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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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Oxidative Stress and Antioxidant Defenses in Biology

Sami Ahmad
TL;DR: This work focuses on the development and regulation of antioxidant defenses in Escherichia coli and Salmonella typhimurium, and on the mechanisms of oxidative modification of low density lipoprotein.
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New trends in photobiology. The interaction of UVA radiation with cultured cells.

TL;DR: This work concerning the interaction of UVA radiation with cultured cells is reviewed with particular emphasis on the involvement of cellular oxidative stress in the biological effects of this radiation on eucaryotic cells.
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Nitric oxide potentiates hydrogen peroxide-induced killing of Escherichia coli.

TL;DR: Exposure to NO resulted in minimal toxicity, but greatly potentiated (up to 1,000-fold) H2O2-mediated killing, as evaluated by a clonogenic assay, and a possible mechanism of modulation of H1N1-mediated toxicity is suggested.
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Cell cycle control, checkpoint mechanisms, and genotoxic stress.

TL;DR: This review focuses on mammalian cell cycle checkpoint functions, their role in maintaining DNA stability during the cell cycle following exposure to genotoxic agents, and the gene products that act in checkpoint function signal transduction cascades.
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Effects of irradiance and ultraviolet radiation on photoadaptation in the zooxanthellae of Aiptasia pallida: primary production, photoinhibition, and enzymic defenses against oxygen toxicity

TL;DR: Differences in enzyme activity between CZ and FIZ suggest an important role for the host in the protection of zooxanthellae against the direct effects of environmentally realistic UV while the photosynthetic performance of zo X-rayed in situ may not be as well protected.
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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