Parental exposure to bisphenol A affects pharyngeal cartilage development and causes global transcriptomic changes in...

As one of the most common endocrine-disrupting chemicals (EDCs), bisphenol A (BPA) is a threat to aquatic ecosystems. Despite a rich literature addressing the adverse effects of BPA on various systems in fish models, the potential impact of parental BPA exposure on offspring pharyngeal cartilage development is poorly understood.

Adult zebrafish (F0) were exposed to BPA (1.0 μM) or control for 7 days. Eggs (F1) were collected and exposed to BPA (control, 0.05, 0.1, 1, 10 μM) until 120 h post-fertilization. Histomorphometrical essay was used to quantitatively and qualitatively assess the effects of BPA on pharyngeal cartilage development. RNA sequencing (RNA-seq) was used to discover differentially expressed genes (DEGs), and KEGG pathway and GO enrichment analysis were performed to interpret functional ontology.

Parental BPA exposure affected hatchability and heart rates of F1 progeny. By pathology analysis, parental BPA exposure caused craniofacial deformity, characterized by wider angles of cartilage elements, disrupted pharyngeal chondrocytes and promoted apoptosis and elongation of head length. RNA-seq suggested that many DEGs were involved in multiple biological processes and signaling pathways; defense responses, reactive oxygen species metabolic process, apoptosis, p53 signaling pathway and MAPK signaling pathway were closely associated with the toxicity of parental BPA exposure.

Parental BPA exposure affected chondrogenesis in the viscerocranium of zebrafish offspring and led to global transcriptomic changes involved in apoptosis, hyperplasia and oxidative stress. These newly identified gene expression patterns, pathways and gene networks of zebrafish eleutheroembryos after early-life waterborne BPA exposure, may lead to severe and permanent morphological and functional consequences.