PMID: 9194529May 1, 1997Paper

Decrease of heart protein kinase C and cyclin-dependent kinase precedes death in perinatal asphyxia of the rat

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
B LubecG Lubec

Abstract

Acidosis, energy depletion, overstimulation by excitatory amino acids, and free radical-mediated reactions are the major current concepts for the explanation of damage and death resulting from asphyxia. Impaired phosphorylation by protein kinase C (PKC) represents another mechanism incriminated for cell death. We used an unsophisticated perinatal asphyxia model to study heart protein kinases PKC and cyclin dependent kinase (CDK). Tissue pH, ATP, the antioxidant enzymes superoxide dismutase, catalase, and glutathion peroxidase, lipid peroxidation products, carbonyls, and aromatic hydroxylation were also tested. Electron spin resonance was applied to demonstrate the possible presence of radical adducts. An ELISA method was used to determine cell death. PKC activity and mRNA decreased with the length of the asphyctic periods and were paralleled by CDK and pH, whereas cell death gradually increased. No evidence was found for the involvement of active oxygen species or a radical adduct, and no energy depletion was observed. We conclude that impaired protein phosphorylation and/or acidosis may play a role in the pathobiochemistry of death from perinatal asphyxia in the rat.

Citations

Jun 1, 2011·The EPMA Journal·Paola MoralesEdgardo Rojas-Mancilla
Jul 21, 2010·Neurotoxicity Research·Mario Herrera-MarschitzPeter J Gebicke-Haerter
Mar 28, 2018·Molecular Neurobiology·Jean Pierre Mendes LimaDaniela Uziel
Feb 13, 2001·Biochemical and Biophysical Research Communications·B C YooG Lubec
Feb 23, 2000·Experimental Neurology·W MosgoellerB Lubec
Jun 1, 1999·Life Sciences·O LabudovaB Lubec

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