Fig. 1

A summary of extrinsic, intrinsic and membrane stress apoptotic pathways. a DNA damages lead to activation of p53 that promotes the expression of pro-apoptotic proteins such as BAX and consequently permeabilization of the outer membrane of mitochondria and release of cytochrome C followed by formation of a large multieric complex namely Apoptosom through participation of cytochrome C, dATP and apoptotic protease-activating factor-1 (APAF-1). b Activation of p53 by ionizing radiation leads to downstream transactivation of death receptor and death ligand that trigger extrinsic apoptotic pathway followed by complex formation between death receptor and its cognate ligand. Complex formation results in receptor trimerization and consequently formation of death inducing signal complex (DISC) by participation of FADD (Fas-associated death domain) mediated by DD (death domain). c Apoptosis might be prompted by production of ceramide as a second messanger which is activated by double strand breaks (DSBs) and reactive oxygen species (ROS) and as a result activation of sphingomyelinase followed by hydrolysis of sphyngomyelin and release of ceramide. The outcome of apoptosis is caspase activation which results in cell death due to production of apoptosome, death inducing signaling complex (DISC) and ceramide in intrinsic, extrinsic and memberane stress apoptotic pathways, respectively