Mitochondrial oxidative stress: implications for cell death.

@article{citeulike:1838583, abstract = {In addition to the established role of the mitochondria in energy metabolism, regulation of cell death has emerged as a second major function of these organelles. This seems to be intimately linked to their generation of reactive oxygen species (ROS), which have been implicated in mtDNA mutations, aging, and cell death. Mitochondrial regulation of apoptosis occurs by mechanisms, which have been conserved through evolution. Thus, many lethal agents target the mitochondria and cause release of cytochrome c and other pro-apoptotic proteins into the cytoplasm. Cytochrome c release is initiated by the dissociation of the hemoprotein from its binding to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and increases the level of soluble cytochrome c in the intermembrane space. Subsequent release of the hemoprotein occurs by pore formation mediated by pro-apoptotic Bcl-2 family proteins, or by Ca(2+) and ROS-triggered mitochondrial permeability transition, although the latter pathway might be more closely associated with necrosis. Taken together, these findings have placed the mitochondria in the focus of current cell death research.}, address = {Institute of Environmental Medicine, Karolinska Institutet, S-171 77 Stockholm, Sweden. Sten.Orrenius@ki.se}, author = {Orrenius, S. and Gogvadze, V. and Zhivotovsky, B. }, citeulike-article-id = {1838583}, doi = {http://dx.doi.org/10.1146/annurev.pharmtox.47.120505.105122}, issn = {0362-1642}, journal = {Annu Rev Pharmacol Toxicol}, keywords = {cardiolipin}, pages = {143--183}, posted-at = {2008-04-12 19:58:43}, priority = {2}, title = {Mitochondrial oxidative stress: implications for cell death.}, url = {http://dx.doi.org/10.1146/annurev.pharmtox.47.120505.105122}, volume = {47}, year = {2007} }

TY - JOUR ID - citeulike:1838583 L3 - citeulike-article-id:1838583 TI - Mitochondrial oxidative stress: implications for cell death. JF - Annu Rev Pharmacol Toxicol VL - 47 SP - 143 EP - 183 AD - Institute of Environmental Medicine, Karolinska Institutet, S-171 77 Stockholm, Sweden. Sten.Orrenius@ki.se SN - 0362-1642 N2 - In addition to the established role of the mitochondria in energy metabolism, regulation of cell death has emerged as a second major function of these organelles. This seems to be intimately linked to their generation of reactive oxygen species (ROS), which have been implicated in mtDNA mutations, aging, and cell death. Mitochondrial regulation of apoptosis occurs by mechanisms, which have been conserved through evolution. Thus, many lethal agents target the mitochondria and cause release of cytochrome c and other pro-apoptotic proteins into the cytoplasm. Cytochrome c release is initiated by the dissociation of the hemoprotein from its binding to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and increases the level of soluble cytochrome c in the intermembrane space. Subsequent release of the hemoprotein occurs by pore formation mediated by pro-apoptotic Bcl-2 family proteins, or by Ca(2+) and ROS-triggered mitochondrial permeability transition, although the latter pathway might be more closely associated with necrosis. Taken together, these findings have placed the mitochondria in the focus of current cell death research. KW - cardiolipin AU - Orrenius, S AU - Gogvadze, V AU - Zhivotovsky, B PY - 2007/// UR - http://dx.doi.org/10.1146/annurev.pharmtox.47.120505.105122 ER -