Bcl-2 functions in an antioxidant pathway to prevent apoptosis Export

@article{citeulike:819704, abstract = {SummaryBcl-2 inhibits most types of apoptotic cell death, implying a common mechanism of lethality. Bcl-2 is localized to intracellular sites of oxygen free radical generation including mitochondria, endoplasmic reticula, and nuclear membranes. Antioxidants that scavenge peroxides, N-acetylcysteine and glutathione peroxidase, countered apoptotic death, while manganese superoxide dismutase did not. Bcl-2 protected cells from H2O2- and menadione-induced oxidative deaths. Bcl-2 did not prevent the cyanide-resistant oxidative burst generated by menadione. Two model systems of apoptosis showed no increment in cyanide-resistant respiration, and generation of endogenous peroxides continued at an inherent rate that was unaltered by Bcl-2. Following an apoptotic signal, cells sustained progressive lipid peroxidation. Overexpression of Bcl-2 functioned to suppress lipid peroxidation completely. We propose a model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation.}, author = {Hockenbery, David M. and Oltvai, Zoltan N. and Yin, Xiao-Ming and Milliman, Curt L. and Korsmeyer, Stanley J.}, citeulike-article-id = {819704}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/0092-8674(93)80066-N}, citeulike-linkout-1 = {http://www.sciencedirect.com/science/article/B6WSN-4DXBC74-6/2/2ec157acaa90ed0bfe622d96ac8bbec7}, day = {22}, doi = {10.1016/0092-8674(93)80066-N}, journal = {Cell}, keywords = {apoptosis, apoptotic-balance, bcl2, oxidative-stress}, month = {October}, number = {2}, pages = {241--251}, posted-at = {2006-08-28 13:26:34}, priority = {2}, title = {Bcl-2 functions in an antioxidant pathway to prevent apoptosis}, url = {http://dx.doi.org/10.1016/0092-8674(93)80066-N}, volume = {75}, year = {1993} }

TY - JOUR ID - citeulike:819704 L3 - citeulike-article-id:819704 N2 - SummaryBcl-2 inhibits most types of apoptotic cell death, implying a common mechanism of lethality. Bcl-2 is localized to intracellular sites of oxygen free radical generation including mitochondria, endoplasmic reticula, and nuclear membranes. Antioxidants that scavenge peroxides, N-acetylcysteine and glutathione peroxidase, countered apoptotic death, while manganese superoxide dismutase did not. Bcl-2 protected cells from H2O2- and menadione-induced oxidative deaths. Bcl-2 did not prevent the cyanide-resistant oxidative burst generated by menadione. Two model systems of apoptosis showed no increment in cyanide-resistant respiration, and generation of endogenous peroxides continued at an inherent rate that was unaltered by Bcl-2. Following an apoptotic signal, cells sustained progressive lipid peroxidation. Overexpression of Bcl-2 functioned to suppress lipid peroxidation completely. We propose a model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation. IS - 2 JF - Cell EP - 251 TI - Bcl-2 functions in an antioxidant pathway to prevent apoptosis VL - 75 SP - 241 KW - apoptosis KW - apoptotic-balance KW - bcl2 KW - oxidative-stress AU - Hockenbery, David AU - Oltvai, Zoltan AU - Yin, Xiao-Ming AU - Milliman, Curt AU - Korsmeyer, Stanley PY - 1993/10/22/ UR - http://dx.doi.org/10.1016/0092-8674(93)80066-N ER -