Free Magnesium Levels Research Articles

MAGT1-mediated disturbance of Mg2+ homeostasis lead to exhausted of HBV-infected NK and CD8+ T cells

The magnesium transporter 1 (MAGT1) is a critical regulator of basal intracellular free magnesium ([Mg2+]i) levels. It has been shown that MAGT1 was involved in the disorder in Mg2+ homeostasis after Epstein-Barr virus (EBV) infection. Here, we identified the effects of MAGT1-mediated disturbance of Mg2+ homeostasis on chronic hepatitis B virus (HBV)-infected natural killer (NK) and CD8+ T cells. The expression of MAGT1 was gradually decreased with the increase of infected time in CD8+ T cells, but not with that in NK cells, of the patients. Decreased level of intracellular free Mg2+ ([Mg2+]i) leads to defective expression of programmed cell death 1 (PD-1) and the NK activating receptor (NKG2D) in NK and CD8+ T cells. Our data illustrate that [Mg2+]i plays a key role in control of HBV infection.

Magnesium oxide supplements for the treatment of post-chemotherapy sleep disturbance.

175 Background: While every cancer patient suffers from anxiety and sleep disturbance during cancer treatment, many physicians do not recognize that these problems can continue long after treatment has ended. Many cancer patients feel increased anxiety immediately after treatment ends when they find themselves “on their own,” without the protection of the medical armamentarium. The fear of recurrence, uncertainty about the future, a sense of vulnerability, awareness of mortality, and grief for the loss of a disease-free life all contribute to anxiety and sleep disturbance long term. Magnesium has been used for sleep induction and relaxation for centuries. The primary mechanism by which sleep is enhanced is by muscle relaxation. Magnesium induces muscle relaxation by preventing calcium from binding to troponin, parvalbumin, myosin, and calmodulin, thereby blocking muscle contraction. High levels of free magnesium competitively bind these proteins, and the slow dissociation of bound magnesium provides prolonged relaxation. It is for this reason that magnesium has a long history of use as a tocolytic in labor, as an adjunct to asthma treatment, and as a powerful laxative. Methods: 23 patients in a primary care practice reported continued anxiety and difficulty with sleep initiation following chemotherapy and/or radiation for various forms of cancer. Rather than use SSRIs, benzodiazepines, or sleep medications, all patients were started on an over the counter 1,000 mg magnesium oxide supplement, taken 1 hour before bedtime for 2 weeks. Results: Four patients dropped out before the end of the study period due to magnesium-induced diarrhea. 19 patients completed the 2-week study. Of these, 14 reported a noticeable reduction of sleep latency and an improvement in sleep quality. 11 also reported a subjective sense of reduced anxiety overall. 5 reported an improvement in nocturnal leg cramps, which had been interfering with sleep quality. Conclusions: Overall, magnesium proved to be a well-tolerated treatment for sleep disturbance and anxiety in the majority of the patients studied.

Quadruplex-Flanking Stem Structures Modulate the Stability and Metal Ion Preferences of RNA Mimics of GFP.

The spinach family of RNA aptamers are RNA mimics of green fluorescent protein (GFP) that have previously been designed to address the challenges of imaging RNA inside living cells. However, relatively low levels of free intracellular magnesium limited the practical use of these aptamers. Recent cell-based selections identified the broccoli RNA aptamer, which requires less magnesium for fluorescence, but the basis for magnesium preference remained unclear. Here, we find that the broccoli RNA structure is very similar to that of baby spinach, a truncated version of the spinach aptamer. Differences in stability and metal ion preferences between these two aptamers, and among broccoli mutants, are primarily associated with the sequence and structure of predicted quadruplex-flanking stem structures. Mutation of purine-purine pairs in broccoli at the terminal stem-quadruplex transition caused reversion of broccoli to a higher magnesium dependence. Unique duplex-to-quadruplex transitions in GFP-mimic RNAs likely explain their sensitivity to magnesium for stability and fluorescence. Thus, optimizations designed to improve aptamers should take into consideration the role of metal ions in stabilizing the transitions and interactions between independently folding RNA structural motifs.

Effects of magnesium supplementation on electrophysiological remodeling of cardiac myocytes in L-NAME induced hypertensive rats.

