MitoPlantRedoxV1, Main, Exploration, bibRecord, 000090

Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.

Identifieur interne : 000090 ( Main/Exploration ); précédent : 000089; suivant : 000091

Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.

Source :

Free radical biology & medicine [ 1873-4596 ] ; 2019.

RBID : pubmed:30395972

Descripteurs français

KwdFr :
- Altération de l'ADN (effets des radiations), Altération de l'ADN (génétique), Antioxydants (pharmacologie), Espèces réactives de l'oxygène (métabolisme), Humains (MeSH), Lignée cellulaire tumorale (MeSH), Mitochondries (effets des radiations), Mitochondries (métabolisme), Protéomique (MeSH), Radiothérapie par ions lourds (effets indésirables), Réparation de l'ADN (effets des radiations), Réparation de l'ADN (génétique), Transport d'électrons (effets des radiations), Tumeurs (génétique), Tumeurs (métabolisme), Tumeurs (radiothérapie).
MESH :
- effets des radiations : Altération de l'ADN, Mitochondries, Réparation de l'ADN, Transport d'électrons.
- effets indésirables : Radiothérapie par ions lourds.
- génétique : Altération de l'ADN, Réparation de l'ADN, Tumeurs.
- métabolisme : Espèces réactives de l'oxygène, Mitochondries, Tumeurs.
- pharmacologie : Antioxydants.
- radiothérapie : Tumeurs.
- Humains, Lignée cellulaire tumorale, Protéomique.

English descriptors

KwdEn :
- Antioxidants (pharmacology), Cell Line, Tumor (MeSH), DNA Damage (genetics), DNA Damage (radiation effects), DNA Repair (genetics), DNA Repair (radiation effects), Electron Transport (radiation effects), Heavy Ion Radiotherapy (adverse effects), Humans (MeSH), Mitochondria (metabolism), Mitochondria (radiation effects), Neoplasms (genetics), Neoplasms (metabolism), Neoplasms (radiotherapy), Proteomics (MeSH), Reactive Oxygen Species (metabolism).
MESH :
- chemical , metabolism : Reactive Oxygen Species.
- chemical , pharmacology : Antioxidants.
- adverse effects : Heavy Ion Radiotherapy.
- genetics : DNA Damage, DNA Repair, Neoplasms.
- metabolism : Mitochondria, Neoplasms.
- radiation effects : DNA Damage, DNA Repair, Electron Transport, Mitochondria.
- radiotherapy : Neoplasms.
- Cell Line, Tumor, Humans, Proteomics.

Abstract

Heavy ion radiotherapy has shown great promise for cancer therapy. Understanding the cellular response mechanism to heavy ion radiation is required to explore measures of overcoming devastating side effects. Here, we performed a quantitative proteomic analysis to investigate the mechanism of carbon ion irradiation on human AHH-1 lymphoblastoid cells. We identified 4602 proteins and quantified 4569 proteins showing high coverage in the mitochondria. Data are available via ProteomeXchange with identifier PXD008351. After stringent filtering, 290 proteins were found to be significantly up-regulated and 16 proteins were down-regulated. Functional analysis revealed that these up-regulated proteins were enriched in the process of DNA damage repair, mitochondrial ribosome, and particularly mitochondrial respiratory chain, accounting for approximately 50% of the accumulated proteins. Bioinformatics and functional analysis demonstrated that these up-regulated mitochondrial respiratory chain proteins enhanced ATP production and simultaneously reactive oxygen species release. More importantly, increased reactive oxygen species led to secondary organelle injury and lagged DNA double-strand breaks. Consistently, the expression of antioxidant enzymes was up-regulated for free radical scavenging. The mechanism of lagged secondary injury originated from disturbances in the mitochondrial respiratory chain. Our results provided a novel target for cell self-repair against heavy ion radiation-induced cellular damage.

