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PubMed1988

Mitochondrial inclusions in renal epithelial cells of magnesium-deficient rats.

In rats with prolonged magnesium deficiency, paracrystalline inclusions in mitochondria were found frequently in the epithelial cells of the thick ascending limb of Henle, especially in the region of the upper medulla. The inclusions presented a variegated appearance. Some were filamentous aggregates, many had alternating dark and light bands, and others were elongated rectangular densities. They were not found in tubules with calcific deposits where the cells showed degenerative changes. This suggested that the inclusions were probably due to altered cell metabolism and not products of cell degeneration.

Animals↗
PubMed1985

Enhanced distal absorption of potassium by magnesium-deficient rats.

The effect of acute potassium infusion on renal tubular reabsorption of potassium by magnesium-deficient and pair-fed control rats has been studied by the recollection micropuncture method. During potassium chloride infusion, the amount of potassium remaining in the distal tubule is lower in magnesium-deficient than in pair-fed rats. This could be due to a reduction in potassium secretion or to an enhancement of potassium reabsorption. The present study demonstrates enhanced renal potassium retention in the magnesium-deficient rat, and is in contrast to previous reports of renal potassium wasting in this circumstance.

Absorption↗
PubMed1994

Combined effects of magnesium deficiency and an atherogenic level of low density lipoprotein on uptake and metabolism of low density lipoprotein by cultured human endothelial cells. I. Biochemical data.

The effects of magnesium deficiency on uptake and metabolism of low density lipoprotein (LDL) were investigated using human arterial endothelial cells cultured in media containing various concentrations of magnesium (100-1000 microM) and a high concentration of LDL (2 mg LDL cholesterol/ml) labelled with [3H]cholesteryl linoleate. The LDL uptake was time-dependent and increased for up to 8 h in both the magnesium-deficient and magnesium-sufficient treatments. The extent of LDL uptake progressively increased with the decrease in magnesium concentration of the medium. Surface-bound LDL also increased in a similar manner during the incubation but less extensively than the LDL uptake. The majority of radioactivity from internalized LDL was detected in unesterified cholesterol at all time points in both the magnesium deficiency and sufficiency groups. Only small amounts of radioactivity were found in cholesteryl esters. These findings indicate that most LDL taken up by the cells was rapidly hydrolysed but not readily re-esterified. The lack of re-esterification may be due to a relative deficiency of acyl-CoA:cholesterol acyltransferase (ACAT) and the presence of large amounts of unesterified cholesterol.

Analysis of Variance↗
PubMed1993

Oxidative modification of triglyceride-rich lipoproteins in hypertriglyceridemic rats following magnesium deficiency.

Hypertriglyceridemia observed in magnesium (Mg)-deficient rats was associated with a significant increase in the very low-density lipoprotein (VLDL) plus low-density lipoprotein (LDL) fractions. The results from in vitro copper-induced lipid peroxidation, expressed in terms of conjugated dienes and thiobarbituric acid reactive substances content, showed that VLDL + LDL particles from Mg-deficient rats were more susceptible to oxidative damage than lipoproteins from control rats. These results suggest that the mechanism responsible for the atherogenicity and tissue damage characteristic of Mg deficiency may be mediated by an increased susceptibility of triglyceride-rich lipoproteins to peroxidation in hypertriglyceridemic animals.

Animals↗
PubMed1998

Reappraisal of the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rat. Effects of treatment with potassium citrate or the combination magnesium citrate and potassium citrate.

There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.

Animals↗
PubMed1989

Superoxide anion in polymorphonuclear leukocytes of hairless rats suffering from magnesium-deficiency dermatitis.

Clinical and histological studies were made on magnesium-deficiency dermatitis produced on a new strain of hairless rats. Superoxide anion generation in polymorphonuclear leukocytes (PMNs) and the inhibitory effect of some antioxidants and anti-inflammatory agents against the elicited dermatitis were also examined. From the detection of increased superoxide production and effective actions of inhibitors including superoxide dismutase, cepharanthine, 4-4'-diamono-diphenylsulphone and 5,4,11,14-eicosatetraynoic acid (ETYA), it is indicated that superoxide anion or related activated oxygen may be responsible for magnesium-deficiency dermatitis as an inflammatory mediator and that the dermatitis may be related to lipoxygenase metabolites derived from arachidonic acid.

Animals↗
PubMed2002

THC aggravates rat muricide behavior induced by two levels of magnesium deficiency.

A severe magnesium deprivation induces an interspecific aggressive behavior (muricidal behavior, MB) in different strains of rats. Delta9-tetrahydrocannabinol (THC) is also known to induce MB even after a single injection (11 mg/kg) in starving, isolated rats. In the present work, we investigated the MB behavior, for six successive assays 1 h delayed, of two groups of male Long-Evans rats fed 50- or 150-ppm Mg(2+)-deficient diets, for 42 days after a single injection of THC at doses (2, 4 or 8 mg/kg) that did not induce aggressiveness in control rats. This treatment led to Mg(2+) plasma levels of 5+/-0.3 and 12.3+/-0.9 mg/ml vs. 21+/-1.5 mg/ml initially. In the 50-ppm Mg-deficient rat group, all the rats were muricidal but the MB pattern was severely aggravated by THC. In the 150-ppm Mg-deficient rat group, no rat was muricidal but all doses of THC induced a 100% MB. In addition, by quantifying the three phases of MB, we showed through six consecutive hourly muricidal assays, that the two first phases (attack latency and attack on the living mouse) decreased progressively, whereas the third phase (attack on the dead mouse) increased dramatically. This indicates firstly that Mg-deprivation decreases the responsiveness threshold of rats to THC. Secondly, these very low doses of THC induced an aggravation of MB and an acquired hyper-aggressiveness in both 50- and 150-ppm Mg-deficient rats, probably involving different neurotransmitters, mainly serotonin, which is decreased by both treatments.

