氧化还原与细胞凋亡的关联

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-κB、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。

Redox signaling and apoptosis

The regulatory role of cellular redox state during apoptosis is still controversial. Redox signaling cantransduce signals upstream to mitochondria and initiate apoptosis. On the other hand, release of mitochondrialcytochrome C triggers generation of reactive oxygen species (ROS) and makes apoptotic cells much moreoxidized. 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 theapoptosis-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-sensi-tive gene NF-kB. Simple redox signaling theory is difficult to explain how apoptosis happen,but each redoxsignaling plays a different role in the apoptosis process.