Fig. 5

Schematic diagram illustrating the mechanisms by which PFOA exposure disrupts thyroid hormone synthesis. In the physiological state, TSH triggers TSH-dependent signalings to regulate gene expression and protein glycosylation of NIS, which is responsible for iodide uptake and is the critical molecule for thyroid hormone synthesis. Thyroid hormones exert their effects on target cells throughout multiple systems to regulate various physiological processes, including metabolism, growth, and development of the body. Exposure to PFOA can disrupt the glycosylation process of NIS, which in turn inhibits the translocation of NIS to the plasma membrane. This inhibition leads to a decrease in the uptake of iodide and subsequently results in reduced levels of thyroid hormones in zebrafish larvae. TSH: Thyroid Stimulating Hormone; TSHR: Thyroid Stimulating Hormone Receptor; NIS: Na+ /I− Symporter; TR: Thyroid Hormone Receptor; I-: iodide ion; PFOA: Perfluorooctanoic Acid.