Aggression↗
PubMed1989

Cardiovascular consequences of magnesium deficiency and loss: pathogenesis, prevalence and manifestations--magnesium and chloride loss in refractory potassium repletion.

Dietary magnesium (Mg) deficiency is more prevalent than generally suspected and can cause cardiovascular lesions leading to disease at all stages of life. The average American diet is deficient in Mg, especially in the young, in alcoholic persons, and in those under stress or with diseases or receiving certain drug therapies, who have increased Mg needs. Otherwise normal, Mg-deficient diets cause arterial and myocardial lesions in all animals studied, and diets that are atherogenic, thrombogenic and cardiovasopathic, as well as Mg-deficient, intensify the cardiovascular lesions, whereas Mg supplementation prevents them. Diuretics and digitalis can intensify an underlying Mg deficiency, leading to cardiac arrhythmias that are refractory unless Mg is added to the regimen. Potassium (K) depletion in diuretic-treated hypertensive patients has been linked to an increased incidence of ventricular ectopy and sudden death. K supplementation alone is not the answer. Mg has been found to be necessary to intracellular K repletion in these patients. Because patients with congestive heart failure and others receiving diuretic therapy are also prone to chloride loss leading to metabolic alkalosis that also interferes with K repletion, the addition of Mg and chloride supplements in addition to the K seems prudent.

Cardiovascular Agents↗
PubMed1980

Aromatic amines (serotonin and histamine) and magnesium deficiency in the rat.

Rats were made deficient by giving a 4 mg Mg/100 g diet. The control diet content was 40 mg Mg/100 g. Serotonin injected to magnesium deficient and control rats was metabolized at the same rate in both groups and the urinary derivatives were similar. Serotonin catabolism can occur in liver as shown by isolated hepatocyte technique. Hyperemia of the ears and dermatosis appeared in magnesium deficient rats, while histaminemia rised. This allergy-like crisis was delayed and milder, when the food intake was reduced. The evolution of histaminemia was studied in parallel with the different white blood cells, during three periods of magnesium deficiency. An important rise of total white blood cells, specially poly morphonuclear and eosinophil cells was observed. The peak for eosinophils occured before the histaminemia and basophils peaks. Basophils cells found only in magnesium deficient group were partly degranualted.

Animals↗
PubMed1988

Changes in intestinal calcium transport and binding in magnesium-deficient chicks.

Disruption of membrane integrity and function has been reported previously as one of the predominant effects of magnesium deficiency. In the current study, we have examined the uptake and binding of calcium by intestinal brush border membrane vesicles from chicks and investigated the effects of Mg deficiency on these processes. Both uptake and binding of calcium were significantly decreased in the membrane vesicles from animals given the magnesium-deficient diet. In addition, the calcium-binding activity of proteins isolated by chromatography on DE-52 cellulose of mucosal extracts was altered by the magnesium deficiency.

Animals↗
PubMed1993

Intracellular magnesium deficiency in acute myocardial infarction.

It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.

Adult↗
PubMed1996

Evidence for magnesium deficiency in the pathogenesis of bronchopulmonary dysplasia (BPD).

Bronchopulmonary dysplasia (BPD) has been defined as a requirement for oxygen for more than 28 days because of chronic pulmonary changes, usually in a premature infant. About 50 per cent of very low birth weight (VLBW) infants who weigh 1 kg at birth and who survive 28 days will develop BPD. Since 80 per cent of fetal accretion of magnesium occurs during the third trimester, this population is also at risk for magnesium deficiency. This paper reviews evidence for a role of magnesium deficiency in the pathogenesis of BPD. Pathology in BPD that may be caused or aggravated by magnesium deficiency is noted. Agents or mediators that are increased in BPD and in BPD include: oxygen free radicals; the inflammatory cytokines interleukin (IL)-1 and IL-6, and tumour necrosis factor-alpha; vaso- and bronchoconstrictors thromboxane A2 (TXA2) and serotonin: vasoconstrictor, endothelin-1 (ET-1); and bronchoconstrictor, histamine. Magnesium deficiency increases the susceptibility of cells and tissues to peroxidation, worsens the inflammatory reaction, reduces the immune response, exaggerates catecholamine release in stress, and diminishes energy metabolism. Possibly because of the danger of magnesium toxicity and the difficulty in studying the preterm VLBW neonate, little is known about magnesium supplementation in this group. Such information must be gained through controlled studies on the effect of antepartum exposure to maternally administered magnesium sulphate on the VLBW infant, through carefully monitored postnatal administration of magnesium in an intensive care setting, or through evaluations of combined pre- and postnatal supplementation.

Animals↗
PubMedDate not supplied

Magnesium deficiency in critical illness.

Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma. Magnesium regulates hundreds of enzyme systems. By regulating enzymes controlling intracellular calcium, Mg affects smooth muscle vasoconstriction, important to the underlying pathophysiology of several critical illnesses. The principle causes of Mg deficiency are gastrointestinal and renal losses; however, the diagnosis is difficult to make because of the limitations of serum Mg levels, the most common assessment of Mg status. Magnesium tolerance testing and ionized Mg2+ are alternative laboratory assessments; however, each has its own difficulties in the ICU setting. The use of Mg therapy is supported by clinical trials in the treatment of symptomatic hypomagnesemia and preeclampsia and is recommended for torsade de pointes. Magnesium therapy is not supported in the treatment of acute myocardial infarction and is presently undergoing evaluation for the treatment of severe asthma exacerbation, for the prevention of post-coronary bypass grafting dysrhythmias, and as a neuroprotective agent in acute cerebral ischemia.

Asthma↗