DOI: 10.1016/j.freeradbiomed.2018.10.449
PubMed: 30395972

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Xu, Ping" sort="Xu, Ping" uniqKey="Xu P" first="Ping" last="Xu">Ping Xu</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.</title>
<author><name sortKey="Fan, Peng Cheng" sort="Fan, Peng Cheng" uniqKey="Fan P" first="Peng-Cheng" last="Fan">Peng-Cheng Fan</name>
<affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China; Key Laboratory of the Plateau of Environmental Damage Control, General Hospital of Lanzhou, Lanzhou 730050, China.</nlm:affiliation>
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<author><name sortKey="Zhang, Yao" sort="Zhang, Yao" uniqKey="Zhang Y" first="Yao" last="Zhang">Yao Zhang</name>
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<author><name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name>
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<author><name sortKey="Wei, Wei" sort="Wei, Wei" uniqKey="Wei W" first="Wei" last="Wei">Wei Wei</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206</wicri:regionArea>
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<author><name sortKey="Zhou, Yan Xia" sort="Zhou, Yan Xia" uniqKey="Zhou Y" first="Yan-Xia" last="Zhou">Yan-Xia Zhou</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206</wicri:regionArea>
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<author><name sortKey="Xie, Yi" sort="Xie, Yi" uniqKey="Xie Y" first="Yi" last="Xie">Yi Xie</name>
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<author><name sortKey="Wang, Xin" sort="Wang, Xin" uniqKey="Wang X" first="Xin" last="Wang">Xin Wang</name>
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<author><name sortKey="Qi, Ying Zi" sort="Qi, Ying Zi" uniqKey="Qi Y" first="Ying-Zi" last="Qi">Ying-Zi Qi</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206</wicri:regionArea>
<wicri:noRegion>Beijing102206</wicri:noRegion>
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<author><name sortKey="Chang, Lei" sort="Chang, Lei" uniqKey="Chang L" first="Lei" last="Chang">Lei Chang</name>
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<wicri:regionArea>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206</wicri:regionArea>
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<author><name sortKey="Jia, Zheng Ping" sort="Jia, Zheng Ping" uniqKey="Jia Z" first="Zheng-Ping" last="Jia">Zheng-Ping Jia</name>
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<author><name sortKey="Zhou, Zhe" sort="Zhou, Zhe" uniqKey="Zhou Z" first="Zhe" last="Zhou">Zhe Zhou</name>
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<wicri:regionArea>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850</wicri:regionArea>
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<author><name sortKey="Guan, Hua" sort="Guan, Hua" uniqKey="Guan H" first="Hua" last="Guan">Hua Guan</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850</wicri:regionArea>
<placeName><settlement type="city">Pékin</settlement>
</placeName>
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<author><name sortKey="Zhang, Hong" sort="Zhang, Hong" uniqKey="Zhang H" first="Hong" last="Zhang">Hong Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000</wicri:regionArea>
<wicri:noRegion>Lanzhou 730000</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Xu, Ping" sort="Xu, Ping" uniqKey="Xu P" first="Ping" last="Xu">Ping Xu</name>
<affiliation wicri:level="4"><nlm:affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; Key Laboratory of Combinatorial Biosynthesis and Drug Discovery of Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071, China. Electronic address: xuping@mail.ncpsb.org.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; Key Laboratory of Combinatorial Biosynthesis and Drug Discovery of Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071</wicri:regionArea>
<placeName><settlement type="city">Wuhan</settlement>
<region type="région">Hubei</region>
</placeName>
<orgName type="university">Université de Wuhan</orgName>
<placeName><settlement type="city">Wuhan</settlement>
<region type="province">Hubei</region>
</placeName>
</affiliation>
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<author><name sortKey="Zhou, Ping Kun" sort="Zhou, Ping Kun" uniqKey="Zhou P" first="Ping-Kun" last="Zhou">Ping-Kun Zhou</name>
<affiliation wicri:level="1"><nlm:affiliation>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China. Electronic address: zhoupk@bmi.ac.cn.</nlm:affiliation>
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<placeName><settlement type="city">Pékin</settlement>
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<series><title level="j">Free radical biology & medicine</title>
<idno type="eISSN">1873-4596</idno>
<imprint><date when="2019" type="published">2019</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidants (pharmacology)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>DNA Damage (genetics)</term>
