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Decabromodiphenyl ethane induced hyperactivity in developing zebrafish at environmentally relevant concentrations.

Jianghuan Hua1, Xiulin Wang2, Jiaping Zhu3

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Summary

Decabromodiphenyl ethane (DBDPE) exposure in zebrafish embryos caused developmental neurotoxicity, leading to hyperactivity. Higher concentrations disrupted the cholinergic system, suggesting potential ecological risks.

Keywords:
Decabromodiphenyl ethaneDevelopmental toxicityHyperactivityMotor behaviorZebrafish embryos/larvae

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Area of Science:

  • Environmental Science
  • Toxicology
  • Neuroscience

Background:

  • Decabromodiphenyl ethane (DBDPE) is a widely used flame retardant with increasing environmental presence.
  • Concerns exist regarding its potential developmental neurotoxicity and bioaccumulation in biota.

Purpose of the Study:

  • To investigate the developmental neurotoxicity of DBDPE in zebrafish embryos.
  • To elucidate the underlying mechanisms of DBDPE-induced neurotoxicity at different concentrations.

Main Methods:

  • Zebrafish embryos were exposed to varying concentrations of DBDPE (2.91–97.12 μg/L) until 120 hours post-fertilization.
  • Assessed body burdens, bioaccumulation factors, locomotor activity, neurotransmitter levels, protein expression, and performed molecular docking.

Main Results:

  • DBDPE exposure led to concentration-dependent bioaccumulation and hyperactivity in zebrafish larvae.
  • Lower DBDPE concentrations decreased neurotransmitters and specific proteins, while higher concentrations increased acetylcholine and ChAT activity, inhibiting nAChRs.
  • Molecular docking suggested interactions between DBDPE and α1-TUBULIN, SYN2a, and ChAT.

Conclusions:

  • DBDPE induces developmental neurotoxicity and hyperactivity in zebrafish, with distinct mechanisms at lower and higher exposure levels.
  • Higher concentrations likely disrupt the cholinergic system, with ChAT as a potential target.
  • Findings provide insights for ecological risk assessment of DBDPE.