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Effect of hyperoxia on cortical neuronal nuclear function and programmed cell death mechanisms
Journal article   Peer reviewed

Effect of hyperoxia on cortical neuronal nuclear function and programmed cell death mechanisms

Eddie Chang, Kristie Hornick, Karen I Fritz, Om P Mishra and Maria Delivoria-Papadopoulos
Neurochemical research, v 32(7), pp 1142-1149
Jul 2007
DOI: https://doi.org/10.1007/s11064-007-9282-4
PMID: 17401666
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

Animals Animals, Newborn Apoptosis - physiology bcl-2-Associated X Protein - metabolism Calcium - metabolism Calcium-Transporting ATPases - metabolism Cell Nucleus - metabolism Cerebral Cortex - cytology Humans Hyperoxia Lipid Peroxidation Neurons - cytology Neurons - physiology Phosphates - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Swine
There is growing concern over detrimental neurologic effects to human newborns caused by increased inspired oxygen concentrations. We hypothesize that hyperoxia (FiO(2)>0.95) results in increased high-affinity Ca(2+)-ATPase activity, Ca(2+)-influx, and proapoptotic protein expression in cortical neuronal nuclei of newborn piglets. Neuronal cerebral energy metabolism was documented by determining ATP and phosphocreatine levels. Neuronal nuclear conjugated dienes and fluorescent compounds were measured as indices of lipid peroxidation. High-affinity Ca(2+)-ATPase activity and ATP-dependent Ca(2+)-influx were determined to document neuronal nuclear membrane function. Hyperoxia resulted in increases in lipid peroxidation, high-affinity Ca(2+)-ATPase activity, ATP-dependent Ca(2+)-influx, and Bax/Bcl-2 ratio in the cortical neuronal nuclei of newborn piglets. We conclude that hyperoxia results in modification of neuronal nuclear membrane function leading to increased nuclear Ca(2+)-influx, and propose that hyperoxia-induced increases in intranuclear Ca(2+) activates the Ca(2+)/calmodulin-dependent protein kinase pathway, triggering increased CREB protein-mediated apoptotic protein expression in hyperoxic neurons.

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Web of Science research areas
Biochemistry & Molecular Biology
Neurosciences
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