Das Bad Radkersburger ErholungssystemRegion Bad RadkersburgIhre Partner in Bad RadkersburgKommunikation und Kontakt


for the assessment of stress intensity and stress compatibility in large groups

Institute for Applied Stress Research




Submit Abstracts

Full Papers

Honorary Commitee

List of Participants



to I.A.S.

eins.gif (43 Byte)


H. Zollner 

Institut of Biochemistry University of Graz

Magnesium is an ubiquitous element in nature; 2.1% of the earth crust is formed by magnesium. In the body it is the second most abundant cation second to potassium. 60% of the total magnesium (270-420 mg/kg body wt.) is localized in bone, 39% in soft tissue and the remaining 1% in extracellular fluids. Rat liver cells contain 23 nmoles/mg dry wt. 50% are found in the endoplasmatic reticulum, 20 % in mitochondria and the rest in cytosol. The major part (94%) of cytosolic magnesium is bound to proteins, membranes, nucleic acids and intermediary metabolites. 41% is chelated to ATP. Only 2% of total cell magnesium is in the biological active ionized form. In mitochondria about 0.9% magnesium is free (total: 32 nmoles/mg protein). The remainder is bound to membranes, proteins, ATP,ADP, Pi, citrate ect. Again ATPMg complex dominates with 53%. The concentration of ionized magnesium in cytosol and mitochondria is about the same.

An outstanding property of Mg++ is its tendency to form chelates. The physicochemical bases for this behavior is the very small ionic radius.

Quite a large number of enzymes are reported to be affected by this cation  in one or the other way. It may act as cofactor, activator and/or inhibitor or the  real substrate may be a Mg complex and it influences enzyme equilibria. In addition, variation of Mg++ concentration influences the free energy of ATP hydrolysis.

Total Mg++ content and free cellular Mg++ concentration in cells is controlled by hormones, ligand gated ion channels and exchange carriers. α-Adrenergic- or ß-adrenergic receptor agonists stimulate Mg++ efflux. Insulin  antagonizes ß-adrenergic receptor stimulated Mg++ efflux. prostaglandin-E2 stimulate Mg++ influx in kidney tubule cells like insulin in platelets and lymphocytes. On the other hand  secretion of insulin, secretin, parathyroid hormone and catecholamines is modulated by Mg++.

Activation of the NMDA receptor of neuronal cells or of the muscarinic receptor increases  cytosolic Mg++. Arg-vasopressin, endothelin-1 or depletion of inositol-1,4,5-trisphosphate sensitive Ca++ stores, resulted in elevated levels of ionized Mg++ in muscle cells. 

Efflux is catalyzed by a sodium/Mg++ exchanger in most cells and rat liver cells in addition contain a Ca++ /Mg++ exchanger. 

In isolated mitochondria Mg++ concentration is modulated by the respiratory state, the membrane potential and the extramitochondrial Mg++ and phosphate.

Mg++ has  yet not been considered as a regulator of gene expression. Recently a signal pathway was described for the regulation of the prodynorphin gene by Ca++. In this pathway Ca++ binds to a repressor called DREAM. Sequence analysis showed that this protein may contain a Mg++ binding site and it was speculated that Mg++ could also regulate this pathway. There are also some other findings for a possible effect of Mg++ on gene expression.

Mg++may also play a role in apoptosis. Triggering apoptosis by stimulation of the cell death  receptor Fas in primary B-cells led to an increase of cytosolic Mg++ and this increase in Mg++ is an early event in  the signaling pathway. In addition glycodeoxycholic acid induction of  apoptosis in rat liver cells is mediated by an increase in cytosolic Mg++, and Bax induced opening of the permeability transition pore of mitochondria, an other event in the apoptotic signaling pathway, is Mg++ dependent. 

However also protecting effects have been reported. The  opening of the permeability transition pore induced by the ganglioside GD3 or Ca++ was prevented by Mg++.

Strong evidence for an antioxidant and antiinflammatory effect of Mg++ was found in Mg++ deficient animals. Mg++ deficiency led to myocardial necrosis, fibrosis vascular lesions and is regarded as an atherosclerosis risk factor;  antioxidants or Mg++ protected. 

This review shows that in the recent years we have gained new insights in the molecular and cellular action of Mg++ but only part of the effects can be explained on a biochemical molecular basis.

BAd RAdkersburg




ZurückWeiterNach ObenSuchenSitemap / HilfeEmail an den Webmaster