Raingeard Damien, Bilbao Eider, Sáez-Morquecho Cristina, de Cerio Oihane Díaz, Orbea Amaia, Cancio Ibon, Cajaraville Miren P
Laboratory of Cell Biology and Histology, Department of Zoology and Animal Cell Biology, University of the Basque Country, PO BOX 644, E-48080 Bilbao, Basque Country, Spain.
Mar Genomics. 2009 Sep-Dec;2(3-4):201-13. doi: 10.1016/j.margen.2009.10.004. Epub 2009 Nov 20.
In November 2002 the tanker Prestige released more than 60,000t of a heavy fuel oil which spread over Galician waters and the Biscay Bay, affecting coastal ecosystems. Polycyclic aromatic hydrocarbons are the main components of the Prestige fuel oil and induce biotransformation metabolism and peroxisome proliferation in marine organisms. In vertebrates, this later response involves peroxisome proliferator-activated receptors (PPARs), transcription factors belonging to the nuclear receptor superfamily, that act upon heterodimerization with the retinoid X receptor (RXR). In order to assess the possible biological effects of the Prestige oil spill in the Biscay Bay, male and female juvenile and adult European hakes Merluccius merluccius were sampled in June and December 2004 and 2005. PCR screening of hake liver cDNA with degenerate primers resulted in cloning and sequencing of cDNA fragments of PPARα (1011bp), PPARγ (812bp), RXR (270bp) and of the PPARα target gene palmitoyl-CoA oxidase (AOX1, 792bp). Fragments of another 9 toxicologically relevant genes were also cloned and sequenced. PPARα mRNA expression was not significantly different among groups. In juvenile females transcription of PPARγ, RXR and AOX1 significantly increased in June 2005 when compared to June 2004. In adult males levels of AOX1 decreased in the same period. AOX1 and 7-ethoxyresorufin O-deethylase (EROD) activities, measured as exposure biomarkers, differed between years only in males sampled in June. EROD activity was higher in 2004 than in 2005 in adults, whereas both juvenile and adults showed higher AOX1 activity in 2005. The lack of historical data previous to the accident or in areas not affected by the accident did not allow to relate observed variations in gene transcription levels and enzyme activities to the Prestige oil spill. Reported data could be useful for comparison purposes for future studies in European hake and contributes gene sequence information relevant for future toxicological studies.
2002年11月，“威望号”油轮泄漏了6万多吨重质燃料油，这些燃油扩散到加利西亚海域和比斯开湾，影响了沿海生态系统。多环芳烃是“威望号”燃料油的主要成分，可诱导海洋生物的生物转化代谢和过氧化物酶体增殖。在脊椎动物中，后一种反应涉及过氧化物酶体增殖物激活受体（PPARs），它属于核受体超家族的转录因子，与视黄酸X受体（RXR）异源二聚化后发挥作用。为了评估比斯开湾“威望号”漏油事件可能产生的生物学影响，于2004年和2005年6月及12月采集了雄性和雌性欧洲无须鳕幼鱼和成鱼样本。用简并引物对无须鳕肝脏cDNA进行PCR筛选，结果克隆并测序了PPARα（1011bp）、PPARγ（812bp）、RXR（270bp）以及PPARα靶基因棕榈酰辅酶A氧化酶（AOX1，792bp）的cDNA片段。另外9个毒理学相关基因的片段也被克隆并测序。各群体间PPARα mRNA表达无显著差异。与2004年6月相比，2005年6月幼鱼雌性中PPARγ、RXR和AOX1的转录显著增加。同期成年雄性中AOX1水平下降。作为暴露生物标志物测定的AOX1和7-乙氧基异吩恶唑酮O-脱乙基酶（EROD）活性，仅在6月采样的雄性中存在年份差异。2004年成年鱼的EROD活性高于2005年，而2005年幼鱼和成鱼的AOX1活性均较高。事故发生前或未受事故影响地区缺乏历史数据，无法将观察到的基因转录水平和酶活性变化与“威望号”漏油事件联系起来。报告的数据可用于欧洲无须鳕未来研究的比较目的，并为未来毒理学研究提供相关基因序列信息。
