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Journal ArticleDOI

Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro.

James A. Imlay, +2 more
- 29 Apr 1988 - 
- Vol. 240, Iss: 4852, pp 640-642
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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.

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Citations
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Effects of 2-butoxyethanol on hepatic oxidative damage.

TL;DR: The results support the proposal that the induction of hepatic oxidative stress by 2- butoxyethanol in vivo occurs secondary to induction of hemolysis and iron deposition in the liver rather than as a direct action of 2-but oxygenethanol or its main metabolite,2-butoxy acetic acid.
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Cyanide enhances hydrogen peroxide toxicity by recruiting endogenous iron to trigger catastrophic chromosomal fragmentation.

TL;DR: It is proposed that disrupting intracellular iron trafficking is a common strategy employed by the immune system to kill microbes.
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Staphylococcal DNA Repair Is Required for Infection.

TL;DR: It is shown that ROS cause breaks in the staphylococcal DNA, which must be repaired by a two-protein complex known as RexAB; otherwise, the bacterium is killed, and it cannot sustain infection.
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Scavengers of free radical oxygen affect the generation of low molecular weight DNA in stimulated lymphocytes from patients with systemic lupus erythematosus.

TL;DR: It is suggested that the autooxidation and toxicity of high-dose cysteamine preclude its therapeutic use as a free radical scavenger.
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PCNA damage caused by antineoplastic drugs.

TL;DR: Photodynamic crosslinking of nuclear proteins by cytoplasmically localizing drugs, together with other evidence, argues that these drugs may reach the nucleoplasm in amounts sufficient to photodamage important chromosomal enzymes.
References
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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.
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Fenton's reagent revisited

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The catalytic decomposition of hydrogen peroxide by iron salts

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.
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