State Key Laboratory of Freshwater Ecology and Biotechnology , Institute of Hydrobiology, Chinese Academy of Sciences , Wuhan 430072 , China.
School of Chemistry and Environmental Engineering , Wuhan Institute of Technology , Wuhan 430072 , China.
Environ Sci Technol. 2018 Apr 3;52(7):4432-4439. doi: 10.1021/acs.est.8b00700. Epub 2018 Mar 26.
Accumulation of perfluorobutanesulfonate (PFBS) is frequently detected in biota, raising concerns about its ecological safety. However, hazardous effects of PFBS remain largely unexplored, especially for endocrine disrupting potency. In the present study, the multigenerational endocrine disrupting potential of PFBS was investigated by exposing F0 marine medaka eggs to PFBS at different concentrations (0, 1.0, 2.9, and 9.5 μg/L) until sexual maturity. The F1 and F2 generations were reared without continued exposure. Thyroidal disturbances were examined in all three generations. PFBS exposure decreased the levels of 3,5,3'-triiodothyronine (T3) in F0 female blood; however, it increased T3 or thyroxine (T4) levels in F0 brains, in which hyperthyroidism suppressed the local transcription of 5'-deiodinase 2 ( Dio2). Obviously decreased T3 was transferred to F1 eggs, although the parental influences were reversed in F1 larvae. Delayed hatching was coupled with elevated T3 levels in F1 larvae. F1 adults showed comparable symptoms of thyroidal disruption with F0 adults. A slight recovery was noted in the F2 generation, although F2 larvae still exhibited thyroid disruption and synthesized excessive T4. Our results suggested that the offspring suffered more severe dysfunction of the thyroidal axis albeit without direct exposure. This study provided the first molecular insight about PFBS toxicology on the thyroid, beneficial to both human and environmental risk assessment.
全氟丁烷磺酸 (PFBS) 在生物体内经常被检测到,这引起了人们对其生态安全性的关注。然而,PFBS 的危害性影响在很大程度上仍未得到探索,尤其是其对内分泌系统的干扰作用。在本研究中,通过将 F0 海洋斑马鱼卵暴露于不同浓度(0、1.0、2.9 和 9.5μg/L)的 PFBS 中直至性成熟,研究了 PFBS 的多代内分泌干扰潜力。F1 和 F2 代在没有持续暴露的情况下进行繁殖。在所有三代中都检查了甲状腺紊乱情况。PFBS 暴露降低了 F0 雌性血液中的 3,5,3'-三碘甲状腺原氨酸 (T3) 水平;然而,它增加了 F0 大脑中的 T3 或甲状腺素 (T4) 水平,其中甲状腺功能亢进抑制了 5'-脱碘酶 2 (Dio2) 的局部转录。明显减少的 T3 被转移到 F1 卵中,尽管在 F1 幼虫中出现了亲本影响的逆转。F1 幼虫的孵化延迟伴随着 T3 水平升高。F1 成虫表现出与 F0 成虫相似的甲状腺紊乱症状。在 F2 代中观察到轻微的恢复,尽管 F2 幼虫仍表现出甲状腺紊乱并合成过多的 T4。我们的研究结果表明,尽管没有直接暴露,但后代的甲状腺轴功能障碍更为严重。这项研究首次提供了关于 PFBS 对甲状腺毒性的分子见解,有助于人类和环境风险评估。