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全氟辛烷磺酸(PFOS)对三角帆蚌肝胰腺的氧化性损伤
引用本文:潘若雷,杨淑雯,江敏.全氟辛烷磺酸(PFOS)对三角帆蚌肝胰腺的氧化性损伤[J].生态毒理学报,2016,11(6):112-120.
作者姓名:潘若雷  杨淑雯  江敏
作者单位:1. 上海海洋大学水产与生命学院,上海,201306;2. 上海海洋大学水产与生命学院,上海201306;上海市水产养殖工程技术研究中心,上海201306
基金项目:上海市高校知识服务平台项目(ZF1206);上海市教委重点学科建设项目(J50701)
摘    要:PFOS是典型的持久性有机污染物,迁移能力强,具有较高的生物可利用性和蓄积能力,且具有广泛的生物毒性。为探究PFOS对淡水底栖生物的毒性作用机制,以三角帆蚌为研究对象,进行了不同剂量(0.1、1.0、5.0 mg·L-1)的PFOS胁迫和净水恢复实验,期间对受试生物肝胰腺中的谷胱甘肽(GSH)含量、谷胱甘肽-S转移酶(GST)活性、超氧化物歧化酶(SOD)活性,以及谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性进行了连续测定。结果发现,低浓度胁迫(0.1 mg·L-1)对各项指标均有不同程度的诱导作用,且持续时间较长;而在中高浓度PFOS胁迫下,则呈现出明显的诱导向抑制过渡的时间效应。GSH含量和GST活性具有较高的相关性(P0.05)。恢复实验中,所测指标普遍未恢复到对照组水平,说明P FOS胁迫损伤的恢复需要更长的时间。研究表明,PFOS对三角帆蚌肝胰腺的氧化胁迫显著,并能快速地激活肝胰腺细胞的解毒代谢;但长期的PFOS胁迫则会造成肝胰腺细胞的实质性损伤。

关 键 词:PFOS  三角帆蚌  肝胰腺  酶活性  毒性机理
收稿时间:1/4/2016 12:00:00 AM
修稿时间:2/1/2016 12:00:00 AM

Perfluorooctane Sulfonate (PFOS)-Induced Oxidative Damage in Hepatopancreas of Hyriopsis cumingii
Pan Ruolei,Yang Shuwen,Jiang Min.Perfluorooctane Sulfonate (PFOS)-Induced Oxidative Damage in Hepatopancreas of Hyriopsis cumingii[J].Asian Journal of Ecotoxicology,2016,11(6):112-120.
Authors:Pan Ruolei  Yang Shuwen  Jiang Min
Institution:1. College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China 2. Research and Engineering Center on Aquatic Environment Ecosystem, Shanghai 201306, China
Abstract:Perfluorooctane sulfonate (PFOS) is a typical persistent organic pollutant, which has high levels of bio-availability and can easily migrate in the environment or accumulate in biont. In addition, PFOS has a wide range of biological toxicity. However, few studies have focused on the toxicity mechanism of PFOS on aquatic benthic animals. In this study, we explored the toxic effects of different concentrations (0.1, 1.0 and 5.0 mg?L-1) of PFOS to benthic organisms by testing the activity of glutathione S-transferase (GST), superoxide dismutase (SOD), alanine transaminase (ALT), aspartate transaminase (AST), and the concentration of GSH in the hepatopancreas of PFOS treated Hyriopsis cumingii. In different intensities, we detected long-lasting inductions of GSH, GST and ALT activity in the lower concentration (0.1 mg?L-1) group. In contrast, similar patterns for all biomarkers shifting from induction to inhibition were found in the 1.0 mg?L-1 and 5.0 mg?L-1 groups. As an indicator of oxidative stress, the activity of SOD was significantly inhibited in all the treated groups. Finally, a positive correlation (P<0.05) was found between GSH concentration and GST activity in the 5.0 mg?L-1 group suggesting that the cellular detoxification system was highly motivated. In the restoration experiment, none of the biomarkers had restored to the normal range, and all of the biomarkers showed more instability than the control group, which indicated the dysfunction and suggested that a longer convalescence was needed to repair the damage. In summary, the rapid triggering of cellular detoxification and oxidative stress of the antioxidant system in hepatopancreas of Hyriopsis cumingii was detected during the PFOS treated process. The blocking of toxic metabolic pathways and accumulation of oxidant may be the origin of cellular damage.
Keywords:PFOS  Hyriopsis cumingii  hepatopancreas  enzyme activity  toxic mechanism
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