Embryonic exposure to pentabromobenzene inhibited the inflation of posterior swim bladder in zebrafish larvae.
The emerging flame retardants pentabromobenzene (PBB) has been frequently detected in recent years and may pose exposure risks to wild animals and human beings. In this study, the inflation of posterior swim bladder of zebrafish larvae was used as an endpoint to study the developmental toxicity and putative mechanisms associated with PBB toxicity. Our results showed that embryonic exposure to PBB could significantly inhibit the inflation of posterior swim bladders. Reduced T3 levels and transcriptional changes of crh and pomc were observed in PBB treated zebrafish larvae at 120 hpf. However, key regulators of thyroid and adrenocortical system involved in the synthesis (tsh), biological conversion (ugt1ab, dio2) and functional regulation (trα, trβ, gr) showed no significant changes. Further data revealed that prlra was the only gene that was altered among the detected genes at 96 h post fertilization (hpf). At 120 hpf, the morphology of swim bladder indicated deflation in treatments at 0.25 μM and higher. In addition, the mRNA levels of anxa5, prlra, prlrb, atp1b2 and slc12a10 were all significantly changed at 120 hpf. Taken together, we suppose that embryonic exposure to PBB inhibited the inflation of swim bladder in zebrafish probably via prlra mediated pathways. The observed changes of thyroid and adrenocortical parameters might be indirect effects evoked by PBB exposure. Overall, our results provide important data and indications for future toxicological study and risk assessment of the emerging flame retardants PBB.