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Hindbrain defects induced by Di-butyl phthalate (DBP) in developing zebrafish embryos
Evelyn Paquette1, Naomi Mumper1, Alissa Rodrigues1
1Department of Biology, Sacred Heart University, Fairfield, CT, United States of America.
Neurotoxicology and Teratology
|April 27, 2022
Summary
Di-butyl phthalate (DBP) is a common plasticizer leaching into aquatic environments. DBP exposure during zebrafish embryonic development disrupts hindbrain structure and cranial motor neuron patterning.
Area of Science:
- Environmental toxicology
- Developmental neurobiology
- Aquatic toxicology
Background:
- Di-butyl phthalate (DBP) is a widespread plasticizer contaminating soil and water.
- Phthalates leach into aquatic ecosystems due to their non-covalent binding to plastic polymers.
- While endocrine disruption by DBP is studied, its developmental neurotoxicity is less understood.
Purpose of the Study:
- To investigate the developmental neurotoxicity of Di-butyl phthalate (DBP) in zebrafish embryos.
- To assess the impact of environmentally relevant DBP concentrations on neurodevelopment.
Main Methods:
- Zebrafish embryos at pre-gastrulation stage were exposed to 2.5 μM DBP.
- Hindbrain structure, rhombomere patterning, and cranial motor neuron development were analyzed at 72 hours post fertilization (hpf).
- Specific focus on branchiomotor neuron and Mauthner neuron (r4) development.
Main Results:
- DBP exposure disrupted general hindbrain structure and rhombomere patterning.
- Defects in the patterning and migration of hindbrain-specific cranial motor neurons were observed.
- Developmental abnormalities in r4-specific Mauthner neurons were identified.
Conclusions:
- Embryonic exposure to Di-butyl phthalate (DBP) induces significant hindbrain defects.
- DBP impacts the development and differentiation of neurons originating in the hindbrain.
- This study highlights the potential neurodevelopmental risks of DBP in aquatic environments.

