Reactive Oxygen and Apoptosis

Abstract

Apoptosis – programmed cell death–was first described as a distinct morphological form of cell death characterized by cell shrinkage, membrane disrupture, and chromatin condensation which finally leads to cell fragmentation (Kerr et al. 1972). Internucleosomal DNA cleavage is one early hallmark in the process of cell death (Wyllie 1980). The patterns of this type of cell death during development suggest a distinct genetic program for cell death that is triggered in the cells (Sulston and Horvitz 1977; Wyllie 1980; Abrams et al. 1993; Green and Scott 1994). Further support comes from the isolation of mutants of the nematode Caenorhabditis elegans which are, unlike the wild type, defective for developmental cell death (Ellis and Horvitz 1986; Hengartner 1992).

Apoptosis appears to be a general property of most cells (Vaux 1993), being fundamental for the organization and life span of any organism to control homeostasis and cell populations. Apoptosis is necessary to achieve an adequate balance between sufficient survival of cells and overwhelming proliferation and expansion. This is of particular importance to prevent malignant growth, but it is also necessary to limit expansion of immune cells challenged by pathogens or other stimuli, and as a defense mechanism to remove self-reactive lymphocytes (Wyllie 1980; Arends and Wyllie 1991; Ellis et al. 1991; Raff 1992; Steller 1995). Apoptosis, in contrast to necrosis, is a biochemically active metabolic process (Cohen 1993; Williams and Smith 1993). Cells enter apoptotic pathways as a response to a variety of primary triggers, like the presence or absence of hormonal...