Other Cell Death Mechanisms

Necrosis is an alternate mode of cell death, which differs from apoptosis in significant ways. Necrosis is characterized by swelling of the cell and its organelles, including the mitochondria. Subsequently, cell membranes lose their integrity, and cellular constituents, including many degradative enzymes, leak into the surrounding tissue. This leakage often damages contiguous cells, and causes local exudative inflammation. Thus, unlike apoptosis, necrotic cell death is chaotic, and generally detrimental to the tissues in which it occurs (94,101).

Necrosis is generally induced by highly noxious stimuli, such as cytotoxins, hyperthermia, hypoxia, metabolic poisons, and direct cell or tissue trauma. In some pathological conditions—ischemic injury, for example—both apoptotic and necrotic cell death may occur. Cells are thought to die by necrosis, rather than apoptosis, when they experience more severe insults. In addition, cells may die by necrosis when one or more components of an apoptotic pathway are inactivated, which can occur as a consequence of mutation or physiological processes. For example, senescent human fibroblasts may become resistant to apoptosis-inducing signals because they cannot stabilize p53 in response to damage (73). As a result, senescent cells die by necrosis, rather than apoptosis. Necrosis, and the accompanying inflammation reactions, may increase during aging owing to age-related defects in the cellular machinery that controls and/or carries out apoptosis.

Recently, cell death pathways with both unique characteristics and characteristics of both apoptosis and necrosis have been described (112). These alternative cell death modes are generally distinguishable by their morphological characteristics, differential sensitivities to pharmacologic agents, and/or biochemical reactions. At present, little is known about how these alternative pathways impact normal or pathological physiology. However, some of them are prominent in age-related neurodegenerative diseases (112).

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