The molecular mechanisms and physiological consequences of oxidative stress: lessons from a model bacterium
By J. Imlay. Nature Reviews Microbiology, 2013
1,510 citations recorded by the source corpus.
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.
Subfields: Genetics, Inorganic Chemistry, Molecular Medicine
View Paper: https://www.semanticscholar.org/paper/79a28740f10e8c0e2575a7bd6dcfab27d04dc0e3
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In Molecular Medicine
Citations in the corpus
- Biofilms as Promoters of Bacterial Antibiotic Resistance and Tolerance (2020, background): “Ferrous iron from iron-sulfur clusters is oxidized to ferric iron in the Fenton reaction which yields extremely reactive and harmful hydroxyl radicals that oxidize vital macromolecules such as DNA, proteins, and lipids [120,121].”
- The Biology of Streptococcus mutans (2019, background): “…2 , and its more damaging breakdown products hydroxyl radical and superoxide anion, can rapidly cause irreversible cellular damage by triggering mismetallation of enzymes, by damaging proteins through oxidation of sulfurous amino acids and metal-binding sites, and by disturbing DNA integrity ( 84).”
- Antibiotics induce redox-related physiological alterations as part of their lethality (2014, background): “In purine nucleotides, the C8 position is particularly close to the complexed Fe (86) and hence would be favorably disposed to react with a newly generated hydroxyl radical (71) or with an iron-oxo radical (76).”
- 13 reasons why the brain is susceptible to oxidative stress (2018, background): “-] in the picomolar range, Imlay [219] estimates the half-time for mononuclear enzyme damage is still ~20min owing to favourable kinetics (k ~106 M−1 s−1).”