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Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage
Fan, Peng-Cheng1,2,3; Zhang, Yao1,4,5; Wang, Yu2; Wei, Wei1; Zhou, Yan-Xia1; Xie, Yi6; Wang, Xin3; Qi, Ying-Zi1; Chang, Lei1; Jia, Zheng-Ping
刊名FREE RADICAL BIOLOGY AND MEDICINE
2019-01
卷号130页码:436-445
关键词Quantitative proteomics Mitochondria Heavy ion radiation iTRAQ Oxidative stress
ISSN号0891-5849
DOI10.1016/j.freeradbiomed.2018.10.449
英文摘要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.
资助项目Guangzhou science and technology innovation & development project[201802020016]
WOS关键词DOUBLE-STRAND BREAKS ; CELLS ; IRRADIATION ; EXPRESSION ; EXPOSURE ; GENE ; RADIOTHERAPY ; GLUTATHIONE ; GAMMA-H2AX ; PROTECTION
WOS研究方向Biochemistry & Molecular Biology ; Endocrinology & Metabolism
语种英语
出版者ELSEVIER SCIENCE INC
WOS记录号WOS:000455347000040
内容类型期刊论文
源URL[http://119.78.100.186/handle/113462/64487]  
专题中国科学院近代物理研究所
通讯作者Xu, Ping; Zhou, Ping-Kun
作者单位1.Beijing Inst Radiat Med, Beijing Proteome Res Ctr, Natl Ctr Prot Sci Beijing, State Key Lab Prote, Beijing 102206, Peoples R China
2.Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, Beijing Key Lab Radiobiol, Beijing 100850, Peoples R China
3.Gen Hosp Lanzhou, Key Lab Plateau Environm Damage Control, Lanzhou 730050, Gansu, Peoples R China
4.Sun Yat Sen Univ, Coll Ecol & Evolut, State Key Lab Biocontrol, Guangzhou 510275, Guangdong, Peoples R China
5.Sun Yat Sen Univ, Coll Ecol & Evolut, Guangdong Prov Key Lab Plant Resources, Guangzhou 510275, Guangdong, Peoples R China
6.Chinese Acad Sci, Inst Modern Phys, Dept Heavy Ion Radiat Med, Lanzhou 730000, Gansu, Peoples R China
7.Wuhan Univ, Sch Pharmaceut Sci, Minist Educ, Key Lab Combinatorial Biosynth & Drug Discovery, Wuhan 430071, Hubei, Peoples R China
推荐引用方式
GB/T 7714
Fan, Peng-Cheng,Zhang, Yao,Wang, Yu,et al. Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage[J]. FREE RADICAL BIOLOGY AND MEDICINE,2019,130:436-445.
APA Fan, Peng-Cheng.,Zhang, Yao.,Wang, Yu.,Wei, Wei.,Zhou, Yan-Xia.,...&Zhou, Ping-Kun.(2019).Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage.FREE RADICAL BIOLOGY AND MEDICINE,130,436-445.
MLA Fan, Peng-Cheng,et al."Quantitative proteomics reveals mitochondrial respiratory chain as a dominant target for carbon ion radiation: Delayed reactive oxygen species generation caused DNA damage".FREE RADICAL BIOLOGY AND MEDICINE 130(2019):436-445.
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