Common Killing Mechanism for Bactericidal Antibacterial CompoundsRosenthal, 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 Abstract Author Information 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: firstname.lastname@example.org. The authors have no funding or conflicts of interest to disclose. © 2013 Lippincott Williams & Wilkins, Inc.