| Literature DB >> 25666086 |
Abstract
Microorganisms are vulnerable to elevated levels of intracellular reactive oxygen species (ROS). This situation has led to proposals that many natural stresses might be toxic specifically because they accelerate endogenous ROS formation. Such a mechanism has been convincingly demonstrated for redox-cycling compounds. However, the evidence is much weaker for most other stressors. The hypothesis that clinical antibiotics generate lethal ROS stress has attracted much attention, and the author discusses some aspects of evidence that support or oppose this idea. Importantly, even if all cellular electron flow were somehow diverted to ROS formation, the resultant doses of H2O2 and O2(-) would more likely be bacteriostatic than bacteriocidal unless key defense mechanisms were simultaneously blocked.Entities:
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Year: 2015 PMID: 25666086 PMCID: PMC4380616 DOI: 10.1016/j.mib.2015.01.004
Source DB: PubMed Journal: Curr Opin Microbiol ISSN: 1369-5274 Impact factor: 7.934