Related Experiment Video
Updated: Oct 18, 2025
Using Immunofluorescence to Detect PM2.5-induced DNA Damage in Zebrafish Embryo Hearts
Published on: February 15, 2021
Cardiac developmental toxicity and transcriptome analyses of zebrafish (Danio rerio) embryos exposed to Mancozeb
Yongfeng Wang1, Zhiquan Yu1, Zunpan Fan1
1Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Hubei 430030, PR China.
Abstract:
Mancozeb (MZ), an antibacterial pesticide, has been linked to reproductive toxicity, neurotoxicity, and endocrine disruption. However, whether MZ has cardiactoxicity is unclear. In this study, the cardiotoxic effects of exposure to environment-related MZ concentrations ranging from 1.88 μM to 7.52 μM were evaluated at the larval stage of zebrafish. Transcriptome sequencing predicted the mechanism of MZ-induced cardiac developmental toxicity in zebrafish by enrichment analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). Consistent with morphological changes, the osm, pfkfb3, foxh1, stc1, and nrarpb genes may effect normal development of zebrafish heart by activating NOTCH signaling pathways, resulting in pericardial edema, myocardial fibrosis, and congestion in the heart area. Moreover, differential gene expression analysis indicated that cyp-related genes (cyp1c2 and cyp3c3) were significantly upregulated after MZ treatment, which may be related to apoptosis of myocardial cells. These results were verified by real-time quantitative RT-qPCR and acridine orange staining. Our findings suggest that MZ-mediated cardiotoxic development of zebrafish larvae may be related to the activation of Notch and apoptosis-related signaling pathways.
Insights
Mancozeb (MZ) pesticide exposure causes zebrafish heart defects by affecting Notch and apoptosis pathways. This study reveals potential cardiotoxicity from environmental MZ concentrations.
Area of Science:
- Environmental toxicology
- Developmental biology
- Cardiovascular research
Background:
- Mancozeb (MZ) is an antibacterial pesticide with known reproductive, neurotoxic, and endocrine-disrupting effects.
- The potential cardiotoxicity of Mancozeb remains largely unexplored.
- Zebrafish larvae are a valuable model for studying developmental toxicity.
Purpose of the Study:
- To investigate the cardiotoxic effects of environmentally relevant Mancozeb (MZ) concentrations on zebrafish larvae.
- To elucidate the molecular mechanisms underlying MZ-induced cardiac developmental toxicity.
Main Methods:
- Zebrafish larvae were exposed to MZ concentrations ranging from 1.88 μM to 7.52 μM.
- Transcriptome sequencing, KEGG, and GO enrichment analysis were used to predict molecular mechanisms.
- Real-time quantitative RT-qPCR and acridine orange staining validated gene expression and apoptosis.
Main Results:
- MZ exposure led to morphological changes including pericardial edema, myocardial fibrosis, and cardiac congestion in zebrafish larvae.
- Transcriptome analysis indicated that MZ activates NOTCH signaling pathways, involving genes like osm, pfkfb3, foxh1, stc1, and nrarpb.
- Upregulation of cyp-related genes (cyp1c2, cyp3c3) was observed, suggesting a role in myocardial cell apoptosis.
Conclusions:
- Mancozeb (MZ) exposure induces cardiotoxicity during zebrafish larval development.
- The cardiotoxic effects are associated with the activation of Notch signaling and apoptosis-related pathways.
- These findings highlight potential risks of environmental MZ exposure to cardiovascular development.
