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

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BIOCHEMISTRY OF MAGNESIUM

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.

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