Anti-oxidant adaptation in the AML cells supersensitive to hydrogen peroxide.
Identifieur interne : 000E93 ( Main/Exploration ); précédent : 000E92; suivant : 000E94Anti-oxidant adaptation in the AML cells supersensitive to hydrogen peroxide.
Auteurs : Yoon-Kyeong Oh [Corée du Sud] ; Tae-Bum Lee ; Cheol-Hee ChoiSource :
- Biochemical and biophysical research communications [ 0006-291X ] ; 2004.
Descripteurs français
- KwdFr :
- ADN complémentaire (métabolisme), Antioxydants (pharmacologie), Catalase (métabolisme), Espèces réactives de l'oxygène (MeSH), Humains (MeSH), Leucémie aigüe myéloïde (métabolisme), Lignée cellulaire tumorale (MeSH), Oxydants (pharmacologie), Oxydoréduction (MeSH), Peroxyde d'hydrogène (pharmacologie), Régulation négative (MeSH), Spectrométrie de fluorescence (MeSH), Séquençage par oligonucléotides en batterie (MeSH).
- MESH :
- métabolisme : ADN complémentaire, Catalase, Leucémie aigüe myéloïde.
- pharmacologie : Antioxydants, Oxydants, Peroxyde d'hydrogène.
- Espèces réactives de l'oxygène, Humains, Lignée cellulaire tumorale, Oxydoréduction, Régulation négative, Spectrométrie de fluorescence, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Antioxidants (pharmacology), Catalase (metabolism), Cell Line, Tumor (MeSH), DNA, Complementary (metabolism), Down-Regulation (MeSH), Humans (MeSH), Hydrogen Peroxide (pharmacology), Leukemia, Myeloid, Acute (metabolism), Oligonucleotide Array Sequence Analysis (MeSH), Oxidants (pharmacology), Oxidation-Reduction (MeSH), Reactive Oxygen Species (MeSH), Spectrometry, Fluorescence (MeSH).
- MESH :
- chemical , metabolism : Catalase, DNA, Complementary.
- chemical , pharmacology : Antioxidants, Hydrogen Peroxide, Oxidants.
- metabolism : Leukemia, Myeloid, Acute.
- Cell Line, Tumor, Down-Regulation, Humans, Oligonucleotide Array Sequence Analysis, Oxidation-Reduction, Reactive Oxygen Species, Spectrometry, Fluorescence.
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:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<author><name sortKey="Oh, Yoon Kyeong" sort="Oh, Yoon Kyeong" uniqKey="Oh Y" first="Yoon-Kyeong" last="Oh">Yoon-Kyeong Oh</name>
<affiliation wicri:level="1"><nlm:affiliation>Research Center for Resistant Cells, Chosun University, Gwangju 501-759, Republic of Korea.</nlm:affiliation>
<country xml:lang="fr">Corée du Sud</country>
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<author><name sortKey="Lee, Tae Bum" sort="Lee, Tae Bum" uniqKey="Lee T" first="Tae-Bum" last="Lee">Tae-Bum Lee</name>
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<author><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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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidants (pharmacology)</term>
<term>Catalase (metabolism)</term>
<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>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><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>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term>
<term>DNA, Complementary</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term>
<term>Hydrogen Peroxide</term>
<term>Oxidants</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leukemia, Myeloid, Acute</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ADN complémentaire</term>
<term>Catalase</term>
<term>Leucémie aigüe myéloïde</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term>
<term>Oxydants</term>
<term>Peroxyde d'hydrogène</term>
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<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Down-Regulation</term>
<term>Humans</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Oxidation-Reduction</term>
<term>Reactive Oxygen Species</term>
<term>Spectrometry, Fluorescence</term>
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<term>Humains</term>
<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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<front><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>
</front>
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<ArticleTitle>Anti-oxidant adaptation in the AML cells supersensitive to hydrogen peroxide.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
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