Poly- and perfluoroalkyl substances (PFAS) are a class of endocrine disrupting chemicals (EDCs) reported to alter thyroid function. Iodide uptake by thyroid follicular cells, an early step in the synthesis of thyroid hormones, is a potential target for thyroid disruption by EDCs. The aim of the present study was to evaluate the acute effects of perfluorooctane sulfonic acid (PFOS) and perfluorooctane carboxylic acid (PFOA), two of the most abundant PFAS in the environment, on iodide transport by thyroid follicular cells in vitro. Dynamic changes in intracellular iodide concentration were monitored by live cell imaging using YFP-H148Q/I152, a genetically encoded fluorescent iodide biosensor. PFOS, but not PFOA, acutely and reversibly inhibited iodide accumulation by FRTL-5 thyrocytes, as well as by HEK-293 cells transiently expressing the Sodium Iodide Symporter (NIS). PFOS prevented NIS-mediated iodide uptake and reduced intracellular iodide concentration in iodide-containing cells, mimicking the effect of the NIS inhibitor perchlorate. PFOS did not affect iodide efflux from thyroid cells. The results of this study suggest that disruption of iodide homeostasis in thyroid cells may be a potential mechanism for anti-thyroid health effects of PFOS. The study also confirms the utility of the YFP-H148Q/I152 cell-based assay to screen environmental PFAS, and other EDCs, for anti-thyroid activity.

聚全氟烷基物质（PFAS）是一类内分泌干扰化学物质（EDC），据报道会改变甲状腺功能。甲状腺滤泡细胞摄取碘化物是甲状腺激素合成的早期步骤，是EDC破坏甲状腺的潜在目标。本研究的目的是评估全氟辛烷磺酸（PFOS）和全氟辛烷羧酸（PFOA）（环境中两种最丰富的PFAS）对甲状腺滤泡细胞在体外碘化物转运的急性作用。。使用YFP-H148Q / I152（一种基因编码的荧光碘化物生物传感器）通过活细胞成像监测细胞内碘化物浓度的动态变化。全氟辛烷磺酸（而非全氟辛烷磺酸）不但可逆地抑制FRTL-5甲状腺细胞以及瞬时表达碘化钠转运蛋白（NIS）的HEK-293细胞的碘化物积累。全氟辛烷磺酸可防止NIS介导的碘化物吸收并降低含碘化物细胞中细胞内碘化物的浓度，从而模仿NIS抑制剂高氯酸盐的作用。全氟辛烷磺酸不影响甲状腺细胞的碘流出。这项研究的结果表明，破坏甲状腺细胞中的碘稳态可能是全氟辛烷磺酸抗甲状腺健康作用的潜在机制。这项研究还证实了基于YFP-H148Q / I152细胞的测定法可用于筛选环境PFAS和其他EDC，