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Hyperoxia in cell culture. A non-apoptotic programmed cell death
1CardioPulmonary Research Institute, Winthrop-University Hospital, SUNY Stony Brook School of Medicine, Mineola 11501, USA. jkazzaz@winthrop.org
Annals of the New York Academy of Sciences
|February 11, 2000
Abstract:
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.