Akademik Veri Yönetim Sistemi
TURKIYE KLINIKLERI TIP BILIMLERI DERGISI, cilt.29, sa.6, ss.1677-1686, 2009 (SCI-Expanded)
Apoptosis and necrosis are two important cell death forms. Depending on the intensity and duration of the stimulus, either apoptosis or necrosis can take place. Biochemical and pathological findings are very different in both death forms but at the same time have some common features. These differences help us to distinguish necrosis and apoptosis in tissues. Cell shrinkage, chromatin condensation, formation of cytoplasmic blebs and apoptotic bodies and phagocytosis of these apoptotic cells by the macrophages without forming tissue damage are the four important events in apoptosis pathology. Bcl-2 family and caspases are the major mediators of apoptotic pathways. Intrinsic pathway, by the activation of caspases-8 and 10 and formation of death-inducing signal complex (DISC) and extrinsic pathway, by the activation of caspase-9 and apoptosome complex formation, both induce caspase-3. At this last step, caspase-3 causes typical fragmentation of DNA. Bcl-2 family has either apoptotic or anti-apoptotic members. According to the balance between bcl-2 proteins, pro-apoptotic or anti-apoptotic signals affect the mitochondria. If apoptotic signals are dominated cytochrome c is released from the mitochondria to form the apoptosome complex. Induced apoptosis causes organ insufficiency and inhibition of apoptosis causes hyperplasia and cancer. Apoptosis defects are important in developmental, otoimmune and neurodegenerative diseases and in cancer progress. In recent years, researches on the induction and blockage of apoptotic signal molecules, have presented a novel approach to the control of cancer progression. In this article, recent literature data on apoptosis regulatory molecules, its relationship with diseases and apoptosis detection methods were reviewed and were discussed.