Developmental retardation, reduced fecundity, and modulated expression of the defensome in the intertidal copepod Tigriopus japonicus exposed to BDE-47 and PFOS

• The repercussions of BDE-47 and PFOS were occurred on development and fecundity.
• BDE-47 and PFOS can induce oxidative stress through the generation of ROS.
• The expression of defensome was changed in response to BDE-47 and PFOS.
• ROS-induced DNA damage in BDE-47 and PFOS exposure lead to apoptosis and DNA repair.

2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and perfluorooctane sulfonate (PFOS) are widely dispersed persistent organic pollutants (POPs) in the marine ecosystem. However, their toxic effects on marine organisms are still poorly understood. In this study, we investigated the effects of BDE-47 and PFOS on development and reproduction at the organismal level and reactive oxygen species (ROS) production and gene expression patterns of the defensome at the cellular level in the intertidal copepod Tigriopus japonicus. In copepods exposed to BDE-47 and PFOS, we observed developmental retardation and reduced fecundity, suggesting repercussions on in vivo endpoints through alterations to the normal molting and reproduction system of T. japonicus. BDE-47 and PFOS increased levels of ROS in T. japonicus in a concentration-dependent manner, indicating that POPs can induce oxidative stress through the generation of ROS. Additionally, transcript profiles of genes related to detoxification (e.g., CYPs), antioxidant functions (e.g., GST- sigma, catalase, MnSOD), apoptosis (e.g., p53, Rb), and cellular proliferation (e.g., PCNA) were modulated over 72 h in response to BDE-47 (120 μg/L) and PFOS (1000 μg/L). These findings indicate that BDE-47 and PFOS can induce oxidative stress-mediated DNA damage repair systems with transcriptional regulation of detoxification, antioxidant, and apoptosis-related genes, resulting in developmental retardation and reduced fecundity in the copepod T. japonicus.