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In vivo analysis of the process of o...

Park, Sungkyung.

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In vivo analysis of the process of oxidative DNA damage of Escherichia coli.

Record Type:	Electronic resources : Monograph/item
Title/Author:	In vivo analysis of the process of oxidative DNA damage of Escherichia coli./
Author:	Park, Sungkyung.
Description:	113 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-07, Section: B, page: 3540.
Contained By:	Dissertation Abstracts International66-07B.
Subject:	Biology, Microbiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3182346
ISBN:	9780542230585

In vivo analysis of the process of oxidative DNA damage of Escherichia coli.
Park, Sungkyung.

In vivo analysis of the process of oxidative DNA damage of Escherichia coli. - 113 p.

Source: Dissertation Abstracts International, Volume: 66-07, Section: B, page: 3540.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2005.

The goal of this work was to study the mechanism of oxidative DNA damage in Escherichia coli. Both exogenously added and endogenously produced hydrogen peroxide (H2O2) were toxic. The bactericidal effect of exogenous H2O2 was potentiated when cells were pre-grown with poor sulfur sources and followed by transient cystine exposure. Cell death was due to an unusually rapid rate of DNA damage. Iron chelators relieved the killing, indicating that intracellular free iron mediated the conversion of H2O2 into a hydroxyl radical, the direct effector of DNA damage. The cystine treatment caused a temporary loss of cysteine homeostasis, with intracellular pools increasing about eight-fold. In vitro analysis demonstrated that cysteine reduces ferric iron with exceptional speed. This action permits free iron to redox cycle rapidly in the presence of H2O2, thereby augmenting the rate at which hydroxyl radicals are formed. During routine growth, cells maintain small cysteine pools, and cysteine is not a major contributor to DNA damage. Thus, the homeostatic control of cysteine levels is important in conferring resistance to oxidants.

ISBN: 9780542230585Subjects--Topical Terms:

1017734
Biology, Microbiology.

In vivo analysis of the process of oxidative DNA damage of Escherichia coli.
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020 $a 9780542230585
035 $a (UnM)AAI3182346
035 $a AAI3182346
040 $a UnM $c UnM
100 1 $a Park, Sungkyung. $3 1910456
245 1 0 $a In vivo analysis of the process of oxidative DNA damage of Escherichia coli.
300 $a 113 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-07, Section: B, page: 3540.
500 $a Adviser: James A. Imlay.
502 $a Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2005.
520 $a The goal of this work was to study the mechanism of oxidative DNA damage in Escherichia coli. Both exogenously added and endogenously produced hydrogen peroxide (H2O2) were toxic. The bactericidal effect of exogenous H2O2 was potentiated when cells were pre-grown with poor sulfur sources and followed by transient cystine exposure. Cell death was due to an unusually rapid rate of DNA damage. Iron chelators relieved the killing, indicating that intracellular free iron mediated the conversion of H2O2 into a hydroxyl radical, the direct effector of DNA damage. The cystine treatment caused a temporary loss of cysteine homeostasis, with intracellular pools increasing about eight-fold. In vitro analysis demonstrated that cysteine reduces ferric iron with exceptional speed. This action permits free iron to redox cycle rapidly in the presence of H2O2, thereby augmenting the rate at which hydroxyl radicals are formed. During routine growth, cells maintain small cysteine pools, and cysteine is not a major contributor to DNA damage. Thus, the homeostatic control of cysteine levels is important in conferring resistance to oxidants.
520 $a To investigate the toxicity of endogenously produced H2O 2 an Hpx- mutant which lacks H2O 2-scavenging enzymes was constructed. Aerobically grown Hpx- cells showed a growth defect. They formed long filaments and exhibited high rates of mutagenesis, both indicators of DNA damage. Hpx- recA cells died rapidly when they were aerated, even though the accumulated level of intracellular H2O2 was less than 1 micromolar. Spin-trap experiments detected substantial hydroxyl radicals and iron chelators eliminated both the phenotypic defects and hydroxyl-radical formation, thereby confirming that the Fenton reaction was responsible. An Hpx- oxyR strain exhibited more DNA lesions than did the Hpx- mutant, indicating that the OxyR stress response induced a protein that suppressed DNA damage. This protein was Dps, an iron-sequestration protein, since Hpx- dps mutants exhibited sensitivity similar to that of the Hpx - oxyR mutant. These results reveal that aerobic E. coli generates sufficient H2O2 to create toxic levels of DNA damage.
520 $a Thus, we conclude that the vulnerability of cells to oxidative DNA damage is strongly determined by their ability to control free iron and cysteine and to scavenge H2O2.
590 $a School code: 0090.
650 4 $a Biology, Microbiology. $3 1017734
690 $a 0410
710 2 0 $a University of Illinois at Urbana-Champaign. $3 626646
773 0 $t Dissertation Abstracts International $g 66-07B.
790 1 0 $a Imlay, James A., $e advisor
790 $a 0090
791 $a Ph.D.
792 $a 2005
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3182346