摘要
为探究海洋环境中持久性有机污染物——全氟辛烷磺酸(PFOS)的生物毒性效应,以半滑舌鳎肝脏细胞(HTLC)为研究对象,将其暴露于含不同浓度PFOS的DMEM-F12培养基中,分别染毒24、48、72 h后,利用噻唑蓝比色法(MTT)和透射电镜实验评价PFOS的细胞毒性;同时测定活性氧自由基(ROS)和超氧化物歧化酶(SOD)活性来探讨PFOS对细胞的氧化损伤效应。结果发现,细胞活性随PFOS浓度升高呈先促进后抑制趋势,当PFOS浓度达到1 000%mol·L-1时细胞活性受到显著抑制(P<0.01);电镜结果显示PFOS能引起与代谢相关的细胞器如线粒体、内质网等发生肿胀甚至破损;与对照组相比,ROS含量和SOD活性分别在20%mol·L-1、200%mol·L-1开始出现显著性差异(P<0.05),证实在PFOS引起的氧化应激反应中SOD起到了清除自由基作用以维持细胞稳态。研究表明,PFOS对海洋鱼类细胞具有一定的生物毒性,能引起细胞产生氧化应激反应,并进一步破坏生物膜系统,从而导致细胞增殖和多种代谢途径受到抑制。
MTT assay and transmission election microscope （TEM） were used to analyze the cytotoxicity of perflu- orooctane sulfonate （PFOS） on liver cells of Cynoglossus semilaevis （HTLC）. Reactive oxygen species （ROS） and superoxide dismutase （SOD） activity were applied to evaluate the oxidative damage of HTLC exposed to different concentrations of PFOS for 24, 48, 72 h, respectively. The results indicated that cell activity was promoted under the low concentration of PFOS. However, the activity was inhibited obviously when PFOS concentration increased to 1 000 μmol · L ^-1（P〈0.01）. TEM results showed that organelles relevant to metabolism, such as intracellular mi- tochondria and endoplasmic reticulum, would swell and/or be damaged under the condition of high PFOS concen- tration in HTLC. ROS contents and SOD activity also displayed significant difference at 20μmol · L ^-1 and 200 μmol · L ^-1 of PFOS, respectively （P〈0.05）, indicating that SOD can maintain the cellular homeostasis by removing free radicals induced in the process of oxidative stress caused by PFOS. The results confirmed that the proliferation and metabolic pathways can be inhibited significantly by PFOS in HTLC by the oxidative stress and then the de- struction of the biomembrane system of HTLC in marine fish.
出处
《生态毒理学报》
CAS
CSCD
北大核心
2015年第4期162-169,共8页
Asian Journal of Ecotoxicology
基金
国家海洋局海洋公益性科研专项(201105013)
国家自然科学基金(21377032)
国家海洋局近岸海域生态环境重点实验室开放基金(201506)