Hypertension is one of the major risk factors of cardiac hypertrophy and magnesium deficiency is suggested to be a contributing factor in the progression of this complication. In this study, we aimed to investigate the relationship between intracellular free Mg(2+) levels and electrophysiological changes developed in the myocardium of L-NAME induced hypertensive rats. Hypertension was induced by administration of 40mg/kg of L-NAME for 6weeks, while magnesium treated rats fed with a diet supplemented with 1g/kg of MgO for the same period. L-NAME administration for 6weeks elicited a significant increase in blood pressure which was corrected with MgO treatment; thereby cardiac hypertrophy developing secondary to hypertension was prevented. Cytosolic free magnesium levels of ventricular myocytes were significantly decreased with hypertension and magnesium administration restored these changes. Hypertension significantly decreased the fractional shortening with slowing of shortening kinetics in left ventricular myocytes whereas magnesium treatment was capable of restoring hypertension-induced contractile dysfunction. Long-term magnesium treatment significantly restored the hypertension-induced prolongation in action potentials of ventricular myocytes and suppressed Ito and Iss currents. In contrast, hypertension dependent decrement in intracellular Mg(2+) level did not cause a significant change in L-type Ca(2+) currents, SR Ca(2+) content and NCX activity. Nevertheless, hypertension mediated increase in superoxide anion, hydrogen peroxide and protein oxidation mitigated with magnesium treatment. In conclusion, magnesium administration improves mechanical abnormalities observed in hypertensive rat ventricular myocytes due to reduced oxidative stress. It is likely that, changes in intracellular magnesium balance may contribute to the pathophysiology of chronic heart diseases.

Alcohol Intoxication May Exacerbate the Effects of Blunt Cranial Trauma Through Changes in Brain Free Magnesium Levels

Moderate to high levels of alcohol decrease brain intracellular free magnesium concentration, a factor known to be critical in brain injury. Phosphorus magnetic resonance spectroscopy was used to examine changes to brain free magnesium concentration after blunt cranial trauma in alcohol-intoxicated rats. Rats exposed acutely or chronically to alcohol sufficient to increase blood alcohol levels to between 150 and 350 mg/dL demonstrated a brain free magnesium level that was 20-50% less than in nonintoxicated animals (p < 0.01). After injury, brain free magnesium levels declined more rapidly and to a greater extent in alcohol-affected animals than in nonintoxicated control animals (p < 0.001). As both preinjury depletion of magnesium and degree of magnesium decline after brain injury have been associated with poor recovery, these findings suggest that moderate to severe alcohol intoxication may predispose the brain to a worse outcome by reducing brain free magnesium levels, both before and after injury.

Magnesium in acute and chronic brain injury: an update

While brain free magnesium levels have been shown to decline in a number of acute and chronic brain pathologies, the mechanisms of such decline and the potential for magnesium administration as a therapeutic intervention are still unclear. In acute brain injury, magnesium therapy has failed in recent clinical trials of trauma, presumably because of an intact blood brain barrier at the time of administration reducing central penetration. Under such conditions, magnesium's peripheral effects on cardiovascular parameters may dominate over the central, and potentially neuroprotective, effects of the compound. In contrast, magnesium has been demonstrated to be beneficial in lacunar strokes, albeit that recent animal studies indicate that this effect is without any significant reduction of lesion size. Postnatal magnesium has also been shown to improve neurological outcome in term neonates with perinatal asphyxia, although this may be limited to cases of mild to moderate brain injury; no effect is observed following severe brain injury. Prenatal magnesium has been reported to be beneficial for outcome in very preterm infants, although this may only be at low doses. Combination therapies are also showing promise in experimental studies, with combined magnesium and mild hypothermia as well as magnesium and polyethylene glycol proving effective in ischemic stroke and in spinal cord injury, respectively. With respect to chronic brain injury, recent results indicate that magnesium deficient mice are susceptible to developing Parkinson's disease, which is consistent with earlier findings that magnesium deficiency over a number of generations is associated with the development of Parkinson's disease. The latter was associated with the appearance of variants of the TRPM channels. Our recent studies have shown that Parkinson's disease is associated with reduced TRPM2 and TRPM7 channel mRNA expression. Taken together, a more complete picture is emerging of the role of magnesium in brain injury, its therapeutic potential as well the mechanisms associated with its decline.

