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摄食全氟辛烷磺酸或全氟辛酸日粮的三文鱼的脂质过氧化和氧化应激反应。

Lipid peroxidation and oxidative stress responses of salmon fed a diet containing perfluorooctane sulfonic- or perfluorooctane carboxylic acids.

机构信息

Department of Biology, Norwegian University of Science and Technology (NTNU), 7491 Trondheim, Norway.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2011 Nov;154(4):288-95. doi: 10.1016/j.cbpc.2011.06.012. Epub 2011 Jun 30.

DOI:10.1016/j.cbpc.2011.06.012
PMID:21742055
Abstract

The present study was conducted to evaluate the effects of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on lipid β-oxidation and oxidative stress responses in Atlantic salmon liver and kidney tissues. We quantified changes in the expression levels of peroxisome proliferator-activated receptors (PPARs) and acyl-CoA oxidase (ACOX1) enzyme whose transcription is induced by PPARs. In addition, we analyzed gene expression patterns for enzymatic antioxidants (superoxide dismutase: SOD, catalase: CAT and glutathione peroxidase: GPx). Thiobarbituric acid reactive substances (TBARS) were analyzed as a measure for lipid peroxidation. Juvenile Atlantic salmon were repeatedly force-fed food spiked with PFOA or PFOS at 0.2mg/kg, and samples were collected after 0, 2, 5 and 8 days and after a 7 days recovery period. Our data showed that exposure of salmon to PFOS or PFOA produced changes (either increased or decreased) in mRNA expression for PPARs, ACOX1, oxidative stress responses and lipid peroxidation (TBARS) and these responses showed marked organ differences, associated with tissue bioaccumulation patterns and dependent on exposure time. Given that a classical reaction during reactive oxygen species (ROS)-induced damage involves the peroxidation of lipids, our study demonstrates that salmon continuously exposed to dietary PFOS or PFOA dose showed alteration in peroxisomal responses and oxidative stress responses, with higher severity in the kidney, compared to liver. Overall, our data suggest that ROS-mediated oxidative damage maybe a significant and putative toxic effect of PFOA and PFOS in fish as has been reported in mammals.

摘要

本研究旨在评估全氟辛烷磺酸(PFOS)和全氟辛酸(PFOA)对大西洋鲑鱼肝脏和肾脏组织中脂类β-氧化和氧化应激反应的影响。我们量化了过氧化物酶体增殖物激活受体(PPARs)和酰基辅酶 A 氧化酶(ACOX1)的表达水平变化,这两种酶的转录受 PPARs 诱导。此外,我们还分析了抗氧化酶(超氧化物歧化酶:SOD、过氧化氢酶:CAT 和谷胱甘肽过氧化物酶:GPx)的基因表达模式。丙二醛(TBARS)被分析作为脂质过氧化的衡量标准。我们用含有 0.2mg/kg PFOA 或 PFOS 的食物反复灌喂幼大西洋鲑鱼,在 0、2、5 和 8 天以及 7 天恢复期后采集样本。我们的数据表明,暴露于 PFOS 或 PFOA 会导致鲑鱼的 PPARs、ACOX1、氧化应激反应和脂质过氧化(TBARS)的 mRNA 表达发生变化(增加或减少),这些反应表现出明显的器官差异,与组织生物积累模式有关,并取决于暴露时间。鉴于活性氧(ROS)诱导损伤过程中的经典反应涉及脂质的过氧化,我们的研究表明,连续暴露于膳食 PFOS 或 PFOA 剂量的鲑鱼表现出过氧化物酶体反应和氧化应激反应的改变,与肝脏相比,肾脏的严重程度更高。总的来说,我们的数据表明,ROS 介导的氧化损伤可能是 PFOA 和 PFOS 在鱼类中一种重要的、潜在的毒性作用,这在哺乳动物中已有报道。

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