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Essay / Research Paper Abstract
This 10 page paper provides an overview of the existing research. Nitric oxide induced apoptosis, or cell death, has been the focus of a considerable amount of research, especially in terms of efforts to prevent or treat disease. It has been recognized, for example, that assessing the impacts of nitric oxide induced apoptosis may be beneficial in reducing cancer metastasis, reducing the impacts of dementia, and addressing the problems related types of disease. Bibliography lists 10 sources.
Page Count:
10 pages (~225 words per page)
File: MH11_MHNitriO.rtf
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especially in terms of efforts to prevent or treat disease. It has been recognized, for example, that assessing the impacts of nitric oxide induced apoptosis may be beneficial in
reducing cancer metastasis, reducing the impacts of dementia, and addressing the problems related types of disease. Determining the effect of nitric oxide induced apoptosis on p53 activity in human
disease, then, requires an assessment of a considerable body of research. 2-The role of nitric oxide on apoptosis Apoptosis can be described as a "process of programmed cell death
or cell suicide" (RCDRG, 2004). Apoptosis often occurs as an essential counterbalance to cell proliferation, and has been studied in the assessment of disease progression, tumor growth, and even
in trophoblast cells that proliferate during pregnancy (RCDRG, 2004). Nitric oxide (NO) plays a significant role in cell apoptosis, as well as acting as a mitigating agent in
a variety of other physiological processes. Nitric oxide acts as a signaling molecule to regulate a range of processes in tissues, including the following: "vasodilation , neuronal function,
inflammation and immune function" (RCDRG, 2004). Further, NO has also been assessed as a component in the regulation of cell necrosis and apoptosis, as well as in the protection from
apoptosis in particular cell types (RCDRG, 2004). "Nitric oxide has been demonstrated to inhibit apoptosis in a number of cell types including leukocytes, hepatocytes, trophoblasts and endothelial cells" (RCDRG,
2004). The anti-apoptotic effects of nitric oxide occur in conjunction with a number of different mediating mechanisms, including " nitrosylation and inactivation of many of the caspases including caspase 3,
caspase 1 and caspase 8. Other mechanisms include activating p53, upregulating heat shock protein 70 (and consequently blocking recruitment of pro-caspase 9 to the Apaf-1 apoptosome), upregulating Bcl-2 and Bcl-XL
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