Hagenaars A, Knapen D, Meyer I J, van der Ven K, Hoff P, De Coen W
Department of Biology, Research Unit Ecophysiology, Biochemistry and Toxicology, University of Antwerp, Antwerp, Belgium.
Aquat Toxicol. 2008 Jul 7;88(3):155-63. doi: 10.1016/j.aquatox.2008.04.002. Epub 2008 Apr 11.
Perfluorooctane sulfonate (PFOS) has been manufactured for over 50 years in increasing quantities and has been used for several industrial and commercial aims. Due to persistence and bioaccumulation of this pollutant, it can be found worldwide in wildlife and humans. Biochemical effects of PFOS exposure are mainly studied in mammalian model species and information about effects on fish species remain largely scarce. This lack of toxicity data points out that there is an urgent need for the mechanistic molecular understanding of the mode of action of this pollutant. In the present study, common carp (Cyprinus carpio) was exposed through water for 14 days at concentrations of 0.1, 0.5 and 1 mg/l PFOS. Liver was selected as target tissue. Custom microarrays were constructed from cDNA libraries obtained with Suppression Subtractive Hybridization-Polymerase Chain Reaction (SSH-PCR) experiments. Microarray data revealed that the expression of several genes in the liver was influenced by PFOS exposure and real-time PCR was used to confirm these gene expression changes. The affected genes were mainly involved in energy metabolism, reproduction and stress response. Furthermore, the relative condition factor, the hepatosomatic index, and the available glycogen reserves of the exposed fish were significantly lower after 14 days of exposure than in the control fish. At all levels of biological organization, indications of a trade-off between the metabolic cost of toxicant exposure on one hand and processes vital to the survival of the organism on the other hand were seen. Our results support the prediction that increases in energy expenditure negatively affects processes vital to the survival of an organism, such as growth.
全氟辛烷磺酸（PFOS）已生产了50多年，产量不断增加，并已用于多种工业和商业目的。由于这种污染物具有持久性和生物累积性，因此在全球范围内的野生动物和人类体内都能发现它。PFOS暴露的生化效应主要在哺乳动物模型物种中进行研究，而关于其对鱼类影响的信息仍然非常匮乏。缺乏毒性数据表明，迫切需要从分子机制上了解这种污染物的作用方式。在本研究中，将鲤鱼（Cyprinus carpio）置于浓度为0.1、0.5和1毫克/升的PFOS水中暴露14天。选择肝脏作为靶组织。通过抑制性消减杂交-聚合酶链反应（SSH-PCR）实验获得的cDNA文库构建了定制微阵列。微阵列数据显示，PFOS暴露会影响肝脏中多个基因的表达，并使用实时PCR来确认这些基因表达的变化。受影响的基因主要参与能量代谢、繁殖和应激反应。此外，暴露14天后，暴露组鱼的相对状况因子、肝体指数和糖原储备量均显著低于对照组鱼。在生物组织的各个层面上，都可以看到一方面是有毒物质暴露的代谢成本，另一方面是对生物体生存至关重要的过程之间存在权衡的迹象。我们的结果支持了这样的预测，即能量消耗的增加会对生物体生存至关重要的过程（如生长）产生负面影响。