<term>DNA Damage (radiation effects)</term>
<term>DNA Repair (genetics)</term>
<term>DNA Repair (radiation effects)</term>
<term>Electron Transport (radiation effects)</term>
<term>Heavy Ion Radiotherapy (adverse effects)</term>
<term>Humans (MeSH)</term>
<term>Mitochondria (metabolism)</term>
<term>Mitochondria (radiation effects)</term>
<term>Neoplasms (genetics)</term>
<term>Neoplasms (metabolism)</term>
<term>Neoplasms (radiotherapy)</term>
<term>Proteomics (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Altération de l'ADN (effets des radiations)</term>
<term>Altération de l'ADN (génétique)</term>
<term>Antioxydants (pharmacologie)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mitochondries (effets des radiations)</term>
<term>Mitochondries (métabolisme)</term>
<term>Protéomique (MeSH)</term>
<term>Radiothérapie par ions lourds (effets indésirables)</term>
<term>Réparation de l'ADN (effets des radiations)</term>
<term>Réparation de l'ADN (génétique)</term>
<term>Transport d'électrons (effets des radiations)</term>
<term>Tumeurs (génétique)</term>
<term>Tumeurs (métabolisme)</term>
<term>Tumeurs (radiothérapie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term>
</keywords>
<keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Heavy Ion Radiotherapy</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Altération de l'ADN</term>
<term>Mitochondries</term>
<term>Réparation de l'ADN</term>
<term>Transport d'électrons</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Radiothérapie par ions lourds</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Damage</term>
<term>DNA Repair</term>
<term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Altération de l'ADN</term>
<term>Réparation de l'ADN</term>
<term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term>
<term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term>
<term>Mitochondries</term>
<term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term>
</keywords>
<keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>DNA Damage</term>
<term>DNA Repair</term>
<term>Electron Transport</term>
<term>Mitochondria</term>
</keywords>
<keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="radiothérapie" xml:lang="fr"><term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Humans</term>
<term>Proteomics</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Protéomique</term>
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<front><div type="abstract" xml:lang="en">Heavy ion radiotherapy has shown great promise for cancer therapy. Understanding the cellular response mechanism to heavy ion radiation is required to explore measures of overcoming devastating side effects. Here, we performed a quantitative proteomic analysis to investigate the mechanism of carbon ion irradiation on human AHH-1 lymphoblastoid cells. We identified 4602 proteins and quantified 4569 proteins showing high coverage in the mitochondria. Data are available via ProteomeXchange with identifier PXD008351. After stringent filtering, 290 proteins were found to be significantly up-regulated and 16 proteins were down-regulated. Functional analysis revealed that these up-regulated proteins were enriched in the process of DNA damage repair, mitochondrial ribosome, and particularly mitochondrial respiratory chain, accounting for approximately 50% of the accumulated proteins. Bioinformatics and functional analysis demonstrated that these up-regulated mitochondrial respiratory chain proteins enhanced ATP production and simultaneously reactive oxygen species release. More importantly, increased reactive oxygen species led to secondary organelle injury and lagged DNA double-strand breaks. Consistently, the expression of antioxidant enzymes was up-regulated for free radical scavenging. The mechanism of lagged secondary injury originated from disturbances in the mitochondrial respiratory chain. Our results provided a novel target for cell self-repair against heavy ion radiation-induced cellular damage.</div>
</front>
</TEI>
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<DateCompleted><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>17</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>130</Volume>
<PubDate><Year>2019</Year>
<Month>01</Month>
</PubDate>
</JournalIssue>
<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.</ArticleTitle>
<Pagination><MedlinePgn>436-445</MedlinePgn>
</Pagination>
