6:2 Chlorinated polyfluorinated ether sulfonate, a PFOS alternative, induces embryotoxicity and disrupts cardiac development in zebrafish embryos

• Published in: Aquatic toxicology Vol. 185; pp. 67 - 75
• Main Authors: Shi, Guohui, Cui, Qianqian, Pan, Yitao, Sheng, Nan, Sun, Sujie, Guo, Yong, Dai, Jiayin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-04-2017
• Subjects: Alkanesulfonates - chemistry; Alkanesulfonates - toxicity; Alkanesulfonic Acids - chemistry; Alkanesulfonic Acids - toxicity; Animals; Cardiac development; Developmental toxicity; Embryo, Nonmammalian - drug effects; Embryo, Nonmammalian - metabolism; Erythrocytes - drug effects; F-53B; Fluorocarbons - chemistry; Fluorocarbons - toxicity; Gene Expression Regulation, Developmental - drug effects; Heart - drug effects; Heart - embryology; Larva - drug effects; RNA, Messenger - genetics; RNA, Messenger - metabolism; Water Pollutants, Chemical - toxicity; Wnt signaling pathway; Zebrafish; Zebrafish - embryology; Zebrafish - genetics; Zebrafish Proteins - genetics; Zebrafish Proteins - metabolism; Zebrafish; Cardiac development; F-53B; Wnt signaling pathway; Developmental toxicity
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/j.aquatox.2017.02.002

•F–53B caused delayed hatching, increased the occurrence of malformations, and reduced survival.•Exposure to 3mg/L F–53B resulted in high accumulation of the compound in zebrafish embryos.•F–53B induced cardiac toxicity and reduced heart rate.•F–53B might affect Wnt signaling pathway and decrease the erythrocyte numbers.
As an alternative to perfluorooctanesulfonate (PFOS), 6:2 chlorinated polyfluorinated ether sulfonate (commercial name: F-53B) has been used as a mist suppressant in Chinese electroplating industries for over 30 years. It has been found in the environment and fish, and one acute assay indicated F–53B was moderately toxic. However, the toxicological information on this compound was incomplete and insufficient for assessment of their environment impact. The object of this study was to examine the developmental toxicity of F–53B using zebrafish embryos. Zebrafish embryos were incubated in 6-well plates with various concentrations of F–53B (1.5, 3, 6, and 12mg/L) from 6 to 132h post fertilization (hpf). Results showed that F–53B exposure induced developmental toxicity, including delayed hatching, increased occurrence of malformations, and reduced survival. Malformations, including pericardial and yolk sac edemas, abnormal spines, bent tails, and uninflated swim bladders, appeared at 84 hpf, and increased with time course and dose. A decrease in survival percentages was noted in the 6 and 12mg/L F-53B-treated groups at 132 hpf. Continuous exposure to 3mg/L F–53B resulted in high accumulation levels in zebrafish embryos, suggesting an inability for embryos to eliminate this compound and a high cumulative risk to fish. We also examined the cardiac function of embryos at specific developmental stages following exposure to different concentrations, and found that F–53B induced cardiac toxicity and reduced heart rate. Even under low F–53B concentration, o-dianisidine staining results showed significant decrease of relative erythrocyte number at 72 hpf before the appearance of observed effects of F–53B on the heart. To elucidate the underlying molecular changes, genes involved in normal cardiac development were analyzed using real-time qPCR in the whole-body of zebrafish embryos. F–53B inhibited the mRNA expression of β-catenin (ctnnb2) and wnt3a. The mRNA levels of β-catenin targeted genes (nkx2.5 and sox9b), which play critical roles in cardiogenesis, were also reduced after exposure. Thus, exposure to F–53B impaired the development of zebrafish embryos and disrupted cardiac development, which might be mediated by effects on the Wnt signaling pathway and decrease of erythrocyte numbers.