Antioxidant Astaxanthin Co-Treatment Protects Zebrafish from Dimethomorph-Induced Cardiovascular Toxicity

Dimethomorph (DIM) is a commonly applied morpholine fungicide, yet its potential toxicity to non-target organisms raises significant environmental concerns. This study aims to elucidate the toxicological effects of DIM on zebrafish, with a particular focus on its cardiovascular impacts. Zebrafish embryos were exposed to a range of DIM concentrations for 48 h, and their cardiac and vascular performance was meticulously assessed to determine the extent of cardiovascular toxicity. The findings revealed notable cardiac hypertrophy, evidenced by a substantial enlargement in heart size, alongside a dose-dependent reduction in heart rate. These observations suggest direct impairment of cardiac function following DIM exposure. To further investigate the molecular underpinnings of these effects, gene expression analysis was conducted using quantitative real-time PCR (qRT-PCR). The results demonstrated significant alterations in the expression of key genes associated with cardiovascular development and function, providing mechanistic insights into DIM's toxic effects. In addition to cardiac abnormalities, DIM exposure led to a significant increase in the metabolic rate of the zebrafish embryos, indicating a potential disruption in energy homeostasis. To explore possible protective measures, a rescue experiment was performed using Astaxanthin, a potent antioxidant. Notably, Astaxanthin treatment partially mitigated the observed cardiac and metabolic phenotypes, suggesting its potential as a therapeutic agent to counteract DIM-induced toxicity. In summary, this study provides compelling evidence of the cardiovascular toxicity of DIM in zebrafish, highlighting its potential to disrupt cardiac function and metabolic regulation. The observed effects underscore the importance of re-evaluating the environmental impact of DIM and emphasize the need for further research to fully understand its mechanisms of toxicity. The findings also suggest that Astaxanthin (AST) could serve as a protective agent against DIM-induced toxicity, opening avenues for future studies aimed at mitigating the adverse effects of this widely used fungicide. This research study contributes to the growing body of knowledge on the environmental and health risks associated with pesticide use, advocating for more stringent regulations and safer alternatives.

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Journal
International Journal of Molecular Sciences
Published
2026-04-01
DOI
https://doi.org/10.3390/ijms27073211
Primary Topic
Environmental Toxicology and Ecotoxicology
Type
article
Field-Weighted Citation Impact
0.00

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article

Antioxidant Astaxanthin Co-Treatment Protects Zebrafish from Dimethomorph-Induced Cardiovascular Toxicity

Chung‐Der Hsiao, Yu‐Heng Lai, Ross D. Vasquez, Ferry Saputra et al.
International Journal of Molecular Sciences
Environmental Toxicology and Ecotoxicology
article

Antioxidant Astaxanthin Co-Treatment Protects Zebrafish from Dimethomorph-Induced Cardiovascular Toxicity

Chung‐Der Hsiao, Yu‐Heng Lai, Ross D. Vasquez, Ferry Saputra, Marri Jmelou M. Roldan, Chih-Hsin Hung
article en

Abstract

Dimethomorph (DIM) is a commonly applied morpholine fungicide, yet its potential toxicity to non-target organisms raises significant environmental concerns. This study aims to elucidate the toxicological effects of DIM on zebrafish, with a particular focus on its cardiovascular impacts. Zebrafish embryos were exposed to a range of DIM concentrations for 48 h, and their cardiac and vascular performance was meticulously assessed to determine the extent of cardiovascular toxicity. The findings revealed notable cardiac hypertrophy, evidenced by a substantial enlargement in heart size, alongside a dose-dependent reduction in heart rate. These observations suggest direct impairment of cardiac function following DIM exposure. To further investigate the molecular underpinnings of these effects, gene expression analysis was conducted using quantitative real-time PCR (qRT-PCR). The results demonstrated significant alterations in the expression of key genes associated with cardiovascular development and function, providing mechanistic insights into DIM's toxic effects. In addition to cardiac abnormalities, DIM exposure led to a significant increase in the metabolic rate of the zebrafish embryos, indicating a potential disruption in energy homeostasis. To explore possible protective measures, a rescue experiment was performed using Astaxanthin, a potent antioxidant. Notably, Astaxanthin treatment partially mitigated the observed cardiac and metabolic phenotypes, suggesting its potential as a therapeutic agent to counteract DIM-induced toxicity. In summary, this study provides compelling evidence of the cardiovascular toxicity of DIM in zebrafish, highlighting its potential to disrupt cardiac function and metabolic regulation. The observed effects underscore the importance of re-evaluating the environmental impact of DIM and emphasize the need for further research to fully understand its mechanisms of toxicity. The findings also suggest that Astaxanthin (AST) could serve as a protective agent against DIM-induced toxicity, opening avenues for future studies aimed at mitigating the adverse effects of this widely used fungicide. This research study contributes to the growing body of knowledge on the environmental and health risks associated with pesticide use, advocating for more stringent regulations and safer alternatives.

International Journal of Molecular SciencesVol. 27(7)
Chung Yuan Christian University (TW), Chinese Culture University (TW), Kaohsiung Chang Gung Memorial Hospital (TW), University of Santo Tomas (PH), I-Shou University (TW)
Chung Yuan Christian University, National Science and Technology Council
Openalex Percentile: Top 23%
Environmental Toxicology and Ecotoxicology
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