ABSTRACT
Apoptosis is a cell suicide program that removes damaged, infected, and superfluous cells. The term apoptosis was coined in a classic paper by Kerr et al. in 1972 [1] to describe a distinct mode of cell destruction, which is the major mechanism for elimination of overabundant and unwanted cells during embryonic development, growth, differentiation, and normal cell turnover. It is a programmed sequence of biochemical events triggered by specific physiological and stress stimuli leading to the activation of a set of cysteine proteases known as caspases. These enzymes are the effectors for the programmed disintegration of subcellular structures leading ultimately to cell death. In addition to the involvement of apoptosis in the programming of nor-
mal development, a number of pathological stimuli have been shown to induce apoptosis, including extracellular stress (ionizing and ultraviolet radiation, heat shock, and oxidative and osmotic stress), receptor-mediated processes, growth-factor withdrawal, loss of cell adhesion (anoikis), cytotoxic lymphocytes, and many chemotherapeutic drugs. Radiation biologists were aware of the process before the use of the term
apoptosis and before the phenomenon was widely studied. The rapid death of small lymphocyteswhich is observed following irradiation results from an apoptotic mechanism but was originally termed interphase death because cell death preceded cell division rather than following it as is the case with reproductive or mitotic death. This chapter describes the basic mechanisms of apoptosis, the apoptotic
cascades, and how they may be set in motion by ionizing radiation.
