Short-term reduction in dietary intake of magnesium causes deficits in brain intracellular free Mg 2+ and [H +] i but not high-energy phosphates as observed by in vivo 31P-NMR

Abstract

31P-NMR spectroscopic studies were performed in vivo on brains of rats fed 30–35% normal dietary Mg intake for 6 weeks. Within 2 weeks of the moderately restricted Mg diet serum Mg fell 50%, and brain intracellular free [Mg 2+] i fell 15%; within 3 weeks of restricted diet, brain [Mg 2+] i fell 40% and remained at this level for the additional 3 weeks. Intracellular pH (pH i) progressively rose in a reciprocal manner for 4 weeks. At no interval of time did brain phosphocreatine (PCr), [ATP], or inorganic phosphate change despite the fall in brain [Mg 2+] i, brain pH i and serum Mg. The Mg-deficiency-induced cytosolic loss of protons (resulting in an alkaline cytosol) could be a compensatory mechanism to stabilize [PCr], [ATP] and [ADP] levels via creatine kinase, thus maintaining cytosolic phosphorylation potential. The rise in pH i associated with Mg-deficiency would also account for increased cerebral vascular muscle contractility under these conditions. Lastly, these studies indicate that brain [Mg 2+] i may change without a concomitant change in cell [ATP], and that brain [Mg 2+] i may be a useful marker for total body Mg 2+ status.