Journal ArticleDOI
Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro.
Reads0
Chats0
TLDR
An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide.Abstract:
Exposure of Escherichia coli to low concentrations of hydrogen peroxide results in DNA damage that causes mutagenesis and kills the bacteria, whereas higher concentrations of peroxide reduce the amount of such damage. Earlier studies indicated that the direct DNA oxidant is a derivative of hydrogen peroxide whose formation is dependent on cell metabolism. The generation of this oxidant depends on the availability of both reducing equivalents and an iron species, which together mediate a Fenton reaction in which ferrous iron reduces hydrogen peroxide to a reactive radical. An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide. The direct DNA oxidant both in vivo and in this in vitro system exhibits reactivity unlike that of a free hydroxyl radical and may instead be a ferryl radical.read more
Citations
More filters
Journal ArticleDOI
What Makes a Natural Clay Antibacterial
Lynda B. Williams,David W. Metge,Dennis D. Eberl,Ronald W. Harvey,Amanda G. Turner,Panjai Prapaipong,Amisha T. Poret-Peterson +6 more
TL;DR: Compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains, it is deduced that extracellular processes do not cause cell death.
Journal ArticleDOI
Activation of the cytoplasmic c-Abl tyrosine kinase by reactive oxygen species.
Xiangao Sun,Pradip K. Majumder,Hisashi Shioya,Frank Wu,Shailendra Kumar,Ralph R. Weichselbaum,Surender Kharbanda,Donald Kufe +7 more
TL;DR: It is demonstrated that cytoplasmic c-Abl is involved in the apoptotic response of cells to oxidative stress and that H2O2-induced apoptosis is attenuated in c- Abl-deficient cells.
Journal ArticleDOI
Disorders of iron metabolism. Part 1: molecular basis of iron homoeostasis
TL;DR: Hepcidin, synthesised by hepatocytes in response to iron concentrations, inflammation, hypoxia and erythropoiesis, is the main iron-regulatory hormone, which binds ferroportin on enterocytes, macrophages and hepatocytes triggering its internalisation and lysosomal degradation.
Journal ArticleDOI
DNA damage and apoptosis in hydrogen peroxide-exposed Jurkat cells: bolus addition versus continuous generation of H2O2
Alexandra Barbouti,Paschalis-Thomas Doulias,Lambros Nousis,Margarita Tenopoulou,Dimitrios Galaris +4 more
TL;DR: Observations stress that, apart from the apparent genotoxic and proapoptotic effects of H(2)O(2), it can also exert antiAPoptotic actions when present, even at low concentrations, during the execution of apoptosis.
Journal ArticleDOI
Oxidative damage to DNA constituents by iron-mediated fenton reactions. The deoxyguanosine family.
TL;DR: 7,8-Dihydro-8-oxo-2′-deoxyguanosine is the most abundant DNA-bound product aside from abasic sites, and its formation was more closely analyzed.
References
More filters
Journal ArticleDOI
The biology of oxygen radicals
TL;DR: The reactive superoxide radical, O2-, formerly of concern only to radiation chemists and radiobiologists, is now understood to be a normal product of the biological reduction of molecular oxygen.
Journal ArticleDOI
The catalytic decomposition of hydrogen peroxide by iron salts
Fritz Haber,Joseph Weiss +1 more
TL;DR: Wansbrough-Jones as discussed by the authors gave the manuscript of this paper to Professor Sir William Pope, but the final revision for the press had not been made and in its original from the paper was not suitable for publication in an English journal; but since, Professor Haber had considered carefully how he wished to present the results embodied in it, the form and sequence of the paper remain unmodified.