Calcium, mitochondria and oxidative stress in neuronal pathology - Novel aspects of an enduring theme

被引:187
作者
Chinopoulos, C [1 ]
Adam-Vizi, V [1 ]
机构
[1] Semmelweis Univ, Dept Biochem Med, Neurobiochem Grp, Hungarian Acad Sci,Szentagothai Knowledge Ctr, H-1444 Budapest, Hungary
关键词
alpha-ketoglutarate dehydrogenase; oxidative stress; permeability transition pore; store-operated Ca2+ entry; transient receptor potential; TRPM2; TRPM7;
D O I
10.1111/j.1742-4658.2005.05103.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The interplay among reactive oxygen species (ROS) formation, elevated intracellular calcium concentration and mitochondrial demise is a recurring theme in research focusing on brain pathology, both for acute and chronic neurodegenerative states. However, causality, extent of contribution or the sequence of these events prior to cell death is not yet firmly established. Here we review the role of the alpha-ketoglutarate dehydrogenase complex as a newly identified source of mitochondrial ROS production. Furthermore, based on contemporary reports we examine novel concepts as potential mediators of neuronal injury connecting mitochondria, increased [Ca2+](c) and ROS/reactive nitrogen species (RNS) formation; specifically: (a) the possibility that plasmalemmal nonselective cationic channels contribute to the latent [Ca2+](c) rise in the context of glutamate-induced delayed calcium deregulation; (b)the likelihood of the involvement of the channels in the phenomenon of 'Ca2+ paradox' that might be implicated in ischemia/reperfusion injury; and (c) how ROS/RNS and mitochondrial status could influence the activity of these channels leading to loss of ionic homeostasis and cell death.
引用
收藏
页码:433 / 450
页数:18
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