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<Abstract><AbstractText>Heavy ion radiotherapy has shown great promise for cancer therapy. Understanding the cellular response mechanism to heavy ion radiation is required to explore measures of overcoming devastating side effects. Here, we performed a quantitative proteomic analysis to investigate the mechanism of carbon ion irradiation on human AHH-1 lymphoblastoid cells. We identified 4602 proteins and quantified 4569 proteins showing high coverage in the mitochondria. Data are available via ProteomeXchange with identifier PXD008351. After stringent filtering, 290 proteins were found to be significantly up-regulated and 16 proteins were down-regulated. Functional analysis revealed that these up-regulated proteins were enriched in the process of DNA damage repair, mitochondrial ribosome, and particularly mitochondrial respiratory chain, accounting for approximately 50% of the accumulated proteins. Bioinformatics and functional analysis demonstrated that these up-regulated mitochondrial respiratory chain proteins enhanced ATP production and simultaneously reactive oxygen species release. More importantly, increased reactive oxygen species led to secondary organelle injury and lagged DNA double-strand breaks. Consistently, the expression of antioxidant enzymes was up-regulated for free radical scavenging. The mechanism of lagged secondary injury originated from disturbances in the mitochondrial respiratory chain. Our results provided a novel target for cell self-repair against heavy ion radiation-induced cellular damage.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fan</LastName>
<ForeName>Peng-Cheng</ForeName>
<Initials>PC</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China; Key Laboratory of the Plateau of Environmental Damage Control, General Hospital of Lanzhou, Lanzhou 730050, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; State Key Laboratory of Biocontrol and Guangdong Provincial Key Laboratory of Plant Resources, College of Ecology and Evolution, Sun Yat-Sen University, Guangzhou 510275, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yu</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Wei</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Yan-Xia</ForeName>
<Initials>YX</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xie</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of the Plateau of Environmental Damage Control, General Hospital of Lanzhou, Lanzhou 730050, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qi</LastName>
<ForeName>Ying-Zi</ForeName>
<Initials>YZ</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>Lei</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jia</LastName>
<ForeName>Zheng-Ping</ForeName>
<Initials>ZP</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of the Plateau of Environmental Damage Control, General Hospital of Lanzhou, Lanzhou 730050, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Zhe</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Guan</LastName>
<ForeName>Hua</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Hong</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Ping</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Proteomics, National Center for Protein Sciences Beijing, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing102206, China; Key Laboratory of Combinatorial Biosynthesis and Drug Discovery of Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071, China. Electronic address: xuping@mail.ncpsb.org.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Ping-Kun</ForeName>
<Initials>PK</Initials>
<AffiliationInfo><Affiliation>Beijing Key Laboratory for Radiobiology, Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing 100850, China. Electronic address: zhoupk@bmi.ac.cn.</Affiliation>
</AffiliationInfo>
</Author>
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<Month>11</Month>
<Day>03</Day>
</ArticleDate>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Fan, Peng Cheng" sort="Fan, Peng Cheng" uniqKey="Fan P" first="Peng-Cheng" last="Fan">Peng-Cheng Fan</name>
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<name sortKey="Qi, Ying Zi" sort="Qi, Ying Zi" uniqKey="Qi Y" first="Ying-Zi" last="Qi">Ying-Zi Qi</name>
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<name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name>
<name sortKey="Wei, Wei" sort="Wei, Wei" uniqKey="Wei W" first="Wei" last="Wei">Wei Wei</name>
<name sortKey="Xie, Yi" sort="Xie, Yi" uniqKey="Xie Y" first="Yi" last="Xie">Yi Xie</name>
<name sortKey="Xu, Ping" sort="Xu, Ping" uniqKey="Xu P" first="Ping" last="Xu">Ping Xu</name>
<name sortKey="Zhang, Hong" sort="Zhang, Hong" uniqKey="Zhang H" first="Hong" last="Zhang">Hong Zhang</name>
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<name sortKey="Zhou, Ping Kun" sort="Zhou, Ping Kun" uniqKey="Zhou P" first="Ping-Kun" last="Zhou">Ping-Kun Zhou</name>
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	Serveur d'exploration sur les mitochondries dans l'oxydoréduction chez les plantes
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Serveur d'exploration sur les mitochondries dans l'oxydoréduction chez les plantes

Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.

Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.

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