全氟辛酸对大肠杆菌的氧化胁迫和膜损伤

全氟辛酸(perfluorooctanoic acid,PFOA)因其具有极高的化学稳定性和良好的疏水疏油性而在工业生产中广泛使用,但近年来被认为是一种在环境中广泛分布的持久性有机污染物.利用流式细胞术等检测技术,研究了PFOA对大肠杆菌(Escherichia coli,E.coli)的氧化胁迫和膜损伤,并对其毒性作用机制进行了初步的探索.结果表明,在PFOA胁迫下,大肠杆菌胞内活性氧(reactive oxygen species,ROS)含量增加,膜脂肪酸不饱和度降低,丙二醛(malondialdehyde,MDA)浓度升高、细胞膜通透性增大、跨膜电位降低,而细胞膜上的Na+K+-ATPase、Ca2+Mg2+-ATPase活性随时间的延长代偿性地先上升后降低.由此说明,在PFOA胁迫下,大肠杆菌细胞内升高的ROS与细胞膜不饱和脂肪酸发生过氧化反应,降低膜脂肪酸的饱和度,使得MDA在细胞内积累,进一步引起细胞膜损伤及其上相关ATPase活性降低,最终导致大肠杆菌细胞失活或死亡.实验结果对研究PFOA胁迫下环境生态毒理提供更多依据.

Effect of PFOA on Oxidative Stress and Membrane Damage of Escherichia coli

Perfluorooctanoic acid (PFOA) is widely used in industrial production because of its strong chemical stabilities and good hydrophobic and oleophobic properties. It was considered to be a widespread persistent organic pollutant in environment in recent years. The oxidative stress and membrane damage of Escherichia coli exposed to PFOA were measured by flow cytometry (FCM) and the toxic mechanism of PFOA was also preliminarily explored. The results showed that, under the stress of PFOA, the intracellular reactive oxygen species (ROS) content of E. coli increased, the unsaturation degree of fatty acid decreased, the malondialdehyde (MDA) content increased, the membrane permeability increased, the membrane potential decreased, and the activities of Na⁺K⁺-ATPase and Ca²⁺Mg²⁺-ATPase showed a compensatory increase first and then decreased. Therefore, owing to the stress of PFOA, the higher intracellular ROS in E. coli reacted with membrane unsaturated fatty acids by peroxidation,and then reduced cell membrane fatty acid saturation, accumulated MDA in cells, and further caused damage to cell membrane, reduced the ATPase activity, and eventually resulted in inactivation or apoptosis of E. coli. This study provided more evidence for the further study on environmental ecological toxicology of PFOA.