Moving forward with reactive oxygen species involvement in antimicrobial lethality

Xilin Zhao, Yuzhi Hong, Karl Drlica

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Support for the contribution of reactive oxygen species (ROS) to antimicrobial lethality has been refined and strengthened. Killing by diverse antimicrobials is enhanced by defects in genes that protect against ROS, inhibited by compounds that block hydroxyl radical accumulation, and is associated with surges in intracellular ROS. Moreover, support has emerged for a genetic pathway that controls the level of ROS. Since some antimicrobials kill in the absence of ROS, ROS must add to, rather than replace, known killing mechanisms. New work has addressed many of the questions concerning the specificity of dyes used to detect intracellular ROS and the specificity of perturbations that influence ROS surges. However, complexities associated with killing under anaerobic conditions remain to be resolved. Distinctions among primary lesion formation, resistance, direct lesionmediated killing and a self-destructive stress response are discussed to facilitate efforts to potentiate ROSmediated bacterial killing and improve antimicrobial efficacy.

Original languageEnglish (US)
Article numberdku463
Pages (from-to)639-642
Number of pages4
JournalJournal of Antimicrobial Chemotherapy
Issue number3
StatePublished - Mar 1 2015

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Microbiology (medical)
  • Infectious Diseases
  • Pharmacology (medical)


  • Antibiotics
  • Killing
  • Post-damage cellular response
  • ROS

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