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首页> 外文期刊>Aquatic Toxicology >Effects of North Sea oil and alkylphenols on biomarker responses in juvenile Atlantic cod (Gadus morhua)
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Effects of North Sea oil and alkylphenols on biomarker responses in juvenile Atlantic cod (Gadus morhua)

机译:北海油和烷基酚对大西洋大西洋鳕鱼(Gadus morhua)生物标志物响应的影响

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摘要

A consequence of oil drilling at sea is the release of produced water contaminated with e.g. polycyclic aromatic hydrocarbons (PAH) and alkylphenols. In the present study, juvenile Atlantic cod were exposed to North Sea oil, nonylphenol and a combination of the North Sea oil and an alkylphenol mixture in a flow-through system. A suite of hepatic biomarkers were analysed. Exposure to North Sea oil resulted in strong induction of CYP1A protein levels and EROD activities. Exposure to nonylphenol, on the other hand, resulted in decreased CYP1A levels and EROD activities. Thus, nonylphenol appears to down-regulate CYP1A expression in Atlantic cod. Combined exposure to North Sea oil with an alkylphenol mixture resulted in lower EROD induction, compared to that in fish exposed to North Sea oil alone. This difference was not statistically significant, but still we believe that the alkylphenols have inhibited CYP1A activities in the fish which may have compromised CYP1A mediated metabolism of other xenobiotics, including PAH. CYP3A protein levels were lower, compared to controls, in fish exposed to nonylphenol and the combination of North Sea oil and alkylphenol mixture. In contrast, the oil alone had no effect on CYP3A protein content. North Sea oil exposure, alone or in combination with alkylphenols, caused oxidative stress observed as elevated levels of GSSG content and GR and CAT activities. Interestingly, exposure to nonylphenol resulted in a marked depletion of total glutathione levels. This apparent depletion may be a consequence of increased conjugation of glutathione to nonylphenol followed by excretion. An increase in conjugation enzyme GST activity was observed in the nonylphenol exposed group, although the difference was not significant. No sign of oxidative damage, measured as lipid peroxidation, was observed in any of the exposures experiments. This study suggests that North Sea oil may lead to oxidative stress and altered CYP1A and CYP3A expression. Alkylphenols, present in produced water, resulted in decreased CYP1A and CYP3A protein expression in Atlantic cod.
机译:海上石油钻探的结果是释放出被例如水污染的产出水。多环芳烃(PAH)和烷基酚。在本研究中,大西洋幼鳕鱼在流通系统中暴露于北海油,壬基酚以及北海油和烷基酚混合物的混合物中。分析了一组肝脏生物标志物。暴露于北海石油导致CYP1A蛋白水平和EROD活性的强烈诱导。另一方面,接触壬基酚导致CYP1A水平降低和EROD活性降低。因此,壬基酚似乎下调了大西洋鳕鱼中的CYP1A表达。与单独暴露于北海油中的鱼类相比,将其与烷基苯酚混合物共同暴露于北海油中可降低EROD诱导。这种差异没有统计学意义,但我们仍然认为烷基酚抑制了鱼类中的CYP1A活性,这可能损害了CYP1A介导的其他外源生物的代谢,包括PAH。在暴露于壬基酚以及北海油和烷基酚混合物的混合物中,与对照组相比,CYP3A蛋白水平较低。相反,仅油对CYP3A蛋白含量没有影响。单独或与烷基酚组合使用的北海石油暴露引起氧化应激,这是由于GSSG含量和GR和CAT活性升高所致。有趣的是,暴露于壬基苯酚会导致总谷胱甘肽水平显着减少。这种明显的消耗可能是由于谷胱甘肽与壬基酚的结合增加,然后排泄的结果。在壬基酚暴露组中观察到缀合酶GST活性增加,尽管差异不显着。在任何暴露实验中均未观察到以脂质过氧化为衡量标准的氧化损伤迹象。这项研究表明北海油可能导致氧化应激并改变CYP1A和CYP3A的表达。产水中存在的烷基酚导致大西洋鳕鱼中CYP1A和CYP3A蛋白表达降低。

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