ZFIN ID: ZDB-PUB-180923-12
Transgenerational thyroid endocrine disruption induced by bisphenol S affects the early development of zebrafish offspring
Wei, P., Zhao, F., Zhang, X., Liu, W., Jiang, G., Wang, H., Ru, S.
Date: 2018
Source: Environmental pollution (Barking, Essex : 1987)   243: 800-808 (Journal)
Registered Authors:
Keywords: Bisphenol S, Thyroid endocrine disruption, Transgenerational toxicity, Zebrafish
MeSH Terms:
  • Animals
  • Embryo, Nonmammalian/drug effects
  • Embryonic Development/drug effects
  • Endocrine Disruptors/toxicity
  • Female
  • Larva/drug effects
  • Male
  • Organogenesis/drug effects
  • Phenols/toxicity*
  • Sulfones/toxicity*
  • Thyroid Gland/drug effects*
  • Thyroid Hormones/blood
  • Thyroxine/blood
  • Water Pollutants, Chemical/toxicity
  • Zebrafish/embryology*
PubMed: 30243188 Full text @ Environ. Pollut.
Maternal thyroid hormones (THs) play an essential role in the embryonic and larval development of fish. Previous studies in fish have reported that parental exposure to thyroid disrupting chemicals (TDCs) changed maternal TH levels in the offspring; however, whether this transgenerational thyroid endocrine disruption can further disturb the early development of the offspring still remains largely unknown. Bisphenol S (BPS), a substitute of bisphenol A, has been reported to be a potential TDC. In this study, zebrafish (F0) were exposed to environmentally relevant concentrations (1, 10, and 100 μg/L) of BPS from 2 h post-fertilization to 120 days post-fertilization and then paired to spawn. Plasma levels of thyroxine (T4) were significantly decreased in F0 females while 3,5,3'-triiodothyronine (T3) plasma levels were significantly increased in F0 females and males; moreover, TH content in eggs (F1) spawned by exposed F0 generation exhibited similar changes as the F0 females, with significant decreases in T4 and increases in T3, demonstrating BPS-induced maternal transfer of thyroid endocrine disruption. Further, excessive levels of maternal T3 in the offspring resulted in delayed embryonic development and hatching, swim bladder inflation defect, reduction in motility, developmental neurotoxicity, and lateral stripe hypopigmentation in non-exposed F1 embryos and larvae. These results highlight the adverse effects on the early development of offspring induced by transgenerational thyroid endocrine disruption, which have been ignored by previous studies. Therefore, these results can further improve our understanding of the ecological risks of TDCs.