Cell death/necrosis different from apoptosis

Apoptosis is programed cell death and differs from necrosis in that it results in minimal inflammation and release of genetic material. Although necrosis is the predominant process that follows acute ischemia, apoptosis is important after more minor injury, particularly within the ischemic penumbra. Apoptosis is executed by the production, activation and action of caspases, which are protein-cleaving enzymes that dismantle cytoskeleton proteins and enzymes responsible for cellular repair (Zhang et al. 2004). Neurons are particularly susceptible to caspase-mediated cell death after cerebral ischemia, as demonstrated by the reduction in infarct size by caspase inhibitors in experimental models. 

We also investigated the effect of 1-7 compotmds on the cell cycle (Fig. 11.33). The synthesis of enzymes for DNA replication takes place in the G1 phase, the replication of DNA in the S phase, the synthesis of proteins in the G2 phase, and finally, the cell division in the M phase. Cancer cells proliferate when the regulation of this cell cycle malfunctions. There are two paths in which antitumor agents act on cells one is associated with cell death, and the other one simply slows cell growth. Cell death is classified into apoptosis and necrosis. The spontaneous removal of unwanted cells is called apoptosis, and necrosis refers to cell death related to inflammation caused by bums and poison. After the addition of 1-7, 78.6 % of cells were in the G1 phase compared to 59.8 % in the control group. On the other hand, the rate of apoptosis was not different. Thus, 1-7 slows the transition to the S phase from G1 phase, but it does not induce apoptosis. 

Many of the morphological and biochemical changes that occur in cells that die by necrosis are very different from those that occur in apoptosis. During necrosis cells swell, mitochondria and endoplasmic reticulum lose their structure and become dysfunctional and the nuclear membrane becomes disrupted (Fig. 35-1). Necrotic death is independent of premitochondrial apoptotic proteins such as Bax, cytochrome c release and caspase activation. Necrosis is further distinguished from apoptosis by the fact that necrosis usually occurs as the result of a traumatic physical injury or stroke and cells die en masse, whereas apoptosis typically occurs in individual cells within a population of surviving neighbors. 

Necrotic cell death differs markedly from apoptosis, a morphologically distinct pathway to cell death under the control of conserved genetic elements (Table 1). Apoptotic cell death (a.k.a. programmed cell death or cell suicide) is an active cell death mechanism that functions to remove unwanted cells from a tissue in a controlled, orderly fashion. It generally affects cells in isolation, which exhibit a suite of conserved morphological and biochemical features that contrast sharply with those observed during necrosis. 

Taken together, these results show that lyso-PC may induce different modes of cell death depending on the cell line. Apoptosis prevails in human endothelial cell lines and necrosis is found in rodent endothelial and smooth muscle cell lines. It has been suggested a long time ago that the susceptibility of a cell towards lyso-PC is determined by its amount and distribution in the cellular membranes of various species (Bierbaum et al., 1979). Obviously, there must be specific differences in membrane architecture between human and rodent cells that are responsible for the individual susceptibilities towards the cytotoxic effects of lysophospholipids. Currently these differences are still far from clear and await further investigation. 

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