Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/8512
Title: Mitochondrial Dysfunction and Reactive Oxygen Species in Excitotoxicity and Apoptosis: Implications for the Pathogenesis of Neurodegenerative Diseases
Authors: Rego, A. Cristina 
Oliveira, Catarina R. 
Issue Date: 2003
Citation: Neurochemical Research. 28:10 (2003) 1563-1574
Abstract: In recent years we have witnessed a major interest in the study of the role of mitochondria, not only as ATP producers through oxidative phosphorylation but also as regulators of intracellular Ca2+ homeostasis and endogenous producers of reactive oxygen species (ROS). Interestingly, the mitochondria have been also implicated as central executioners of cell death. Increased mitochondrial Ca2+ overload as a result of excitotoxicity has been associated with the generation of superoxide and may induce the release of proapoptotic mitochondrial proteins, proceeding through DNA fragmentation/condensation and culminating in cell demise by apoptosis and/or necrosis. In addition, these processes have been implicated in the pathogenesis of many neurodegenerative diseases, which share several features of cell death: selective brain areas undergo neurodegeneration, involving mitochondrial dysfunction (mitochondrial complexes are affected), loss of intracellular Ca2+ homeostasis, excitotoxicity, and the extracellular or intracellular accumulation of insoluble protein aggregates in the brain.
URI: http://hdl.handle.net/10316/8512
DOI: 10.1023/A:1025682611389
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais

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