zebrafish.
- Significant alterations in cardiovascular gene expression were observed.
- DIM increased metabolic rate, indicating disrupted energy homeostasis.
- Astaxanthin partially mitigated DIM-induced cardiac and metabolic abnormalities.
Conclusions:
- Dimethomorph exhibits significant cardiovascular and metabolic toxicity in zebrafish.
- Gene expression changes provide mechanistic insights into DIM's toxic effects.
- Astaxanthin demonstrates potential as a counteragent to DIM toxicity.
- Findings underscore the need to re-evaluate DIM's environmental impact and promote safer alternatives.

