World Class University (WCU) program of Chemical Convergence for Energy & Environment (C2E2), School of Chemical and Biological Engineering, College of Engineering, Institute of Chemical Process, Seoul National University (SNU), Seoul 151-744, Republic of Korea.
Environ Sci Technol. 2012 Oct 16;46(20):11299-304. doi: 10.1021/es302379q. Epub 2012 Oct 5.
This study demonstrated Escherichia coli inactivation by cupric ion (Cu[II]), focusing on intracellular generation and consumption of reactive oxygen species (ROS) including superoxide and hydroxyl radials. In the presence of Cu(II), intracellular superoxide levels of E. coli decreased in a concentration-dependent manner, indicating that superoxide radical was used to reduce Cu(II) to Cu(I) in cells. The variation in the hydroxyl radical level by adding Cu(II) was negligible. Molecular oxygen and hydroxyl radical scavengers did not affect the inactivation efficacy of E. coli by Cu(II), excluding the possibility that hydroxyl radicals induced by the copper-mediated reduction of oxygen contributed to the microbiocidal action of Cu(II). However, the inactivation of E. coli by Cu(II) was considerably inhibited and accelerated by a Cu(I)-chelating agent and a Cu(II)-reducing agent, respectively. Our results suggest that the microbiocidal action of Cu(II) is attributable to the cytotoxicity of cellularly generated Cu(I), which does not appear to be associated with oxidative damage by Cu(I)-driven ROS.
本研究旨在探讨铜离子（Cu[II]）对大肠杆菌的灭活作用，重点研究包括超氧自由基和羟自由基在内的细胞内活性氧（ROS）的产生和消耗。在 Cu(II)存在的情况下，大肠杆菌细胞内的超氧自由基水平呈浓度依赖性下降，表明超氧自由基被用于将 Cu(II)还原为细胞内的 Cu(I)。加入 Cu(II)后，羟自由基水平的变化可以忽略不计。添加分子氧和羟自由基清除剂并不影响 Cu(II 对大肠杆菌的灭活效果，这排除了由铜介导的氧还原产生的羟自由基引发铜(II)杀菌作用的可能性。然而，Cu(II)对大肠杆菌的灭活作用分别被 Cu(I)螯合剂和 Cu(II)还原剂显著抑制和加速。我们的结果表明，Cu(II)的杀菌作用归因于细胞内生成的具有细胞毒性的 Cu(I)，而这似乎与 Cu(I)驱动的 ROS 引起的氧化损伤无关。