490: Effect of intravenous magnesium sulfate on free intracellular calcium and magnesium measured in peripheral blood monocytes of women with preeclampsia

AND MAGNESIUM MEASURED IN PERIPHERAL BLOOD MONOCYTES OF WOMEN WITH PREECLAMPSIA JAY BRINGMAN, CHARLES GIBBS, ROBERT AHOKAS, RISA RAMSEY, SYAMAL BHATTACHARYA, ROBERT EGERMAN, University of Tennessee Health Science Center, Obstetrics and Gynecology, Memphis, Tennessee, University of Tennessee Health Science Center, Memphis, Obstetrics and Gynecology, Memphis, Tennessee, University of Tennessee, Obstetrics and Gynecology, Memphis, Tennessee, University of Tennessee Health Science Center, Memphis, General Surgery, Memphis, Tennessee, University of Tennessee Health Science Center, Department of Obstetrics and Gynecology and Internal Medicine, Memphis, Tennessee OBJECTIVE: Intracellular calcium and magnesium are responsible for many cellular functions, including vascular tone and arterial blood flow as calcium channels are known to be magnesium-dependent. We investigated the potential ameliorative effects of magnesium sulfate in preeclampsia by measuring its effect on intracellular free calcium and magnesium in peripheral blood mononuclear cells (PBMCs) as a surrogate of maternal smooth muscle. STUDY DESIGN: After informed consent was obtained, peripheral blood was obtained before and after magnesium sulfate administration to preeclamptic gravidas. Patients were determined to have preeclampsia by ACOG criteria. After Histopaque isolation of PBMCs, intracellular free calcium and magnesium levels were measured ratiometrically using the fluorescent molecular probes Fura-2 and mag Fura-2, respectively. RESULTS: Six patients were included in the study. Intravenous magnesium sulfate resulted in a significant decrease in free intracellular calcium and a significant increase in free intracellular magnesium levels in PBMCs (p 0.0313, p 0.0126, respectively). CONCLUSION: Magnesium sulfate infusion resulted in a lowering of free intracellular calcium and an elevation in free intracellular magnesium levels in PBMCs. Some of the ameliorative effects of intravenous magnesium sulfate may be produced by alterations in intracellular ionic calcium as either a direct effect on contractile proteins or as a secondary messenger for additional processes.

Increase of free Mg2+in the skeletal muscle of chronic fatigue syndrome patients

In a previous study we evaluated muscle blood flow and muscle metabolism in patients diagnosed with chronic fatigue syndrome (CFS). To better understand muscle metabolism in CFS, we re-evaluated our data to calculate free Magnesium levels in skeletal muscle. Magnesium is an essential cofactor in a number of cell processes. A total of 20 CFS patients and 11 controls were evaluated. Phosphorus magnetic resonance spectroscopy from the medial gastrocnemius muscle was used to calculate free Mg2+ from the concentrations and chemical shifts of Pi, PCr, and beta ATP peaks. CFS patients had higher magnesium levels in their muscles relative to controls (0.47 + 0.07 vs 0.36 + 0.06 mM, P < 0.01), although there was no difference in the rate of phosphocreatine recovery in these subjects, as reported earlier. This finding was not associated with abnormal oxidative metabolism as measured by the rate of recovery of phosphocreatine after exercise. In summary, calculation of free Mg2+ levels from previous data showed CFS patients had higher resting free Mg2+ levels compared to sedentary controls.

The cellular ionic basis of hypertension and allied clinical conditions

Two central concepts of human hypertensive disease remain poorly understood: (1) elevated blood pressure as merely one component of an underlying systemic condition, characterized by multiple defects in diverse tissues (eg, “Syndrome X”), and (2) the heterogeneity of hypertension, in which different and even opposite clinical responses to different dietary and drug therapies are routinely observed among equally hypertensive subjects. To help explain these clinical phenomena, a unifying “ionic hypothesis” is proposed, in which steady-state elevations of cytosolic free calcium and suppressed intracellular free magnesium levels, characteristic features of all hypertension, concomitantly alter the function of many tissues. In blood vessels this causes vasoconstriction, arterial stiffness, and/or hypertension; in the heart, cardiac hypertrophy; in platelets, increased aggregation and thrombosis; in fat and skeletal muscle, insulin resistance; in pancreatic beta cells, other endocrine tissues, and sympathetic neurons, potentiated stimulus-secretion coupling resulting in hyperinsulinemia, increased sympathetic nerve activity, and so on. Furthermore, an analysis of cellular biochemical, dietary-nutrient, and hormonal factors that normally regulate steady-state levels of these intracellular ions suggests an ionic equivalent to Laragh's volume-vasoconstriction analysis of hypertension. This provides a cellular-based explanation for the heterogeneity of hypertension and a rational basis for individualizing dietary and drug recommendations among different hypertensive subjects. Copyright © 1999 by W.B. Saunders Company Progress in Cardiovascular Diseases, Vol. 42, No. 1 (July/August), 1999: pp 1-22

Lithium induced changes in intracellular free magnesium concentration in isolated rat ventricular myocytes.

