Institutional members access full text with Ovid®

Share this article on:

Common Killing Mechanism for Bactericidal Antibacterial Compounds

Rosenthal, Kenneth S. PhD*; Risley, Kim M. PhD

Infectious Diseases in Clinical Practice: January 2013 - Volume 21 - Issue 1 - p 38–40
doi: 10.1097/IPC.0b013e318279f1ac
Immunology/Microbiology for ID

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.

From the *Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH and †Department of Biology, University of Mount Union, Alliance, OH.

Correspondence to: Kenneth S. Rosenthal, PhD, Department of Integrative Medical Sciences, Northeast Ohio Medical University, 4209 SR 44, Rootstown, OH 44272. E-mail: ksr@neomed.edu.

The authors have no funding or conflicts of interest to disclose.

© 2013 Lippincott Williams & Wilkins, Inc.