title: Thyroid disruption effects of environmental level perfluorooctane sulfonates (PFOS) in Xenopus laevis.
abstract: Perfluorooctane sulfonate (PFOS), one of the emerging persistent organic pollutants (POPs), has caused growing international concern especially related to the potential disruption in the development and function of thyroid system. Xenopus laevis is an amphibian species widely used as a suitable amphibian model for thyroid disruption research. To study the thyroid disruption effects related to PFOS exposure at environmental low levels, X. laevis tadpoles were exposed to 0.1, 1, 10 and 100 μg/l PFOS in water respectively from stage 46/47 to stage 62. The results showed that the time to metamorphosis (presented by forelimb emergence, FLE) did not significantly change with PFOS exposure, but exhibited an increasing trend (except for 10 μg/l exposure). Partial colloid depletion was observed for PFOS exposure, but no significant histological abnormality was observed in treatment groups. In addition, PFOS exposure resulted in up-regulation of thyroid hormone-regulated genes-thyroid receptor beta A (TRβA), basic transcription element-binding protein (BTEB) and type II deiodinase (DI2) mRNA expression, presented as an inverted U-shaped dose response pattern. However, the mRNA expression of type III deiodinase (DI3) remained unaffected compared with the control. These results demonstrated that PFOS might disrupt the thyroid system in X. laevis tadpoles regarding FLE changes and regulation alternation of thyroid hormone-regulated genes. Our study has raised new concerns for possible thyroid disruption of PFOS in amphibians at environmental relevant levels.
authors.affiliation: Research Center for Import-Export Chemicals Safety of General Administration of Quality Supervision, Inspection and Quarantine of People's Republic of China, Chinese Academy of Inspection and Quarantine, Chaoyang District, Beijing, 100123, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Cheng
authors.forename: Yuan
authors.initials: Y
authors.lastname: Cui
authors.forename: Hui-ming
authors.initials: HM
authors.lastname: Chen
authors.forename: Wen-ping
authors.initials: WP
authors.lastname: Xie
mesh_terms: D017738:Alkanesulfonic Acids / Q000633:toxicity*; D000818:Animals; D001921:Brain / Q000187:drug effects; D004268:DNA-Binding Proteins / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D004781:Environmental Exposure; D005260:Female; D005466:Fluorocarbons / Q000633:toxicity*; D005786:Gene Expression Regulation / Q000187:drug effects; D007453:Iodide Peroxidase / Q000235:genetics; D007814:Larva / Q000187:drug effects; D008297:Male; D008675:Metamorphosis, Biological / Q000187:drug effects*; D013623:Tail / Q000187:drug effects; D013961:Thyroid Gland / Q000187:drug effects* / Q000473:pathology; D037042:Thyroid Hormone Receptors beta / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D029867:Xenopus Proteins / Q000235:genetics; D014982:Xenopus laevis / Q000502:physiology*; D000097564:Iodothyronine Deiodinase Type II
chemical_list: D017738:Alkanesulfonic Acids; D004268:DNA-Binding Proteins; D052244:Endocrine Disruptors; D005466:Fluorocarbons; D007453:Iodide Peroxidase; D037042:Thyroid Hormone Receptors beta; D014157:Transcription Factors; D029867:Xenopus Proteins; D000097564:Iodothyronine Deiodinase Type II; C489674:KLF9 protein, Xenopus; C076994:perfluorooctane sulfonic acid; C117274:iodothyronine deiodinase type III