Cell death mechanism

The suggestion that eNOS-derived NO is implicated in neuronal cell death mechanisms in thiamine deficiency contrasts with current views in cerebral ischemia in which increased eNOS-derived NO is thought to play a neuro-protective role by virtue of its vasodilatory potential. 

Pannunzio, P., Hazell, A. S., Pannunzio, M., Rama Rao, K. V. and Butterworth, R. F. Thiamine deficiency results in metabolic acidosis and energy failure in cerebellar granule cells an in vitro model for the study of cell death mechanisms in Wernicke s encephalopathy. /. Neurosci. Res. 62 286-292, 2000. 

Martin, L. J. Neuronal death in amyotrophic lateral sclerosis is apoptosis possible contribution of a programmed cell death mechanism. /. Neuropathol. Exp. Neurol. 58 459-471, 1999. 

Epithelial cells of the GI tract are exposed to various agents (as indicated in previous sections) and conditions that activate stress-response pathways. This results in either cell survival or cell death. Those cells with inadequate cellular defenses may die by one of three major cell death mechanisms, apoptosis, autophagy or necrosis, depending upon the particular stress conditions. 

How ever, it is important to acknowledge that apoptosis is not the only means for neurons to die. Death of adult neurons in response to pathological challenges also occurs by necrosis, the unregulated cell death mechanism. Necrosis is mediated by increase in intracellular calcium that catalyses activation of Ca + -dependent cystine proteases like, cathepsins and calpains, w hich primarily compromise lysosomal integrity. Subsequently, these cystine proteases in the company of released lysosomal enzymes dismantle structural netw ork of neuron. Additionally, the intracellular pH also plays a major role in necrosis (Syntichaki and Tavemarakis, 2003). 

Jellinger KA. 2000. Cell death mechanisms in Parkinson s disease. J. Neural Transm. 107 1-29... 

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. 

Meseguer, J., M.A. Esteban and V. Mulero. Nonspecific cell-mediated cytotoxicity in the seawater teleosts Sparus aurata and Dicentrarchus labrax) ultrastructural study of target cell death mechanisms. Anat. Rec. 244 499 -505, 1996. 

Proteolytic enzymes are released to the medium because of cell death, mechanical stress, or induced cell lysis. Their presence is expected during fermentation and initial downstream unit operations. Most enzymes of the vacuoles and... 

More than 100 dominant oncogenes have been identified to date. Nearly all the components of the signal transduction chains that transmit signals from the cell exterior to the level of the cell cycle and transcription can be converted by mutations into an oncogenic state. It has to be emphasized that activation of an oncogene is generally not sufficient for transformation of a normal cell into a tumor cell. As outlined in Section 14.8.6, functional inactivation of cell death mechanisms must occur at the same time, and it is the cooperation of defects in oncogenic pathways and in apoptotic pathways that paves the way for the formation of a real tumor. 

Raghupathi R (2004) Cell death mechanisms following traumatic brain injury. Brain Path 14 215-222... 

M. Canete, A. (uarranz. Photodynamic Effects on Cultured Tumor Cells. Cytoskeleton Ahemtions and Cell Death Mechanisms,... 

Orrenius S, Nicotera P, Zhivotovsky B (2011) Cell death mechanisms and their implications in toxicology. Toxicol Sci 119 3-19... 

Nelfinavir inhibits experimentally induced tissue degeneration and cell damage by preventing loss of the mitochondrial membrane potential and even protects mitochondria in cancer cells. However, conversely, it selectively induces a mitochondria-independent cell death mechanism in cancer cells by the so-called endoplasmic reticulum unfolded protein stress response, allowing it to act on otherwise chemoresistant cancer cells [127 ]. 

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