We have examined the effect of exposing isolated rat ventricular myocytes to lithium while measuring cytosolic free magnesium ([Mg2+]i) and calcium ([Ca2+]i) levels with the fluorescent, ion sensitive probes mag-fura-2 and fura-2. There was a significant rise in [Mg2+]i after a 5 min exposure to a solution in which 50% of the sodium had been replaced by Li+, but not when the sodium had been replaced by bis-dimethylammonium (BDA). However, there were significant increases in [Ca2+]i when either Na+ substitute was used. The possibility that Li+, which enters the cells, interferes with the signal from mag-fura-2 was eliminated as Li+ concentrations up to 10 mM had no effect on the dye's fluorescence signal. A possible explanation for these findings is that Li+ displaces Mg2+ from intracellular binding sites. Having considered the binding constants for Mg2+ and Li+ to ATP, we conclude that Li+ can displace Mg2+ from Mg-ATP, thus causing a rise in [Mg2+]i. This work has implications for other studies where Li+ is used as a Na+ substitute.

Loss of cardiac magnesium in experimental heart failure prolongs and destabilizes repolarization in dogs.

We sought to determine whether heart failure results in loss of cardiac magnesium sufficient to alter cellular electrophysiology. Free magnesium has numerous intracellular roles affecting metabolism, excitability and RNA synthesis. Total cardiac magnesium content is reduced in heart failure, but it is unclear whether magnesium loss is primary or iatrogenic. Furthermore, it is unknown whether free magnesium levels are affected or whether a change in free magnesium would alter cellular electrophysiology. Eight mongrel dogs underwent demand ventricular pacing (VVI) at 250 beats/min for 3 weeks to induce heart failure. Sublingual epithelial magnesium was measured before pacing and at death. Left ventricular myocytes were isolated and loaded with Mag-Indo-1 to measure free magnesium ([Mg2+]i); myocytes from eight normal dogs served as controls. To test whether changes in [Mg2+]i in this range could alter cellular repolarization, current-clamped myocytes were dialyzed with 0.5 or 1.0 mmol/liter MgCl2. Mean sublingual epithelial magnesium fell significantly in the paced animals, from 36.9 +/- 0.5 to 33.9 +/- 0.7 mEq/liter (p < 0.01). Mean cardiac [Mg2+]i was significantly lower in the dogs with heart failure--0.49 +/- 0.06 versus 1.06 +/- 0.15 mmol/liter (p < 0.003). Time to 90% repolarization was significantly shorter in cells dialyzed with 1.0 mmol/liter compared with 0.5 mmol/liter MgCl2 in myocytes from normal dogs or dogs with heart failure (596 +/- 34 vs. 760 +/- 58 ms in normal dogs and 586 +/- 29 vs. 838 +/- 98 ms in dogs with heart failure; p < 0.05 for each). Experimental heart failure results in both tissue and cardiac magnesium loss in the absence of drug therapy. Free cardiac magnesium is significantly reduced, possibly contributing to abnormal repolarization in heart failure.

Blood-free magnesium concentration declines following graded experimental traumatic brain injury

Traumatic brain injury has been shown to result in a decrease in brain - free magnesium concentration that is associated with the development of neurologic motor deficits. Although these changes have been well characterized in the brain, changes in free magnesium homeostasis have not been characterized in other fluid compartments. The current experiments use ion selective electrodes to measure alterations in blood - free magnesium concentration following graded experimental brain injury in rats and to compare these changes with subsequent neurologic outcome. After severe impact - acceleration - induced injury, blood - free magnesium levels significantly declined (p<0.05) by 25% and remained depressed for at least 4 days after injury. After moderate injury, the decline in blood - free magnesium was less than that observed in the severe injury group, with respect to both degree of decline and duration of decline. The post - traumatic blood - free magnesium concentration correlated to observed motor deficits as assessed by rotarod evaluation (p<0.001). We conclude that blood - free magnesium levels may be a prognostic indicator of outcome following severe traumatic brain injury.

Direct magnetic resonance determination of aortic distensibility in essential hypertension: relation to age, abdominal visceral fat, and in situ intracellular free magnesium.

