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Anti-oxidant adaptation in the AML cells supersensitive to hydrogen peroxide.

Identifieur interne : 000E93 ( Main/Exploration ); précédent : 000E92; suivant : 000E94

Anti-oxidant adaptation in the AML cells supersensitive to hydrogen peroxide.

Auteurs : Yoon-Kyeong Oh [Corée du Sud] ; Tae-Bum Lee ; Cheol-Hee Choi

Source :

RBID : pubmed:15158439

Descripteurs français

English descriptors

Abstract

The purpose of this study was to investigate the adaptive mechanisms of hydrogen peroxide-supersensitive AML cells against the reactive oxygen species (ROS). Their scavenging capacity against ROS was determined using a fluorometric probe in the doxorubicin-resistant AML-2/DX100 cell characterized by the down-regulation of catalase. AML-2/DX100 cells had more scavenging capacity against endogenous pro-oxidants than did the parental cells AML-2/WT, suggesting that an anti-oxidant adaptation against ROS occurred. cDNA microarrays for 8000 human genes revealed that among 21 anti-oxidant genes, each four gene was up- and down-regulated more than 1.5-fold in AML-2/DX100 compared with AML-2/WT. The mRNA expression of glutathione S-transferase Pi, peroxiredoxin 2, thioredoxin 2, and glutaredoxin was elevated whereas that of peroxiredoxin 3, metallothionein-1F, superoxide dismutase 2, and thioredoxin reductase 1 was depressed. The result indicates that the down-regulation of certain anti-oxidant mechanisms can be compensated for by the up- and down-regulation of the other anti-oxidant mechanisms.

DOI: 10.1016/j.bbrc.2004.04.145
PubMed: 15158439


Affiliations:


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Le document en format XML

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<nlm:affiliation>Research Center for Resistant Cells, Chosun University, Gwangju 501-759, Republic of Korea.</nlm:affiliation>
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<name sortKey="Choi, Cheol Hee" sort="Choi, Cheol Hee" uniqKey="Choi C" first="Cheol-Hee" last="Choi">Cheol-Hee Choi</name>
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<term>Antioxidants (pharmacology)</term>
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<term>Cell Line, Tumor (MeSH)</term>
<term>DNA, Complementary (metabolism)</term>
<term>Down-Regulation (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Hydrogen Peroxide (pharmacology)</term>
<term>Leukemia, Myeloid, Acute (metabolism)</term>
<term>Oligonucleotide Array Sequence Analysis (MeSH)</term>
<term>Oxidants (pharmacology)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Reactive Oxygen Species (MeSH)</term>
<term>Spectrometry, Fluorescence (MeSH)</term>
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<term>ADN complémentaire (métabolisme)</term>
<term>Antioxydants (pharmacologie)</term>
<term>Catalase (métabolisme)</term>
<term>Espèces réactives de l'oxygène (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Leucémie aigüe myéloïde (métabolisme)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Oxydants (pharmacologie)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Peroxyde d'hydrogène (pharmacologie)</term>
<term>Régulation négative (MeSH)</term>
<term>Spectrométrie de fluorescence (MeSH)</term>
<term>Séquençage par oligonucléotides en batterie (MeSH)</term>
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<term>Catalase</term>
<term>DNA, Complementary</term>
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<term>Antioxidants</term>
<term>Hydrogen Peroxide</term>
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<term>Lignée cellulaire tumorale</term>
<term>Oxydoréduction</term>
<term>Régulation négative</term>
<term>Spectrométrie de fluorescence</term>
<term>Séquençage par oligonucléotides en batterie</term>
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<div type="abstract" xml:lang="en">The purpose of this study was to investigate the adaptive mechanisms of hydrogen peroxide-supersensitive AML cells against the reactive oxygen species (ROS). Their scavenging capacity against ROS was determined using a fluorometric probe in the doxorubicin-resistant AML-2/DX100 cell characterized by the down-regulation of catalase. AML-2/DX100 cells had more scavenging capacity against endogenous pro-oxidants than did the parental cells AML-2/WT, suggesting that an anti-oxidant adaptation against ROS occurred. cDNA microarrays for 8000 human genes revealed that among 21 anti-oxidant genes, each four gene was up- and down-regulated more than 1.5-fold in AML-2/DX100 compared with AML-2/WT. The mRNA expression of glutathione S-transferase Pi, peroxiredoxin 2, thioredoxin 2, and glutaredoxin was elevated whereas that of peroxiredoxin 3, metallothionein-1F, superoxide dismutase 2, and thioredoxin reductase 1 was depressed. The result indicates that the down-regulation of certain anti-oxidant mechanisms can be compensated for by the up- and down-regulation of the other anti-oxidant mechanisms.</div>
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