Polyphosphate accumulation and oxidative DNA damage in superoxide dismutase-deficient Escherichia coli

Inorganic polyphosphate is a ubiquitous, linear polymer of phosphate residues linked by high-energy phosphoanhydride bonds. In response to starvation, polyP levels are increased up to 100-fold. It has been proposed that chelation of transition metals by polyP might reduce their toxicity, and that po...

Full description

Saved in:
Bibliographic Details
Published in:Free radical biology & medicine 2001-12, Vol.31 (11), p.1352-1359
Main Authors: Al-Maghrebi, May A, Benov, Ludmil T
Format: Article
Language:English
Subjects:
Cyanides - pharmacology
DNA Damage
Drug Resistance
Escherichia coli
Escherichia coli - enzymology
Free radicals
Hydrogen peroxide
Hydrogen Peroxide - pharmacology
Hydroxyl Radical - metabolism
Hydroxylation
Kinetics
Mutation
Oxidative DNA damage
Oxidative Stress
Polyphosphate
Polyphosphates - metabolism
rpoS gene
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Superoxide dismutase-deficient
Superoxides
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Inorganic polyphosphate is a ubiquitous, linear polymer of phosphate residues linked by high-energy phosphoanhydride bonds. In response to starvation, polyP levels are increased up to 100-fold. It has been proposed that chelation of transition metals by polyP might reduce their toxicity, and that polyP accumulation is vital for survival in stationary phase. SOD-deficient E. coli is unable to survive in stationary phase. We found that deletion of the cytoplasmic SODs does not impair the cell’s capability of synthesizing polyP. However, transient accumulation of polyphosphate correlated with increased resistance to H 2O 2 and protection of DNA against oxidative damage. The reason for this protective effect of polyP is the induction of HPII catalase and DNA repair enzymes as members of the rpoS regulon. PolyP did not directly protect DNA against oxidative damage in vitro and acted as a pro-oxidant by stimulating the production of hydroxyl radical in the Fenton reaction. It is thus suggested that accumulation of poly P and rpoS induction cannot compensate for the lack of cytosolic SODs for survival in stationary phase.
ISSN:0891-5849
1873-4596
DOI:10.1016/S0891-5849(01)00696-7