西亚试剂：A Common Mechanism of Cellular Death Induced by Bactericida

发布时间：2025-07-16

A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics

Michael A. Kohanski,1,2,5,6 Daniel J. Dwyer,1,3,6 Boris Hayete,1,4 Carolyn A. Lawrence,1,2 and James J. Collins1,2,3,4,

1 Center for BioDynamics and Center for Advanced Biotechnology, Boston University, Boston, MA 02215, USA
2 Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA
3 Program in Molecular Biology, Cell Biology, and Biochemistry, Boston University, Boston, MA 02215, USA
4 Bioinformatics Program, Boston University, Boston, MA 02215, USA
5 Boston University School of Medicine, Boston, MA 02118, USA

Corresponding author
James J. Collins
Summary

Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.

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