Summary: The main literature concerning the physiology and biochemistry as well as the pathophysiology and pathobiochemistry of magnesium is reviewed, including:Distribution and physico-chemical state of magnesium in the extracellular and intracellular fluid as well as in the subcellular organelles (membranes, mitochondria, microsomes, ribosomes).Intestinal resorption, transport across membranes and excretion by the kidney.Hormonal regulation of magnesium distribution and its clinical disturbances.Biochemical mechanism and the clinical effects of hypo-and hypermagnesemia. Magnesium-Stoffwechsel: Eine ÜbersichtZusammenfassung: Die wichtigsten Arbeiten über die Physiologie und Biochemie sowie Pathophysiologie und Pathobiochemie des Magnesiums werden dargestellt.Die Darstellung bezieht sich im wesentlichen auf: Die Verteilung und den physikalisch-chemischen Zustand des Mg in der extrazellulären und intrazellulären Flüssigkeit und in den Zellorgänellen (Membranen, Mitochondrien, Mikrosomen, Ribosomen). Die Resorption im Darm, Transport durch Membranen und die Ausscheidung durch die Niere.Die hormonale Regulation der Mg-Verteilung und ihre klinischen Störungen. Biochemische Mechanismen und klinische Erscheinungen bei Hypo-und Hypermagnesiämie.

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Mg2+ transport in rabbit ileal brush border membrane vesicles (BBMV) was characterized by means of a modified mag-fura-2 technique. In the presence of an i>o Na+ gradient, BBMV showed a saturable Mg2+ uptake with a Km of 1.64 mmol l-1. There was no evidence of an overshoot. K+, Li+, and choline+ were as effective as Na+ in stimulating Mg2+ transport. In contrast, only a small amount of Mg2+ transport was observed in the presence either of an o>i Na+ gradient, or in an Na+ equilibrium or in the absence of Na+. Moreover, the findings that Na+ efflux was not stimulated but inhibited by outside Mg2+ and that the nonfluorescent amiloride-analogues DMA and EIPA did not affect Mg2+ transport do not favour the idea of an Mg2+/Na+ antiport system. At Cl- equilibrium, independent of the Na+ gradient, the rate of Mg2+ transport was markedly suppressed compared with the transport rate noted in the presence of an i>o Cl- gradient. The stimulating effect of inside anions could be enhanced by SCN- and decreased by SO2-4. Furthermore, nonfluorescent anion transport antagonist H2-DIDS stimulated Mg2+ transport. These findings indicate that Mg2+ transport can be modulated by inside anions. Mg2+ transport appeared to be electroneutral because it was not dependent on membrane potential. Mg2+ transport was neither stimulated by Bay K8644, a Ca2+ channel agonist, nor inhibited by verapamil, diltiazem, nifedipine and imipramine, the Ca2+ channel antagonists. It, therefore, seems unlikely that Mg2+ uses the Ca2+ transport system.

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Two types of Na(+)-independent Mg(2+) efflux exist in erythrocytes: (1) Mg(2+) efflux in sucrose medium and (2) Mg(2+) efflux in high Cl(-) media such as KCl-, LiCl- or choline Cl-medium. The mechanism of Na(+)-independent Mg(2+) efflux in choline Cl medium was investigated in this study. Non-selective transport by the following transport mechanisms has been excluded: K(+),Cl(-)- and Na(+),K(+),Cl(-)-symport, Na(+)/H(+)-, Na(+)/Mg(2+)-, Na(+)/Ca(2+)- and K(+)(Na(+))/H(+) antiport, Ca(2+)-activated K(+) channel and Mg(2+) leak flux. We suggest that, in choline Cl medium, Na(+)-independent Mg(2+) efflux can be performed by non-selective transport via the choline exchanger. This was supported through inhibition of Mg(2+) efflux by hemicholinum-3 (HC-3), dodecyltrimethylammonium bromide (DoTMA) and cinchona alkaloids, which are inhibitors of the choline exchanger. Increasing concentrations of HC-3 inhibited the efflux of choline and efflux of Mg(2+) to the same degree. The K(d) value for inhibition of [(14)C]choline efflux and for inhibition of Mg(2+) efflux by HC-3 were the same within the experimental error. Inhibition of choline efflux and of Mg(2+) efflux in choline medium occurred as follows: quinine>cinchonine>HC-3>DoTMA. Mg(2+) efflux was reduced to the same degree by these inhibitors as was the [(14)C]choline efflux.

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