The Importance Of Cell Death

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Cell death restrains the superfluity of physiological processes such as embryogenesis, post-embryonic development (Penaloza et al, 2006) and tissue homeostasis and abrogating cell death provokes various diseases such as autoimmune diseases and cancers. (Galluzzi, Maiuri et al. 2007) In the long time of cell death related studies researcher have found dozens of methods to study the death related parameters but none of these method fulfill the requirement. NCCD (Nomenclature Committee on Cell Death) assigned some features for a cell known to be dead which includes. 1) Loss of plasma membrane integrity. 2) Complete destruction of the cell as well as its nucleus. 3) Engulfment of its fractions by neighboring macrophages in vivo. Cell death can be divided into various categories based on morphological appearance (apoptosis, autophagy, necrosis and mitosis associated cell death), enzymatic (with and without involving crucial enzymes such as nucleases, and proteases such as caspases or cathepsins), functional prospects (Physiological or pathological, programmed or accidental) or finally immunologic or non-immunogenic. (Kroemer, Galluzzi et al. 2009). It was earlier believed that the caspases dependent apoptosis governs all regulated cell death in mammalian cells (Fuchs and Steller, 2011; Thompson, 1995). But this perspective has recently changed after Christofferson et al and others have comprehended the non-apoptotic cell death pathway which includes apoptosis inducing factor 1 (AIF1)-dependent parthanatos, caspase-1-dependent pyroptosis, poly(ADP-ribose) polymerase-1 (PARP-1) and receptor interacting protein kinase 1 (RIPK1)- dependent necroptosis (Bergsbaken et al., 2009; Wang et al.,2009; Christofferson and Yuan, 2010). Yang et al h... ... middle of paper ... ...r cell proliferation and survival via high NADPH production and low ROS level (DeNicola, G.M. et al., 2011; Son, J. et al., 2013; Maddocks, O.D. et al., 2013). Glutathione homeostasis may be regulated via NADPH and so either glutathione reduction or high oxidative stress could induce senescence or cell death to a cancer cell (Trachootham D., et al., 2009). Small molecules targeting glutathione antioxidant network such as glutathione itself and glutathione peroxidase e.g. parthenolide (Pei, S. et al., 2013) and ethylisocyanate (Trachootham D., et al., 2006) catalytic subunit of glutamate cysteine ligase and system XC-- e.g. sulfasalazine and Errastin glutathione S-transferase pi 1 and carbonyl reductase e.g. piperlongumine (Raj, L. et al., 2011) could be promising tool to combat cancer stem cell populations which are resistant to radiotherapy induced apoptosis.
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