Binary exposure to hypoxia and perfluorobutane sulfonate disturbs sensory perception and chromatin topography in marine medaka embryos

Perfluorobutane sulfonate (PFBS), an environmental pollutant of emerging concern, is previously shown to dynamically interact with hypoxia on aquatic developmental toxicities. However, the molecular mechanisms underlying the interaction remain unknown. In this follow-up study, marine medaka embryos were exposed to 0 and 3.3 mg/L of PFBS under normoxia (6.9 mg/L) or hypoxia (1.7 mg/L) condition till 15 days post-fertilization. High-throughput transcriptomic sequencing was employed to filter differentially expressed genes and provide mechanistic insight into interactive action between hypoxia and PFBS. The results showed that hypoxia alone and the coexposure paradigm were similarly potent to modify transcriptional profiles, with the majority of genes significantly down-regulated. In contrast, transcriptional toxicity of PFBS was relatively milder. Functional annotation analyses found that hypoxia and coexposure groups mainly impacted phototransduction signaling by decreasing the transcriptions of cyclic nucleotide-gated (CNG) cation channels and retinol transport genes. However, this study demonstrated the first toxicological evidence that toxic effects of PFBS targeted the perception of chemical stimulus through olfactory and gustatory receptors. The addition of PFBS moderately exacerbated the toxic actions of hypoxia, which largely shaped the transcriptional pattern of coexposure group. In addition, gene interactive networks were constructed for hypoxia and coexposure groups, underlining the increased chromatin deacetylation and methylation to epigenetically repress genome-wide transcriptional initiation. Overall, PFBS and hypoxia interact to interrupt the embryonic development of sensory systems, which may compromise the individual fitness and survival, especially during early life stages when precocious perception of food and escape from predators are essential. Copyright © 2020 Elsevier Ltd. All rights reserved.