Intracellular magnesium and magnesium buffering

The development of new techniques for measuring intracellular free Mg²⁺ during the 1980s has provided investigators with the tools needed to produce new insights into the regulation of cellular magnesium. Within the limits of this technology, it appears that all mammalian cells maintain free cytosolic Mg²⁺ levels within the fairly narrow range of 0.25–1 mM. While transport mechanisms and sequestration within cellular organelles will contribute to this regulation, it is binding of Mg²⁺ to an as yet poorly defined system of buffers that is largely responsible for determining the set point of this regulation. The lack of an adequately Mg²⁺-selective ionophore remains an impediment to progress in this area.     

Characterisation of magnesium nutrition and interaction of magnesium and potassium in rice

Magnesium (Mg) is known as one of the essential nutrients for higher plants; yet, the preliminary physiological responses of field crops to its deficiency or excess, particularly to its interaction with potassium (K), remain largely unknown. In this study, we observed that Mg deficiency in rice (Oryza sativa) [less than 1.1 mg g^?1 dry weight (DW) in the shoot] resulted in significant reduction in shoot biomass, decrease in total chlorophyll concentration and net photosynthetic rate and reduction in activities of both nitrate reductase [NR; enzyme classification (EC) 1.6.6.1] and glutamine synthetase (EC 6.3.1.2) in the leaves. However, the Mg‐deficient plant contained higher starch in the leaves, and partitioned larger biomass into roots. Excess of Mg (more than 3.0 mg g^?1 DW in the shoot), together with low K supply, suppressed NR activity and decreased concentration of soluble sugar in the leaves. There were great antagonistic and moderately synergistic effects between K and Mg, but the effects of K were much more significant than those of Mg on their uptake and translocation, NR activity and net photosynthetic rate in the leaves. The optimum weight ratio of K to Mg ranged between 22 and 25 in the leaves at tillering stage. Mg deficiency was not compensated for by moderate supply of K but was aggravated by excess supply of K, suggesting specific roles of Mg in both dry matter production and partition of carbon assimilates in rice.     

Phloem mobility of magnesium

Magnesium-28 was applied to specific leaves of bean (Phaseolus vulgaris) and barley (Hordeum vulgare) plants. After 24 hours, as much as 7% of the absorbed Mg was exported from the treated bean leaves and 11% was transported basipetally from the treated zone of the barley leaves. Transport of Mg did not occur past a heat-killed section of the treated leaf, thereby indicating that translocation took place via the phloem. Mg movement in the phloem was also evident in autoradiograms of bean stem segments in which the xylem was separated from the phloem by a thin sheet of plastic.     

Effect of magnesium supplementation and training on magnesium tissue distribution in rats

The aim of this work is to study the effect of training and Mg supplementation on body pools of Mg and on Mg tissue distribution. Forty male Wistar rats were divided into four groups (n=10): control group (C); trained group (T); Mg-supplemented group (+Mg); and trained and Mg-supplemented group (+MgT). The Mg supplement (100 ppm of Mg) was given in the drinking water for 21 d. The training consisted of swimming during 60% of maximal swimming time obtained in the first session to exhaustion, during 3 wk (5 d a week). The variables measured were: erythrocytes (RBC), hemoglobin (Hb), hematocrit (Hto), total proteins (TP), and Mg in serum, RBC, liver, muscle, bone, and kidney. There was less Mg in liver, muscle, and erythrocyte in trained animals than in control or supplemented animals (T vs C, +MgT vs C and +MgT vs +Mg) (p < 0.01). Trained antimals (T and +MgT) showed higher Mg kidney rates than the untrained ones (p<0.01). There was less bone Mg in control (C) and in supplemented and trained (+MgT) groups than in trained (T) and in supplemented (+Mg) animals (p<0.01). Serum Mg showed a decreasing concentration profile in the following order: +Mg, +MgT, T, C (p<0.01). We conclude that Mg supplementation improves bone and serum Mg levels, but this does not affect Mg status in soft tissues. Maintained exercise leads to a diminution of Mg in the aforementioned soft tissues that is not noticeable in serum, probably provoked by an increase of renal excretion.     

