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Biochemistry Research International
Volume 2012 (2012), Article ID 749845, 9 pages
Review Article

Carbon Monoxide Targeting Mitochondria

1Instituto de Biologia Experimental e Tecnológica (IBET), Apartado 12, 2781-901 Oeiras, Portugal
2Instituto de Tecnologia Química e Biológica (ITQB), Universidade Nova de Lisboa, Apartado 127, 2781-901 Oeiras, Portugal
3CEDOC, Faculdade de Ciência Médicas, Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal

Received 11 November 2011; Accepted 9 January 2012

Academic Editor: Catherine Brenner

Copyright © 2012 Cláudia S. F. Queiroga et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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: cytochrome c oxidase 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.