PUBLICATION
            Diphenyl Phosphate-Induced Toxicity During Embryonic Development
- Authors
 - Mitchell, C.A., Reddam, A., Dasgupta, S., Zhang, S., Stapleton, H.M., Volz, D.C.
 - ID
 - ZDB-PUB-190314-15
 - Date
 - 2019
 - Source
 - Environmental science & technology 53(7): 3908-3916 (Journal)
 - Registered Authors
 - Keywords
 - none
 - MeSH Terms
 - 
    
        
        
            
                
- Flame Retardants*
 - Embryonic Development*
 - Animals
 - Humans
 - Biphenyl Compounds
 - Phosphates
 
 - PubMed
 - 30864794 Full text @ Env. Sci. Tech.
 - CTD
 - 30864794
 
            Citation
        
        
            Mitchell, C.A., Reddam, A., Dasgupta, S., Zhang, S., Stapleton, H.M., Volz, D.C. (2019) Diphenyl Phosphate-Induced Toxicity During Embryonic Development. Environmental science & technology. 53(7):3908-3916.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Diphenyl phosphate (DPHP) is an aryl phosphate ester (APE) used as an industrial catalyst and chemical additive, and is the primary metabolite of flame retardant APEs, including triphenyl phosphate (TPHP). Minimal DPHP-specific toxicity studies have been published despite ubiquitous exposure within human populations following metabolism of TPHP and other APEs. Therefore, the objective of this study was to determine the potential for DPHP-induced toxicity during embryonic development. Using zebrafish as a model, we found that DPHP significantly increased the distance between the sinus venosus and bulbus arteriosis (SV-BA) at 72 h post-fertilization (hpf) following initiation of exposure before and after cardiac looping. Interestingly, pretreatment with D-mannitol mitigated DPHP-induced effects on SV-BA length despite the absence of DPHP effects on pericardial area, suggesting that DPHP-induced cardiac defects are independent of pericardial edema formation. Using mRNA-sequencing, we found that DPHP disrupts pathways related to mitochondrial function and heme biosynthesis; indeed, DPHP significantly decreased hemoglobin levels in situ at 72 hpf following exposure from 24-72 hpf. Overall, our findings suggest that, similar to TPHP, DPHP impacts cardiac development, albeit the potency of DPHP is significantly less than TPHP within developing zebrafish.
            
    
        
        
    
    
    
                
                    
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