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Open AccessJournal ArticleDOI

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.

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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

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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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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Journal ArticleDOI

Superoxide Dismutase AN ENZYMIC FUNCTION FOR ERYTHROCUPREIN (HEMOCUPREIN)

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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Fenton's reagent revisited

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The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen.

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.
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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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