Role of reactive oxygen species in antibiotic action and resistance

被引:374
作者
Dwyer, Daniel J. [1 ,2 ]
Kohanski, Michael A. [1 ,2 ,3 ]
Collins, James J. [1 ,2 ,3 ]
机构
[1] Boston Univ, Howard Hughes Med Inst, Dept Biomed Engn, Ctr BioDynam, Boston, MA 02215 USA
[2] Boston Univ, Ctr Adv Biotechnol, Boston, MA 02215 USA
[3] Boston Univ, Sch Med, Boston, MA 02118 USA
关键词
BASE-EXCISION-REPAIR; POLYMERASES POL-II; ESCHERICHIA-COLI; DNA-POLYMERASES; SOS RESPONSE; OXIDATIVE DAMAGE; GENE-EXPRESSION; MUTAGENESIS; SUPEROXIDE; MECHANISMS;
D O I
10.1016/j.mib.2009.06.018
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The alarming spread of bacterial strains exhibiting resistance to current antibiotic therapies necessitates that we elucidate the specific genetic and biochemical responses underlying drug-mediated cell killing, so as to increase the efficacy of available treatments and develop new antibacterials. Recent research aimed at identifying such cellular contributions has revealed that antibiotics induce changes in metabolism that promote the formation of reactive oxygen species, which play a role in cell death. Here we discuss the relationship between drug-induced oxidative stress, the SOS response and their potential combined contribution to resistance development. Additionally, we describe ways in which these responses are being taken advantage to combat bacterial infections and arrest the rise of resistant strains.
引用
收藏
页码:482 / 489
页数:8
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