中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2004, (2): 81-
氧化还原与细胞凋亡的关联
石 荣,贺福初*
军事医学科学院放射医学研究所基因组蛋白质组实验室,北京 100850
摘 要:细胞内氧化还原状态与细胞凋亡相互关联的机理仍然存在很大争议。细胞内氧化还原状态的改变促进了氧自由基(ROS)的产生和凋亡诱导因子的激活,致使细胞凋亡的同时又加剧了细胞内氧化还原状态的改变。通过激活细胞凋亡信号激酶(ASK-1)、氧化还原转录因子NF-kB、AP-1及Caspase激活,揭示了细胞内氧化还原状态伴随细胞凋亡的不同阶段。
关键词:细胞凋亡;氧化还原;氧自由基
 
Redox signaling and apoptosis
SHI Rong, HE Fu-Chu*
Laboratory of Genome and Proteomic, Institute of Radiation Medicine, Academy of Military Medical Sciences, Beijing 100850, China
Abstract: The regulatory role of cellular redox state during apoptosis is still controversial.  Redox signaling can transduce signals upstream  to mitochondria and initiate apoptosis. On the other hand, release of mitochondrial cytochrome C triggers generation of reactive oxygen species (ROS) and makes apoptotic cells much more oxidized. Although the sequential caspase activation does not have apparent redox-sensitive components, redox signaling provides a separate pathway that is parallel with the caspase cascade. The function of the apoptosis-associated redox change is uncertain. Some studies could provide positive feedback mechanisms, such as activating mitochondrial permeability transition, apoptosis signaling kinase (ASK-1) and redox-sensitive gene NF-kB. Simple redox signaling theory is difficult to explain how apoptosis happen,but each redox signaling plays a different role in the apoptosis process.
Key words: apoptosis; redox; reactive oxygen species(ROS)
 
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