Hyperoxia in cell culture. A non-apoptotic programmed cell death.
Here we discuss the morphological features and our current understanding of the pathways involved in non-apoptotic cell death from O2 toxicity. Preliminary data on hyperoxic signaling indicate that NF-kappa B translocation (and presumptive activation) is not a result of the p42/p44 MAPK pathway, but a likely downstream consequence of activation of the JNK pathway. Our observations suggest the existence of multiple signal transduction pathways in hyperoxia-induced cell death: one involved in the stress response which appears to be NF-kappa B-dependent and another in cell death.
Kazzaz
J A
JA
CardioPulmonary Research Institute, Winthrop-University Hospital, SUNY Stony Brook School of Medicine, Mineola 11501, USA. jkazzaz@winthrop.org
Horowitz
S
S
Li
Y
Y
Mantell
L L
LL
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D016923:Cell Death; D002478:Cells, Cultured; D006801:Humans; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity*; D015398:Signal Transduction
D016328:NF-kappa B; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases; D010100:Oxygen