scholarly journals Carbon Monoxide Targeting Mitochondria

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Cláudia S. F. Queiroga ◽  
Ana S. Almeida ◽  
Helena L. A. Vieira
Keyword(s):  
Carbon Monoxide ◽  
Cell Death ◽  
Mitochondrial Membrane ◽  
Cell Metabolism ◽  
Membrane Permeabilization ◽  
Biological Functions ◽  
Cellular Target ◽  
Cellular Source ◽  
Mitochondrial Membrane Permeabilization

Mitochondria present two key roles on cellular functioning: (i) cell metabolism, being the main cellular source of energy and (ii) modulation of cell death, by mitochondrial membrane permeabilization. Carbon monoxide (CO) is an endogenously produced gaseoustransmitter, which presents several biological functions and is involved in maintaining cell homeostasis and cytoprotection. Herein, mitochondrion is approached as the main cellular target of carbon monoxide (CO). In this paper, two main perspectives concerning CO modulation of mitochondrial functioning are evaluated. First, the role of CO on cellular metabolism, in particular oxidative phosphorylation, is discussed, namely, on: cytochromecoxidase activity, mitochondrial respiration, oxygen consumption, mitochondrial biogenesis, and general cellular energetic status. Second, the mitochondrial pathways involved in cell death inhibition by CO are assessed, in particular the control of mitochondrial membrane permeabilization.

scholarly journals Carbon monoxide prevents hepatic mitochondrial membrane permeabilization

2011 ◽  
Vol 12 (1) ◽  
pp. 10 ◽  
Author(s):  
Cláudia SF Queiroga ◽  
Ana S Almeida ◽  
Paula M Alves ◽  
Catherine Brenner ◽  
Helena LA Vieira
Keyword(s):  
Carbon Monoxide ◽  
Mitochondrial Membrane ◽  
Membrane Permeabilization ◽  
Mitochondrial Membrane Permeabilization

Mitochondrial Membrane Permeabilization in Cell Death

2007 ◽  
Vol 87 (1) ◽  
pp. 99-163 ◽  
Author(s):  
Guido Kroemer ◽  
Lorenzo Galluzzi ◽  
Catherine Brenner
Keyword(s):  
Cell Death ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion ◽  
Membrane Permeabilization ◽  
Critical Event ◽  
Anticancer Chemotherapy ◽  
Intermediate Metabolites ◽  
Mitochondrial Membrane Permeabilization ◽  
End Stage ◽  
Mitochondrial Lipids

Irrespective of the morphological features of end-stage cell death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subcellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to cell death, meaning that mitochondria coordinate the late stage of cellular demise. Pathological cell death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted cell death. Conversely, induction of MMP in tumor cells constitutes the goal of anticancer chemotherapy.

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