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Diphenyl Phosphate-Induced Toxicity During Embryonic Development.

Constance A Mitchell1, Aalekhya Reddam1, Subham Dasgupta1

  • 1Department of Environmental Sciences , University of California , Riverside , California 92521 , United States.

Environmental Science & Technology
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This summary is machine-generated.

Diphenyl phosphate (DPHP), a metabolite of flame retardants, caused cardiac defects in developing zebrafish. This aryl phosphate ester disrupted mitochondrial function and lowered hemoglobin levels, indicating potential developmental toxicity.

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Area of Science:

  • Developmental Toxicology
  • Environmental Health
  • Cardiovascular Research

Background:

  • Diphenyl phosphate (DPHP) is a primary metabolite of aryl phosphate ester (APE) flame retardants.
  • Ubiquitous human exposure to DPHP occurs, yet DPHP-specific toxicity data is limited.
  • Understanding DPHP's impact on embryonic development is crucial due to widespread exposure.

Purpose of the Study:

  • To investigate the potential for DPHP to induce toxicity during embryonic development.
  • To assess DPHP's effects on cardiac development in zebrafish.
  • To elucidate the molecular mechanisms underlying DPHP-induced developmental toxicity.

Main Methods:

  • Zebrafish embryos were exposed to DPHP before and after cardiac looping.
  • Cardiac morphology was assessed by measuring the sinus venosus-bulbus arteriosus (SV-BA) distance.
  • mRNA sequencing was employed to analyze gene expression changes and pathway disruptions.
  • Hemoglobin levels were quantified in exposed zebrafish.

Main Results:

  • DPHP exposure significantly increased SV-BA distance, indicating cardiac defects.
  • DPHP disrupted pathways involved in mitochondrial function and heme biosynthesis.
  • Hemoglobin levels were significantly decreased in DPHP-exposed zebrafish.
  • DPHP's developmental toxicity was less potent than that of triphenyl phosphate (TPHP).

Conclusions:

  • DPHP adversely affects cardiac development in zebrafish embryos.
  • The mechanism involves disruption of mitochondrial function and heme biosynthesis pathways.
  • DPHP poses a developmental risk, though less potent than TPHP.