TY - JOUR
T1 - Necrotic death without mitochondrial dysfunction-delayed death of cardiac myocytes following oxidative stress
AU - Casey, Tammy
AU - Arthur, Peter
AU - Bogoyevitch, M.A.
PY - 2007
Y1 - 2007
N2 - Oxidative stress has been implicated in cell death in range of disease states including ischemia/reperfusion injury of the heart and heart failure.Here we have investigated the mechanisms of cell death following chronic exposure of cardiac myocytes to oxidative stress initiated by hydrogenperoxide. This exposure induced a delayed form of cell death with ultrastructural changes typical of necrosis, and that was accompanied by therelease of lactate dehydrogenase and increased lipid peroxidation. However, this delayed death was not accompanied by the loss of mitochondrialmembrane potential or caspase-3 activation. Furthermore, we could demonstrate that this delayed necrosis was at least partially prevented by pretreatmentwith the hypertrophic stimuli endothelin-1 or leukemic inhibitory factor. Our results suggest that this delayed form necrosis may alsocomprise an ordered series of events involving pathways amenable to therapeutic modulation.© 2006 Elsevier B.V. All rights reserved.
AB - Oxidative stress has been implicated in cell death in range of disease states including ischemia/reperfusion injury of the heart and heart failure.Here we have investigated the mechanisms of cell death following chronic exposure of cardiac myocytes to oxidative stress initiated by hydrogenperoxide. This exposure induced a delayed form of cell death with ultrastructural changes typical of necrosis, and that was accompanied by therelease of lactate dehydrogenase and increased lipid peroxidation. However, this delayed death was not accompanied by the loss of mitochondrialmembrane potential or caspase-3 activation. Furthermore, we could demonstrate that this delayed necrosis was at least partially prevented by pretreatmentwith the hypertrophic stimuli endothelin-1 or leukemic inhibitory factor. Our results suggest that this delayed form necrosis may alsocomprise an ordered series of events involving pathways amenable to therapeutic modulation.© 2006 Elsevier B.V. All rights reserved.
U2 - 10.1016/j.bbamcr.2006.11.013
DO - 10.1016/j.bbamcr.2006.11.013
M3 - Article
VL - 1773
SP - 342
EP - 351
JO - BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
JF - BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
SN - 0167-4889
IS - 3
ER -