Parental exposure to 6:2 chlorinated polyfluorinated ether sulfonate (F-53B) induced transgenerational thyroid hormone disruption in zebrafish.

Abstract Although 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), an alternative to perfluorooctanesulfonate (PFOS), has been regularly detected in different environmental matrices, information regarding its toxicity remains limited. To explore the transgenerational thyroid-disrupting capacity of F-53B, adult zebrafish (F0) were exposed to different concentrations of F-53B (0, 5, 50, or 500 μg/L) for 180 d, with their offspring (F1 and F2) subsequently reared in uncontaminated water. Thyroid disturbances were then examined in the three (F0, F1, and F2) generations. For F0 adult fish, thyroxine (T4) increased in both sexes after exposure to 50 μg/L F-53B, whereas 3,5,3′-triiodothyronine (T3) decreased in all groups, except for 50 μg/L F-53B-treated males. For F1 embryos, parental exposure resulted in F-53B transfer as well as an increase in T4 content. At 5 days post-fertilization, the significant increase in T4 and decrease in T3 were accompanied by a decrease in body length, increase in mortality, and increase in uninflated posterior swim bladder occurrence in F1 larvae. Although thyroid hormone levels were not changed significantly in F1 adult fish or F2 offspring compared with the control, the transcription levels of several genes along the hypothalamus-pituitary-thyroid axis were significantly modified. Our study demonstrated that F-53B possesses transgenerational thyroid-disrupting capability in zebrafish, indicating it might not be a safer alternative to PFOS. Graphical abstract Unlabelled Image Highlights • F-53B exposure disrupted the balance of thyroid hormone levels in F0 adult fish. • Increased T4 levels in F1 eggs were consistent with the T4 level of F0 female serum. • Parental exposed to F-53B altered THs and the HPT axis genes expression in F1 larvae. • Change of TH levels companied with defected swim bladder in F1 larvae. • The change of some HPT axis genes expression still present in F1 adult and F2 larvae. [ABSTRACT FROM AUTHOR]