To investigate the contribution of vascular compliance to essential hypertension (EH), we developed magnetic resonance imaging (MRI) techniques to directly measure aortic distensibility (AD) in the ascending and descending thoracic and abdominal aorta of fasting normal (n= 10) and EH (n=20) subjects. These results were compared with concurrent MR-based measurements of left ventricular mass index (LVMI) and abdominal subcutaneous and visceral fat and with 31P-MR spectroscopic measurement of in situ intracellular free magnesium levels (Mgi) in brain and skeletal muscle. Aortic distensibility in EH was consistently and significantly reduced at all measured sites (2.5+/-0.4, 2.2+/-0.4, 2.3+/-0.4 versus 7.0+/-1.6, 5.1+/-0.3, 7.3+/-0.8 mm Hg(-1) x 10(-3), P<.05), as was Mgi in the brain (284+/-22 versus 383+/-34 micromol/L, P<.05) and skeletal muscle (397+/-10 versus 527+/-36 micromol/L, P<.05). For all subjects, systolic blood pressure (r=-.662, P<.0001) and LVMI (r=-.484, P<.01) were inversely related to AD. AD and brain Mgi were inversely related to age (AD, r=-.792, P<.0001; brain Mgi: r=-.673, P<.05). AD was inversely related to fasting blood glucose (r=-.413, P<.05) and to abdominal visceral fat (r=-.416, P<.05) but not to body mass index (BMI: r=-.328, P=NS) or subcutaneous fat (r=-.157, P=NS). AD was also significantly and positively related to in situ Mgi, both in the brain and skeletal muscle (brain: r=.712, P<.01; skeletal muscle: r=.632, P<.01). We conclude that (1) MR techniques can be used to coordinately and noninvasively assess cardiac, vascular, metabolic, and ionic aspects of hypertensive disease in humans; (2) increased systolic blood pressure and LVMI in EH may at least in part result from decreased AD; (3) decreased Mgi contributes to arterial stiffness in hypertension and may help to explain the characteristic age-related decreases in AD; and (4) decreased AD may be one mechanism by which abdominal visceral fat contributes to cardiovascular risk.

Phosphorus nuclear magnetic resonance spectroscopy: in vivo magnesium measurements in the skeletal muscle of normal subjects.

31P nuclear magnetic resonance spectroscopy was used to study the skeletal muscle of 33 normal males and 32 females. Free intracellular magnesium levels and the ratios of the phosphorus metabolites were determined. Males had significantly lower free magnesium levels (499.8 microM +/- 26.3 microM vs. 530.7 microM +/- 36.0 microM, P = 0.001, d.f. = 63, analysis of variance). The free magnesium level (rs = -0.5431, P = 0.001) and the phosphocreatin/Inorganic phosphate ratio in males (rs = -0.4102, P = 0.018), and the phosphocreatine/Inorganic phosphate ratio in females (rn = -0.4759, P = 0.009) fell with the increasing Minnesota Heart Health Program Questionnaire score.

Effect of aging on intracellular divalent cation metabolism: A link to the increased incidence of hypertension and non-insulin dependent diabetes mellitus in the elderly?

Aging is epidemiologically linked to an increased incidence of hypertension, impaired glucose tolerance and overt non-insulin dependent diabetes mellitus type II (NIDDM). The cellular basis underlying this clinical and epidemiological linkage, cytosolic free calcium (Ca(2+)(i)) and cytosolic free magnesium (Mg(2+)(i)) levels were investigated in elderly subjects and in subjects with essential hypertension (EH) and metabolic diseases. It has been observed that normal aging, as well as hypertension and NIDDM, is characterized by elevated Ca(2+)(i) and suppressed Mg(2+)(i) levels. Furthermore, the divalent ionic defect displayed in EH and NIDDM resembled the normal aging process, i.e., ionic levels in both young and elderly subjects with EH or NIDDM were indistinguishable from those in healthy elderly subjects. The ionic levels predict quantitatively also the extent of elevated blood pressure, and hyperinsulinemic response to oral glucose challenge. Altogether, we suggest that the missing link, responsible for the frequent and increasing clinical coexistence of hypertension, insulin resistance, impaired glucose tolerance, and NIDDM with age, may be ionic in nature, and intrinsic to the normal aging process in Western man.

Adjustment of K' to varying pH and pMg for the creatine kinase, adenylate kinase and ATP hydrolysis equilibria permitting quantitative bioenergetic assessment.

