Ho F Y, Tsang W P, Kong S K, Kwok T T
Department of Biochemistry, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.
Biochem Biophys Res Commun. 2006 Jul 7;345(3):1131-7. doi: 10.1016/j.bbrc.2006.04.178. Epub 2006 May 11.
Hypoxia/reoxygenation insult can be found in many tissues, including heart, brain, and tumor. It is believed that cell death may be resulted after cells were subjected to chronic hypoxia or reoxygenation after chronic hypoxia. The molecular mechanism for reoxygenation induced cell death is so far not clear and will require further study, in particular, to be distinguished from the pathways associated only with chronic hypoxia. In this study, the cell death mechanism in human squamous carcinoma A431 cells after hypoxia/reoxygenation insult is examined. It is demonstrated that although caspase-9 and -3 were activated during both hypoxia and reoxygenation, only those caspases activated during reoxygenation were responsible for reoxygenation induced apoptosis. Activation of caspase-9 and -3 during reoxygenation is believed to be triggered by the ROS formation at the time of reoxygenation. Addition of catalase during reoxygenation was found to attenuate reoxygenation induced apoptosis and caspase activation.
缺氧/复氧损伤可见于许多组织，包括心脏、大脑和肿瘤。据信，细胞在经历慢性缺氧或慢性缺氧后的复氧后可能会导致细胞死亡。复氧诱导细胞死亡的分子机制目前尚不清楚，需要进一步研究，特别是要与仅与慢性缺氧相关的途径区分开来。在本研究中，检测了人鳞状细胞癌A431细胞在缺氧/复氧损伤后的细胞死亡机制。结果表明，虽然半胱天冬酶-9和-3在缺氧和复氧过程中均被激活，但只有在复氧过程中被激活的那些半胱天冬酶才导致复氧诱导的细胞凋亡。复氧过程中半胱天冬酶-9和-3的激活被认为是由复氧时活性氧的形成所触发。发现在复氧过程中添加过氧化氢酶可减轻复氧诱导的细胞凋亡和半胱天冬酶激活。
