Impaired gas bladder inflation in zebrafish exposed to a novel heterocyclic brominated flame retardant tris(2,3-dibromopropyl) isocyanurate.

The teleost gas bladder is a gas-filled internal organ that processes gas exchange and controls buoyancy. Here we report that an emerging heterocyclic brominated flame retardant, tris(2,3-dibromopropyl) isocyanurate (TBC), causes defects in the inflation of the gas bladder of zebrafish larvae. This could cause impaired motility, which can ultimately lead to their death. Exposure to zebrafish embryos revealed that TBC had the most significant influence on the larvae at 72-96 h postfertilization, which coincided with the time that the gas bladder first inflates. Critical factors involved in early zebrafish gas bladder development remained at normal levels, which indicated that TBC caused defects in the inflation of the gas bladder without disrupting early organogenesis. However, the ultrastructure of the gas bladder was altered in the TBC-treated groups: the electron density of cytoplasmic vesicles was changed and the mitochondria were damaged. We deduce that TBC causes damage to mitochondria that influences the secretion of mucus-like material, resulting in defects in gas bladder inflation. For the first time, we report that the gas bladder could be a primary target organ for TBC, and assessment of the gas bladder should be included in toxicity testing protocols of zebrafish embryos.

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