PUBLICATION
            Bifenazate exposure induces cardiotoxicity in zebrafish embryos
- Authors
- Ma, J., Huang, Y., Peng, Y., Xu, Z., Wang, Z., Chen, X., Xie, S., Jiang, P., Zhong, K., Lu, H.
- ID
- ZDB-PUB-210209-3
- Date
- 2021
- Source
- Environmental pollution (Barking, Essex : 1987) 274: 116539 (Journal)
- Registered Authors
- Lu, Huiqiang
- Keywords
- Bifenazate, Calcium signaling pathway, Cardiotoxicity, Heart failure, Oxidative stress
- MeSH Terms
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                - Animals
- Carbamates/metabolism
- Hydrazines
- Oxidative Stress
- Cardiotoxicity*/metabolism
- Embryo, Nonmammalian/metabolism
- Zebrafish*
 
- PubMed
- 33549839 Full text @ Environ. Pollut.
            Citation
        
        
            Ma, J., Huang, Y., Peng, Y., Xu, Z., Wang, Z., Chen, X., Xie, S., Jiang, P., Zhong, K., Lu, H. (2021) Bifenazate exposure induces cardiotoxicity in zebrafish embryos. Environmental pollution (Barking, Essex : 1987). 274:116539.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Bifenazate is a novel acaricide for selective foliar spraying and is widely used to control mites in agricultural production. However, its toxicity to aquatic organisms is unknown. Here, a zebrafish model was used to study bifenazate toxicity to aquatic organisms. Exposure to bifenazate was found to cause severe cardiotoxicity in zebrafish embryos, along with disorders in the gene expression related to heart development. Bifenazate also caused oxidative stress. Cardiotoxicity caused by bifenazate was partially rescued by astaxanthin (an antioxidant), accompanied by cardiac genes and oxidative stress-related indicators becoming normalized. Our results showed that exposure to bifenazate can significantly change the ATPase activity and gene expression levels of the calcium signaling pathway. These led to heart failure, in which the blood accumulated outside the heart without entering it, eventually leading to death. The results indicated that bifenazate exposure caused cardiotoxicity in zebrafish embryos through the induction of oxidative stress and inhibition of the calcium signaling pathway.
            
    
        
        
    
    
    
                
                    
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                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    