Common killing mechanism for bactericidal antibacterial compounds

Kenneth S. Rosenthal, Kim M. Risley

Research output: Contribution to journalArticlepeer-review


Recent findings identify a common toxic mechanism for drugs within 3 bactericidal antimicrobial families, β-lactams, quinolones, and aminoglycosides, beyond the primary target interaction. In vitro studies show that treatment with these compounds blocks cell division, which promotes a buildup of reduced nicotinamide adenine dinucleotide, and its oxidation promotes the production of reactive oxygen species, including hydroxyl radicals. The hydroxyl radical oxidizes guanine to 8-deoxy-guanine. 8-deoxy-guanine can base pair with both deoxycytosine and deoxyadenosine, and this mismatch promotes mutation. The cell's effort to repair closely spaced mismatches with 8-deoxy-guanine causes double-strand breaks in the DNA, which kill the bacteria. These findings identify a common killing mechanism for bactericidal drugs and suggest mechanisms that contribute to the intrinsic susceptibility of bacteria to these drugs.

Original languageEnglish (US)
Pages (from-to)38-40
Number of pages3
JournalInfectious Diseases in Clinical Practice
Issue number1
StatePublished - Jan 1 2013
Externally publishedYes


  • 8-deoxy-guanine
  • DNA damage
  • ampicillin
  • antimicrobials
  • bactericidal
  • hydroxyl radical
  • kanamycin
  • killing mechanism
  • norfloxacin

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases


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