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  • Title: Effects of magnesium sulfate administration during hypoxia on CaM kinase IV and protein tyrosine kinase activities in the cerebral cortex of newborn piglets.
    Author: Mami AG, Ballesteros JR, Fritz KI, Kubin J, Mishra OP, Delivoria-Papadopoulos M.
    Journal: Neurochem Res; 2006 Jan; 31(1):57-62. PubMed ID: 16474997.
    Abstract:
    The present study tested the hypothesis that magnesium sulfate administration prior to hypoxia prevents hypoxia-induced increase in Ca(2+)/Calmodulin-dependent-kinase (CaM Kinase) IV and Protein Tyrosine Kinase (PTK ) activities. Animals were randomly divided into normoxic (Nx), hypoxic (Hx) and magnesium-pretreated hypoxic (Mg(2+)-Hx) groups. Cerebral hypoxia was confirmed biochemically by measuring ATP and phosphocreatine (PCr) levels. CaM Kinase IV and PTK activities were determined in Nx, Hx and Mg(2+)-Hx newborn piglets. There was a significant difference between CaM kinase IV activity (pmoles/mg protein/min) in Nx (270 +/- 49), Mg(2+)-Hx (317 +/- 82) and Hx (574 +/- 41, P < 0.05 vs. Nx and Mg(2+)-Hx) groups. Similarly, there was a significant difference between Protein Tyrosine Kinase activity (pmoles/mg protein/h) in normoxic (378 +/- 68), Mg(2+)-Hx (455 +/- 67) and Hx (922 +/- 66, P < 0.05 vs. Nx and Mg(2+)-Hx ) groups. We conclude that magnesium sulfate administration prior to hypoxia prevents hypoxia-induced increase in CaM Kinase IV and Protein Tyrosine Kinase activities. We propose that by blocking the NMDA receptor ion-channel mediated Ca(2+)-flux, magnesium sulfate administration inhibits the Ca(2+)/calmodulin-dependent activation of CaMKIV and prevents the generation of nitric oxide free radicals and the subsequent increase in PTK activity. As a result, phosphorylation of CREB and Bcl-2 family of proteins is prevented leading to prevention of programmed cell death.
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