Programmed cell death (PCD) is a significant mechanism in both development and homeostasis in adult tissues for the elimination of either superfluous, infected, transformed or damaged cells by the launch of an intrinsic suicide program. One form of PCD is apoptosis, which is distinguished by the maintenance of intact cell membranes during the suicide process to allow adjacent cells to engulf the dying cell so that it does not release its contents and trigger a local inciting reaction. Cells undergoing apoptosis usually display a characteristic morphology, including fragmentation of the cell into membrane-bound apoptotic bodies, nuclear and cytoplasmic condensation and endolytic cleavage of the DNA into small oligonucleosomal fragments (Steller, 1445). The cells or fragments are then phagocytosed by macrophages. Signals that can activate apoptosis can include lineage information, harm due to ionizing radiation or viral infection or extracellular signals. Extrinsic signals may either suppress or promote apoptosis, and the same signals may encourage survival in one cell type and invoke the suicide program in others (Steller, 1447). Invocation of the suicide program involves the synthesis of specific messenger RNA molecules and their translation. PCD can sometimes be concealed by inhibiting transcription or translation (Steller, 1446-7), which provides proof that cell death is mediated by intrinsic cellular mechanisms. This process is necessary for development, tissue homeostasis, and defense against pathogens. Organized life necessitates cell death, and execution of cell death relies on the very machinery of life. Mitochondria, the organelles that produce energy through cellular respiration, integrate death signals arbitrate by proteins belonging to the Bcl-2/Bax family, and kill cells by releasing critical factors such as cytochrome c that activate executioner caspase proteases (Green et al.1309).
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