Nonthermal Dielectric-Barrier Discharge Plasma-Induced Inactivation Involves Oxidative DNA Damage and Membrane Lipid Peroxidation in Escherichia coli

被引:402
作者
Joshi, Suresh G. [1 ,2 ]
Cooper, Moogega [3 ]
Yost, Adam [3 ]
Paff, Michelle [1 ,2 ]
Ercan, Utku K. [4 ]
Fridman, Gregory [4 ]
Friedman, Gary [3 ]
Fridman, Alexander [3 ]
Brooks, Ari D. [1 ,2 ]
机构
[1] Drexel Univ, Coll Med, Dept Surg, Surg Infect Program, Philadelphia, PA 19102 USA
[2] Drexel Univ, Coll Med, Dept Microbiol & Immunol, Philadelphia, PA 19102 USA
[3] Drexel Univ, Div Plasma Biol & Med, AJ Drexel Plasma Inst, Philadelphia, PA 19102 USA
[4] Drexel Univ, Sch Biomed Engn Sci & Hlth Syst, Philadelphia, PA 19102 USA
关键词
SINGLET OXYGEN; REAL-TIME; BIOFILMS; STRESS; EFFICACY;
D O I
10.1128/AAC.01002-10
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Oxidative stress leads to membrane lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce lipid peroxidation in Escherichia coli. Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves membrane lipid peroxidation in E. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for membrane lipid peroxidation, and ROS scavengers, such as alpha-tocopherol (vitamin E), were able to significantly inhibit the extent of lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.
引用
收藏
页码:1053 / 1062
页数:10
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