生物寿命如何调控? 本文揭示, 细胞呼吸中产生的活性氧可能是一决定因素. 在细胞呼吸链中,电子可能过早地从p66Shc逃脱形成易反应的活性氧, 进而造成细胞损伤, 引发细胞凋亡。 该工作可能为p66Shc在缩短动物寿命中的作用提供一个机制性的解释。
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Electron Transfer between Cytochrome c and p66Shc Generates Reactive Oxygen Species that Trigger Mitochondrial Apoptosis
M. Giorgio, E. Migliaccio, F. Orsini, D. Paolucci, M. Moroni, C. Contursi, G. Pelliccia, L. Luzi, S. Minucci, M. Marcaccio, P. Pinton, R. Rizzuto, P. Bernardi, F. Paolucci, and P.G. Pelicci
Energy is produced by mitochondria through a chain of reactions that transfers electrons from substrates to oxygen in the process of respiration. It is believed that electrons can accidentally escape this chain prematurely and form reactive oxygen species (ROS), which cause cell damage. Here, Giorgio et al. show that p66Shc, a protein previously implicated in regulation of apopotosis and life span, is an enzyme that generates ROS by diverting electrons from respiration. This function of p66Shc is activated by environmental stresses, and the generated ROS act as mediators of apoptosis. ROS-induced oxidative stress and apoptosis might explain the role of p66Shc in shortening life span in mammals. Source:Cell 122, 221-233, 2005/7/29
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