摘要
全氟辛烷基磺酸钾(PFOS)和纳米氧化锌(Nano-Zn O)广泛存在于环境中,但是它们复合暴露对水生生物的潜在毒性机制尚未明确。本文探讨PFOS和Nano-Zn O复合暴露对斑马鱼下丘脑-垂体-甲状腺轴(HPT轴)毒性的影响。将斑马鱼胚胎从孵化开始暴露于PFOS(0.2、0.4、0.8 mg·L^(-1))、Nano-Zn O(6.75、12.5、25 mg·L^(-1))、PFOS+Nano-Zn O(0.2+6.75、0.4+12.5、0.8+25 mg·L^(-1))溶液中15 d后,分析幼鱼的发育毒性,体内的甲状腺激素(甲状腺素(T4)和三碘甲状腺氨酸(T3)含量和与甲状腺有关基因(CRF、TSH、NIS、TG和TPO)的表达情况。结果发现复合暴露组与单独暴露组相比,前者显著诱导了幼鱼的畸形率,降低了幼鱼的存活率,并抑制了幼鱼的体长。复合暴露组显著增加了幼鱼体内T3含量,同时抑制体内T4的含量。与单独暴露组相比,复合暴露组显著诱导了CRF和NIS基因的表达,同时抑制了TSHβ和TG基因的表达。而TPO基因的表达水平在单独和复合暴露组中没有显著差异。本研究首次证明了PFOS和Nano-Zn O复合暴露对斑马鱼幼鱼甲状腺轴的干扰效果并对其进行了机制探讨。
Perfluorooctanesulphonic acid potassium salt(PFOS) and Zn O nanoparticles(Nano-Zn O) are widely distributed in the environment. However, the potential toxicity of co-exposure to PFOS and Nano-Zn O remains to be fully elucidated. Our present study investigated the effects of co-exposure to PFOS and Nano-Zn O on the hypothalamic-pituitary-thyroid(HPT) axis in zebrafish. The embryos were exposed to PFOS(0.2, 0.4, 0.8 mg·L^(-1)) single solutions, Nano-Zn O(6.75, 12.5, 25 mg·L^(-1)) single solutions and PFOS plus Nano-Zn O(0.2 + 6.75, 0.4 + 12.5, 0.8 +25 mg·L^(-1)) mixture solutions for 15 days. We analyzed development toxicity, the whole-body content of TH and the expression of genes(corticotropin-releasing factor(CRF), thyroid-stimulating hormone(TSHβ), sodium/iodide symporter(NIS), thyroglobulin(TG), thyroid peroxidase(TPO) related to the HPT axis. Compared with single-exposure groups, the body length and survival rate decreased, the malformation rates increased in co-exposure groups. The triiodothyronine(T3) levels increased and the thyroxine(T4) content decreased in co-exposure groups. Compared with the exposure to PFOS and Nano-Zn O alone, the expression of genes(CRF and NIS) significantly up-regulated and the expression of genes(TSHβ and TG) significantly down-regulated in co-exposure groups. In addition, the expression of TPO gene was unchanged in both the single and co-exposure groups. Our results were the first evidence for the thyroid-disrupting effects of PFOS and Nano-Zn O co-exposure in zebrafish. The results also provide insight into the mechanism of disruption of the thyroid status by PFOS and Nano-Zn O.
出处
《生态毒理学报》
CAS
CSCD
北大核心
2015年第6期144-153,共10页
Asian Journal of Ecotoxicology
基金
哈尔滨工业大学城市水资源与水环境国家重点实验室导向类自主课题(2013DX09)