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III. APOPTOSIS
III.a. Introduction
Apoptosis is an active and precisely regulated process of cell death which is
energy dependent. Apoptosis is also charcctenzed by the absence of membrane rupture,
while apoptotic cells remain metabolically active for many hours or even days after the
initiation of the death process (Ken 1971;Ken 1965; Kerr et al. 1972). Ultrastructural
manifestations of apoptosis include compaction and fragmentation of nuclear chromatin,
cell shrinkage, condensation of cytoplasm, membrane blabbing and convolution of
nuclear outlines (Saikumar et al. 1999; Sharov et al. 1996). Another important
characteristic of apoptosis is the development of membrane bound apoptotic bodies
(apopsomes) and their degradation by phagocytes. Phagocytosis is achieved without the
spillage of cellular content so there is no involvement of inflammatory response (Majno
and Joris 1995). An activation of apoptotic pathways results in the activation of
endogenous endonucleases, which leads to the intranucleosomal chromatin cleavage
(Thompson 1995). However, a classical description of apoptotic and necrotic phenotypes
does not necessarily apply to all circumstances. Intermediate forms of cellular death with
the blend of morphological signs pointing to both apoptosis and necrosis can also be
seen. This phenomenon is termed "secondary necrosis", which represents the
superimposition of signs of necrosis on the cells that already exhibit signs of apoptosis
(Ferlini et a|. 1999; Papassotiropoulos et al. 1996; Wyllie 1997). Apoptosis is considered
to be an essential regulatory factor involved in a number of physiological processes such
as: organogenesis of central nervous system (Clarke et al. 1998; Gordon 1995), breast
involution after weaning (Strange et al. 1995), shedding of endometrium during
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