DNA Damage by Low Concentration of Hydrogen Peroxide

1989 ◽  
Vol 53 (3) ◽  
pp. 835-836 ◽  
Author(s):  
Koichi Yoshinaga ◽  
Kayo Yamamoto ◽  
Hiroe Yoshioka ◽  
Kunihiko Hasegawa
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Low Concentration

scholarly journals DNA damage by low concentration of hydrogen peroxide.

1989 ◽  
Vol 53 (3) ◽  
pp. 835-836
Author(s):  
Koichi YOSHINAGA ◽  
Kayo YAMAMOTO ◽  
Hiroe YOSHIOKA ◽  
Kunihiko HASEGAWA
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Low Concentration

Antioxidative Effect of Rhus javanica Linne Extract Against Hydrogen Peroxide or Menadione Induced Oxidative Stress and DNA Damage in HepG2Cells

2004 ◽  
Vol 9 (2) ◽  
pp. 150-155 ◽  
Author(s):  
Chi-Sung Chun ◽  
Ji-Hyun Kim ◽  
Hyun-Ae Lim ◽  
Ho-Yong Sohn ◽  
Kun-Ho Son ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Antioxidative Effect

scholarly journals Escherichia coli MutM Suppresses Illegitimate Recombination Induced by Oxidative Stress

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 439-446 ◽  
Author(s):  
Masaaki Onda ◽  
Katsuhiro Hanada ◽  
Hirokazu Kawachi ◽  
Hideo Ikeda
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Double Strand Breaks ◽  
Illegitimate Recombination ◽  
Recombination Analysis ◽  
Wild Type ◽  
Strand Breaks ◽  
In The Wild

Abstract DNA damage by oxidative stress is one of the causes of mutagenesis. However, whether or not DNA damage induces illegitimate recombination has not been determined. To study the effect of oxidative stress on illegitimate recombination, we examined the frequency of λbio transducing phage in the presence of hydrogen peroxide and found that this reagent enhances illegitimate recombination. To clarify the types of illegitimate recombination, we examined the effect of mutations in mutM and related genes on the process. The frequency of λbio transducing phage was 5- to 12-fold higher in the mutM mutant than in the wild type, while the frequency in the mutY and mutT mutants was comparable to that of the wild type. Because 7,8-dihydro-8-oxoguanine (8-oxoG) and formamido pyrimidine (Fapy) lesions can be removed from DNA by MutM protein, these lesions are thought to induce illegitimate recombination. Analysis of recombination junctions showed that the recombination at Hotspot I accounts for 22 or 4% of total λbio transducing phages in the wild type or in the mutM mutant, respectively. The preferential increase of recombination at nonhotspot sites with hydrogen peroxide in the mutM mutant was discussed on the basis of a new model, in which 8-oxoG and/or Fapy residues may introduce double-strand breaks into DNA.

Factors which affect DNA strand breakage in human leukocytes exposed to a tumor promoter, phorbol myristate acetate

1982 ◽  
Vol 60 (11) ◽  
pp. 1359-1366 ◽  
Author(s):  
H. C. Birnboim
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Phorbol Myristate Acetate ◽  
Respiratory Burst ◽  
Superoxide Anion ◽  
Tumor Promoter ◽  
Myristate Acetate ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

We have recently reported that phorbol myristate acetate (PMA) induces extensive DNA strand break damage in human peripheral blood leukocytes. The mechanism of action involves superoxide anion and hydrogen peroxide which are generated by phagocytes during the "respiratory burst." In this report, we describe the effect of various inhibitors and scavengers on PMA-induced DNA damage. Azide and cyanide greatly increased the level of damage; sulfhydryl compounds (glutathione, cysteine, and cysteamine) and ascorbate markedly decreased the level of damage. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO) and glycerol also decreased the level of damage but apparently did so by inhibiting the respiratory burst. Diethyldithiocarbamate (DDC) increased the level of DNA damage at low concentrations (<1 mM), but decreased DNA damage at ≥1 mM. The results are consistent with a mechanism involving superoxide anion and hydrogen peroxide, but the precise reaction (free radical or enzymatic) responsible for DNA strand breakage has not been determined. The PMA-stimulated phagocyte is an interesting model system for looking at "active oxygen" mediated DNA damage and factors which influence it.

scholarly journals Labile iron pool correlates with iron content in the nucleus and the formation of oxidative DNA damage in mouse lymphoma L5178Y cell lines.

2003 ◽  
Vol 50 (1) ◽  
pp. 211-215 ◽  
Author(s):  
Marcin Kruszewski ◽  
Teresa Iwaneńko
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Cell Lines ◽  
Oxidative Dna Damage ◽  
Transition Metal Ions ◽  
Dna Lesions ◽  
Labile Iron Pool ◽  
Labile Iron ◽  
Iron Pool ◽  
Mouse Lymphoma

Labile iron pool (LIP) constitutes a crossroad of metabolic pathways of iron-containing compounds and is midway between the cellular need for iron, its uptake and storage. In this study we investigated oxidative DNA damage in relation to the labile iron pool in a pair of mouse lymphoma L5178Y (LY) sublines (LY-R and LY-S) differing in sensitivity to hydrogen peroxide. The LY-R cells, which are hydrogen peroxide-sensitive, contain 3 times more labile iron than the hydrogen peroxide-resistant LY-S cells. Using the comet assay, we compared total DNA breakage in the studied cell lines treated with hydrogen peroxide (25 microM for 30 min at 4 degrees C). More DNA damage was found in LY-R cells than in LY-S cells. We also compared the levels of DNA lesions sensitive to specific DNA repair enzymes in both cell lines treated with H(2)O(2). The levels of endonuclease III-sensitive sites and Fapy-DNA glycosylase-sensitive sites were found to be higher in LY-R cells than in LY-S cells. Our data suggest that the sensitivity of LY-R cells to H(2)O(2) is partially caused by the higher yield of oxidative DNA damage, as compared to that in LY-S cells. The critical factor appears to be the availability of transition metal ions that take part in the OH radical-generating Fenton reaction (very likely in the form of LIP).

Kinetics of the oxidation of diphenyl sulfide with hydrogen peroxide catalyzed by sodium metavanadate

1982 ◽  
Vol 60 (7) ◽  
pp. 848-852 ◽  
Author(s):  
Yoshiro Ogata ◽  
Kazushige Tanaka
Keyword(s):  
Hydrogen Peroxide ◽  
Rate Constant ◽  
Reaction Rate ◽  
Catalytic Amount ◽  
Probable Mechanism ◽  
Initial Concentration ◽  
Sodium Metavanadate ◽  
Low Concentration ◽  
Diphenyl Sulfide ◽  
Kinetics Of

The oxidation of diphenyl sulfide (Ph2S) by hydrogen peroxide in the presence of a catalytic amount of sodium metavanadate (NaVO3) has been studied kinetically by means of iodometry of hydrogen peroxide. The reaction rate is expressed as: v = k[NaVO3]st[Ph2S]2, when the concentration of catalyst is very low and [Ph2S]0/[H2O2]0 > 2, where []st and []0 mean stoichiometric and initial concentration, respectively. The effective oxidant may consist of polymeric as well as monomeric peroxyvanadate in view of the effect of concentration of catalyst on the rate. The main oxidizing species at low concentration of catalyst seems to be diperoxyvanadate VO5−. The rate constant k2 in v = k2[Ph2S]2 tends to decrease with initial concentration of H2O2, which is present in excess of the catalyst. A probable mechanism for the oxidation is discussed.

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