Tetrabromobisphenol A (TBBPA), a ubiquitous environmental pollutant, has been implicated in developmental toxicity of aquatic animals. However, the impact of TBBPA on development and the related mechanism have not been fully elucidated. In this study, using a live imaging technique and transgenic labeling of zebrafish embryos, we described the toxic effects of TBBPA on hematopoietic development in zebrafish. We demonstrated that TBBPA induced erythroid precursor expansion in the intermediate cell mass (ICM), which perturbed the onset of blood circulation at 24–26 hours postfertilization (hpf). Consequently, excessive blood cells accumulated in the posterior blood island (PBI) and vascular cells formed defective caudal veins (CVs), preventing blood cell flow to the heart at 32–34 hpf. We found that the one-cell to 50% epiboly stage was the most sensitive period to TBBPA exposure during hematopoietic development. Furthermore, our results demonstrated that PBI malformation induced by TBBPA resulted from effects on erythroid precursor cells, which might involve THR signaling in complex ways. These findings will improve the understanding of TBBPA-induced developmental toxicity in teleost.
Phenanthrene (Phe) is one of the common polycyclic aromatic hydrocarbons in the environment, and recent studies show that it can cause cardiac developmental toxicity and immunotoxicity. However, it is still unknown whether it can affect the hematopoietic development in aquatic organisms. To address this question, zebrafish ( Danio rerio ) were chronically exposed to Phe at different concentrations. We found that Phe caused structural damage to the renal tubules in the kidney, induced malformed erythrocyte in peripheral blood, and decreased proportion of myeloid cells in adult zebrafish, suggesting possible negative impacts that Phe posed to hematopoietic development. Then, using in situ hybridization technology, we found that Phe decreased the expression of primitive hematopoietic marker genes, specifically gata1 and pu.1 , accompanied by an obstruction of primitive erythrocyte circulation. Furthermore, Phe impaired definitive hematopoiesis, increased aberrations of the transient hematopoietic site (PBI), and reduced the generation of hematopoietic stem cells, ultimately influencing the number of erythrocytes and myeloid cells. The findings suggested that Phe could induce hematopoietic toxicity in zebrafish embryos and pose unknown ecological risks.
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