Cellular magnesium homeostasis

Magnesium, the second most abundant cellular cation after potassium, is essential to regulate numerous cellular functions and enzymes, including ion channels, metabolic cycles, and signaling pathways, as attested by more than 1000 entries in the literature. Despite significant recent progress, however, our understanding of how cells regulate Mg²⁺ homeostasis and transport still remains incomplete. For example, the occurrence of major fluxes of Mg²⁺ in either direction across the plasma membrane of mammalian cells following metabolic or hormonal stimuli has been extensively documented. Yet, the mechanisms ultimately responsible for magnesium extrusion across the cell membrane have not been cloned. Even less is known about the regulation in cellular organelles. The present review is aimed at providing the reader with a comprehensive and up-to-date understanding of the mechanisms enacted by eukaryotic cells to regulate cellular Mg²⁺ homeostasis and how these mechanisms are altered under specific pathological conditions.     

Manipulation of intracellular magnesium levels in Saccharomyces cerevisiae with deletion of magnesium transporters

Magnesium is an important divalent ion for organisms. There have been a number of studies in vitro suggesting that magnesium affects enzyme activity. Surprisingly, there have been few studies to determine the cellular mechanism for magnesium regulation. We wished to determine if magnesium levels could be regulated in vivo. It is known that Saccharomyces cerevisiae has two magnesium transporters (ALR1 and ALR2) across the plasma membrane. We created S. cerevisiae strains with deletion of one (alr1 or alr2) or both (alr1 alr2) transporters. The deletion of ALR1 resulted in a decrease in intracellular magnesium levels. An increase from 5 to 100 mM in the exogenous magnesium level increased the intracellular levels of magnesium in the alr1 and alr1 alr2 strains, whereas the expression of magnesium transporters from S. cerevisiae or Arabidopsis thaliana led to a change of the intracellular levels of magnesium in those strains. The deletion of magnesium transporters in A. cerevisiae and overexpression of magnesium transporters from A. thaliana also affected the intracellular concentrations of a range of metal ions, which suggests that cells use non-specific transporters to help regulate metal homeostasis.     

Histone-produced magnesium extrusion from mitochondria and magnesium binding to histone.

Histone (60 microgram/mg mit. protein) extrudes Mg2+ from mitochondria by 30% with the utilization of endogenous substrates; in the presence of rotenone extrusion drops to about 18%. Dinitrophenol and ADP prevent this effect of histone. Mg2+ extrusion produced by histone depends on histone concentration being at a maximum (100% extrusion) at 107 microgram histone/mit. protein. It was found also that histone alone binds Mg2+ (1.6 nmol Mg2+/microgram histone).     

Axoplasmic free magnesium levels and magnesium extrusion from squid giant axons

The free magnesium concentration in the axoplasm of the giant axon of the squid, Loligo pealei, was estimated by exploting the known sensitivity of the sodium pump to intracellular Mg2+ levels. The Mg- citrate buffer which, when injected into the axon, resulted in no change in sodium efflux was in equilibrium with a Mg2+ level of about 3- -4 mM. Optimal [Mg2+] for the sodium pump is somewhat higher. Total magnesium content of axoplasm was 6.7 mmol/kg, and that of hemolymph was 44 mM. The rate coefficient for 28Mg efflux was about 2 X 10(-3) min-u for a 500-mum axon at 22-25degreesC, with a very high temperature coefficient (Q10=4-5). This efflux is inhibited 95% by injection of apyrase and 75% by removal of external sodium, and seems unaffected by membrane potential or potassium ions. Increased intracellular ADP levels do not affect Mg efflux nor its requirement for Na+/o, but extracellularl magnesium ions do. Activation of 28Mg efflux by Na+/o follows hyperbolic kinetics, with Mg2+/o reducing the affinity of the system for Na+/o. Lanthanum and D600 reversibly inhibit Mg efflux. In the absence of both Na+ and Mg2+, but not in their presence, removal of Ca2+ from the seawater vastly increased 28Mg efflux; this efflux was also strongly inhibited by lanthanum. A small (10(-14) mol cm-2) extra Mg efflux accompanies the conduction of an action potential.     

Role of magnesium in hypertension

Magnesium affects blood pressure by modulating vascular tone and reactivity. It acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Magnesium deficiency has been implicated in the pathogenesis of hypertension with epidemiological and experimental studies demonstrating an inverse correlation between blood pressure and serum magnesium levels. Magnesium also influences glucose and insulin homeostasis, and hypomagnesemia is associated with metabolic syndrome. Although most epidemiological and experimental studies support a role for low magnesium in the pathophysiology of hypertension, data from clinical studies have been less convincing. Furthermore, the therapeutic value of magnesium in the management of hypertension is unclear. The present review addresses the role of magnesium in the regulation of vascular function and blood pressure and discusses the implications of magnesium deficiency in experimental and clinical hypertension, in metabolic syndrome and in pre-eclampsia.