The molecular mechanisms and physiological consequences of oxidative stress: lessons from a model bacterium.
TLDR
This Review summarized the current knowledge of oxidative stress in Escherichia coli, the model organism for which the understanding of damage and defence is most well developed, and proposed strategies to protect themselves with scavenging enzymes and repair systems.Abstract:
Oxic environments are hazardous. Molecular oxygen adventitiously abstracts electrons from many redox enzymes, continuously forming intracellular superoxide and hydrogen peroxide. These species can destroy the activities of metalloenzymes and the integrity of DNA, forcing organisms to protect themselves with scavenging enzymes and repair systems. Nevertheless, elevated levels of oxidants quickly poison bacteria, and both microbial competitors and hostile eukaryotic hosts exploit this vulnerability by assaulting these bacteria with peroxides or superoxide-forming antibiotics. In response, bacteria activate elegant adaptive strategies. In this Review, I summarize our current knowledge of oxidative stress in Escherichia coli, the model organism for which our understanding of damage and defence is most well developed.read more
Citations
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The role of iron and reactive oxygen species in cell death
TL;DR: The different roles of iron in triggering cell death, targets of iron-dependent ROS that mediate cell death and a new form ofIron-dependent cell death termed ferroptosis are described to suggest new therapeutic avenues to treat cancer, organ damage and degenerative disease.
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Free radicals, natural antioxidants, and their reaction mechanisms
TL;DR: The mechanism of action of the natural antioxidant compounds and assays and their reaction mechanisms can help in evaluating the antioxidant activity of various antioxidant compounds as well as in the development of novel antioxidants.
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Molecular mechanisms of biofilm-based antibiotic resistance and tolerance in pathogenic bacteria
Clayton W. Hall,Thien-Fah Mah +1 more
TL;DR: This review summarises both historical and recent scientific data in support of the known biofilm resistance and tolerance mechanisms and suggestions for future work in the field are provided.
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Antibiotics induce redox-related physiological alterations as part of their lethality
Daniel J. Dwyer,Peter Belenky,Jason H. Yang,I. Cody MacDonald,Jeffrey D. Martell,Noriko Takahashi,Clement T Y Chan,Michael A. Lobritz,Dana Braff,Eric G. Schwarz,Jonathan D. Ye,Mekhala Pati,Maarten Vercruysse,Paul S. Ralifo,Kyle R. Allison,Ahmad S. Khalil,Alice Y. Ting,Graham C. Walker,James J. Collins +18 more
TL;DR: This work provides direct evidence that, downstream of their target-specific interactions, bactericidal antibiotics induce complex redox alterations that contribute to cellular damage and death, thus supporting an evolving, expanded model of antibiotic lethality.
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13 reasons why the brain is susceptible to oxidative stress.
TL;DR: 13 reasons why the brain is susceptible to oxidative stress are rationalised and key reasons include inter alia unsaturated lipid enrichment, mitochondria, calcium, glutamate, modest antioxidant defence, redox active transition metals and neurotransmitter auto-oxidation.
References
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Superoxide Dismutase AN ENZYMIC FUNCTION FOR ERYTHROCUPREIN (HEMOCUPREIN)
Joe M. McCord,Irwin Fridovich +1 more
TL;DR: The demonstration that O2·- can reduce ferricytochrome c and tetranitromethane, and that superoxide dismutase, by competing for the superoxide radicals, can markedly inhibit these reactions, is demonstrated.
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The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen.
Alberto Boveris,Britton Chance +1 more
TL;DR: It is postulated that in addition to the well-known flavin reaction, formation of H( 2)O(2) may be due to interaction with an energy-dependent component of the respiratory chain at the cytochrome b level.
Journal ArticleDOI
A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics
TL;DR: The 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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