School of Municipal and Environmental Engineering, Harbin Institute of Technology, Harbin 150090, China; School of public health, Jia Mu Si University, Jiamusi 154007, China.
School of Municipal and Environmental Engineering, Harbin Institute of Technology, Harbin 150090, China.
J Environ Sci (China). 2016 Sep;47:153-164. doi: 10.1016/j.jes.2016.01.018. Epub 2016 Mar 9.
Perfluorooctane sulfonate (PFOS) and ZnO nanoparticles (nano-ZnO) are widely distributed in the environment. However, the potential toxicity of co-exposure to PFOS and nano-ZnO remains to be fully elucidated. The test investigated the effects of co-exposure to PFOS and nano-ZnO on the hypothalamic-pituitary-thyroid (HPT) axis in zebrafish. Zebrafish embryos were exposed to a combination of PFOS (0.2, 0.4, 0.8mg/L) and nano-ZnO (50mg/L) from their early stages of life (0-14days). The whole-body content of TH and the expression of genes and proteins related to the HPT axis were analyzed. The co-exposure decreased the body length and increased the malformation rates compared with exposure to PFOS alone. Co-exposure also increased the triiodothyronine (T3) levels, whereas the thyroxine (T4) content remained unchanged. Compared with the exposure to PFOS alone, exposure to both PFOS (0.8mg/L) and nano-ZnO (50mg/L) significantly up-regulated the expression of corticotropin-releasing factor, sodium/iodidesymporter, iodothyronine deiodinases and thyroid receptors and significantly down-regulated the expression of thyroid-stimulating hormone, thyroglobulin (TG), transthyretin (TTR) and thyroid receptors. The protein expression levels of TG and TTR were also significantly down-regulated in the co-exposure groups. In addition, the expression of the thyroid peroxidase gene was unchanged in all groups. The results demonstrated that PFOS and nano-ZnO co-exposure could cause more serious thyroid-disrupting effects in zebrafish than exposure to PFOS alone. Our results also provide insight into the mechanism of disruption of the thyroid status by PFOS and nano-ZnO.
全氟辛烷磺酸 (PFOS) 和氧化锌纳米粒子 (nano-ZnO) 广泛分布于环境中。然而，PFOS 和 nano-ZnO 共同暴露的潜在毒性仍需充分阐明。本试验研究了 PFOS 和 nano-ZnO 共同暴露对斑马鱼下丘脑-垂体-甲状腺 (HPT) 轴的影响。斑马鱼胚胎从生命早期 (0-14 天) 开始就同时暴露于 PFOS(0.2、0.4、0.8mg/L) 和 nano-ZnO(50mg/L)。分析了全甲状腺素 (TH) 含量和与 HPT 轴相关的基因和蛋白的表达。与单独暴露于 PFOS 相比，共同暴露降低了体长，增加了畸形率。共同暴露还增加了三碘甲状腺原氨酸 (T3) 水平，而甲状腺素 (T4) 含量保持不变。与单独暴露于 PFOS 相比，同时暴露于 PFOS(0.8mg/L)和 nano-ZnO(50mg/L)显著上调了促肾上腺皮质释放因子、钠/碘转运体、甲状腺素脱碘酶和甲状腺受体的表达，显著下调了促甲状腺激素、甲状腺球蛋白 (TG)、转甲状腺素蛋白 (TTR) 和甲状腺受体的表达。共同暴露组 TG 和 TTR 的蛋白表达水平也明显下调。此外，所有组的甲状腺过氧化物酶基因表达均无变化。结果表明，PFOS 和 nano-ZnO 共同暴露比单独暴露于 PFOS 对斑马鱼甲状腺的破坏作用更严重。我们的结果还为 PFOS 和 nano-ZnO 破坏甲状腺状态的机制提供了新的见解。
