الفهرس Only 14 pages are availabe for public view
 |  | from | 110 |  |  |
| | | from | 110 | | |
Abstract
There is increasing evidence that the inflammatory mediators are closely involved in the development of system inflammatory response syndrome (SIRS) and progression to multiple organ dysfunction syndrome (MODS) through induction of programmed cell death or apoptosis in vascular endothelial and\or organ parenchymal cells (Bannerman and Goldblum, 2003). Cytochrome c (Cyt-c) is an intra-mitochondrial protein normally residing in inter-membrane spaces and is involved in the electron transport system for oxidative phosphorylation (Lei et al, 2001). Recent interest has focused on its role as a potential inducer of the intrinsic apoptotic pathway (Fiers et al, 2001). In response to a variety of pathophysiologic stimuli, cytochrome c is released from its normal intra-mitochondrial locations; it traverses the outer mitochondrial membrane, and reaches the cytosol (Wei et al, 2001). Upon reaching the cytosol, and in the presence of deoxy-adenosine triphosphate, cytochrome c binds to Apaf-1 (Apoptotic protease-activation factor 1) a process that leads to caspase 9 recruitment (Green and Reed, 2003).The resulting cyto-c\ Apaf-1\ caspase 9 complex (the so-called apoptosome) can then activate downstream effector caspases culminating in cellular protein degradation, and ultimately, apoptotic cell death (Kroemer et al, 2003).