Physiologists and biochemists frequently ignore the importance of adjusting equilibrium constants to the ionic conditions of the cell prior to calculating a number of bioenergetic and kinetic parameters. The present study examines the effect of pH and free magnesium levels (free [Mg2+]) on the apparent equilibrium constants (K') of creatine kinase (ATP: creatine N-phosphotransferase; EC 2.7.3.2), adenylate kinase (ATP:AMP phosphotransferase; EC 2.7.4.3) and adenosinetriphosphatase (ATP phosphohydrolase; EC 3.6.1.3) reactions. We show how K' can be calculated using the equilibrium constant of a specified chemical reaction (Kref) and the appropriate acid-dissociation and Mg(2+)-binding constants at an ionic strength (I) of 0.25 mol l-1 and 38 degrees C. Substituting the experimentally determined intracellular pH and free [Mg2+] into the equation containing a known Kref and two variables, pH and free [Mg2+], enables K' to be calculated at the experimental ionic conditions. Knowledge of K' permits calculation of cytosolic phosphorylation ratio ([ATP]/[ADP][Pi]), cytosolic free [ADP], free [AMP], standard transformed Gibbs energy of formation (delta fG' degrees ATP) and the transformed Gibbs energy of the system (delta fG' ATP) for the biological system. Such information is vital for the quantification of organ and tissue bioenergetics under physiological and pathophysiological conditions.

Simultaneous Determination of Intracellular Magnesium and pH from the Three 31P NMR Chemical Shifts of ATP

The simultaneous determination of intracellular [MgT]/[ATPT] and pH from the three 31P NMR chemical shifts of ATP has been demonstrated using two-dimensional calibrations. The resulting pH will more accurately represent that of healthy tissue than by using the standard NMR technique. As a result of other possible complexes of MgATP and uncertainties in intracellular pH, errors in the values of KMgATPD(pH), the MgATP NMR shift limits, and thus intracellular magnesium levels are reduced by using this self-consistent analytical method. Direct determination of free magnesium from the (γ − β) shifts of ATP may be more sensitive in the alkaline pH range than with the commonly used (α − β) shifts. In addition, the calibration data sets allow for a graphical representation of the uncertainty in magnesium due to the uncertainty in the measured chemical shifts and pH. Our results indicate that KMgATPD is consistent with the literature and favors a value near 50 μM at pH 7.2, but that free magnesium levels will be lower than most prior estimates.

Do diuretics cause magnesium deficiency?

1. Controlled trials, of which there are few, do not substantiate claims that diuretics play a role in causing magnesium deficiency. Consequently, the vast majority of patients taking conventional doses of thiazide diuretics (i.e. bendrofluazide 2.5 mg day-1 or equivalent) do not need magnesium supplements. On balance, potassium-sparing diuretics tend to increase serum and intracellular magnesium content; this should not be taken as evidence of prior magnesium deficiency. It remains theoretically possible that large doses of loop diuretics given more than once daily for long periods could induce negative magnesium balance and magnesium deficiency. However, it has been difficult to run appropriately controlled trials in conditions where such therapy is needed (i.e. heart failure) and until more reliable information becomes available no absolute recommendation can be made. 2. Methods for the measurement of intracellular free magnesium levels are now available and are more relevant to the assessment of magnesium deficiency than total intracellular magnesium content; the complex relationship between intracellular free and total magnesium content remains to be defined. Future work involving the effect of diuretics on intracellular free magnesium measurements should make every attempt to avoid the errors of trial design and multiple publication that litter current and past literature.

Apparent low free magnesium levels in blue crab vas deferens determined by 31P NMR

1. 1. 31P NMR examination of blue crab vas deferens reveals an α-β ATP chemical shift differences on average of 9.8 ppm. 2. 2. This implies a free magnesium concentration well below 100 μM. 3. 3. Thus crab vas deferens represents a new model for a low free magnesium system. 4. 4. These results also point to a feature of carcine metabolism not previously recognized.

Increased mortality in female rats after brain trauma is associated with lower free Mg2+.

Male and female Sprague-Dawley rat siblings (200-350 g) were monitored by phosphorus magnetic resonance spectroscopy for 4 h after moderate (2.8 atmospheres) fluid-percussion-induced traumatic brain injury. Following injury, two of nine male animals died whereas 100% of all female rats (n = 16) died (p < 0.01). Prior to injury, brain free magnesium concentration in males was 0.58 +/- 0.05 mM and in females 0.41 +/- 0.09. After injury, mean brain free magnesium concentration in males declined to 0.32 +/- 0.06 whereas mean brain free magnesium concentration in ventilated females (n = 6) after injury declined to 0.17 +/- 0.03 (p < 0.05). There were no significant differences between groups with respect to any other measured variables. We conclude that female rats are more susceptible to irreversible injury after brain trauma, and that this increased susceptibility to injury may be related to brain free magnesium levels.