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PubMed1992

Cardioskeletal mitochondrial myopathy associated with chronic magnesium deficiency.

A 3-year-old boy presenting with convulsions and carpopedal spasm had hypomagnesemia and hypermagnesuria due to congenital magnesium-losing nephropathy. Despite chronic oral and intermittent intravenous magnesium supplementation, he remained chronically hypomagnesemic. At age 4, he developed a progressive proximal myopathy and dilated hypertrophic cardiomyopathy that ultimately contributed to his death at age 14 years. Skeletal and cardiac muscle specimens showed a mitochondrial myopathy with increased numbers of enlarged, structurally abnormal mitochondria. Muscle magnesium content was markedly decreased. Chronic oral and intermittent intravenous magnesium supplementation may be inadequate to prevent the progressive cardioskeletal myopathy associated with the chronic magnesium deficiency of congenital magnesium-losing nephropathy.

Biopsy↗
PubMed1991

[Magnesium deficiency and development of late diabetic complications].

Diabetics have a higher prevalence of recurrent angina, myocardial infarction and hypertension compared with healthy individuals. This is partly due to the metabolic control, and partly to the development of nephropathy, but inherited factors also seem to contribute to their development. Another factor, to some extent inherited, could be magnesium-deficiency. Up to 30% of all diabetics suffer from magnesiumdepletion, which in other disease entities has been related to angina pectoris, myocardial infarction, and changes in blood lipids. Furthermore, magnesium-deficiency might be related to the development of hypertension. In diabetes, magnesium-depletion has been linked with the development of retinopathy, and an increase in abortions and malformations in diabetic pregnancies. No intervention trials with magnesium, to elucidate the question of magnesium depletion and diabetic late complications have hitherto been made. No methods for assessing magnesium-status in diabetes are available as yet, to select patients for this type of trial.

Diabetes Mellitus, Type 1↗
PubMed1983

Magnesium deficiency in cystic fibrosis.

We have described the first case of symptomatic magnesium deficiency in a patient with cystic fibrosis and have discussed its causes. Such deficiency probably occurs with significant frequency in cystic fibrosis and should be considered in such patients so that important morbidity can be prevented.

Adult↗
PubMed1976

Magnesium deficiency, requirement and toxicity in the young Japanese quail.

Studies of magnesium deficiency, requirement and toxicity in the young Japanese quail (Coturnix coturnix japonica) were conducted. Day-old birds were fed an adequate purified diet containing 35% soy protein to 2 weeks of age. Residual magnesium in the diet without any added magnesium salts was 21 p.p.m. magnesium was supplied by graded amounts of MgSO4 to a total of 11 levels ranging from 125 to 2,000 p.p.m. Deficiency signs included poor growth, and occasionally excitability, gasping and convulsions. Most mortality occurred during the first 7 days. The maximum dietary magnesium concentrations that produced the minimal significant deviation from normal values for mortality, body weight, hemoglobin and tibia ash was 225, 200, 250 and 250 p.p.m., respectively. Based on these measurements, 300 p.p.m. magnesium is considered adequate to meet the young quail's requirement under the conditions of these experiments. With 2,000 p.p.m. magnesium, the only adverse effect was an increase in mortality. Between 200 and 1,000 p.p.m. magnesium there was a linear relationship between concentration of magnesium in the tibia and the log of the concentration of dietary magnesium. This suggests that tibia magnesium concentration might be useful for bioassay of magnesium in foodstuffs.

Animals↗
PubMedDate not supplied

Selenium concentration and glutathione peroxidase activity in selenium and magnesium deficient rats.

To clarify the effects of selenium (Se) and magnesium (Mg) deficiencies on Se and glutathione peroxidase (GSHPx) status, weanling male Wistar rats weighing 50-60 g were placed on four kinds of diets divided by two levels of Se (0.5 or 0.019 mg/kg) and Mg (500 or 50 mg/kg) for 8 wk. Magnesium deficiency had an influence on distribution of Se, which was increased in muscle and decreased in other tissues. The changes in GSHPx matched those in Se. The levels of Se and GSHPx in most tissues were lower in Se-Mg-deficient rats than in Se-deficient rats. Thus, selenium and Mg deficiencies would make oxidant lesion more serious than Se deficiency.

Animals↗
PubMed2000

Effects of partial and total colectomy on mineral and acid-base homoeostasis in the rat: magnesium deficiency, hyperphosphaturia and osteopathy, in the presence of high serum 1,25-dihydroxyvitamin D but normal parathyroid hormone.

The effects of colectomy on acid-base status, extra-osseous and bone minerals, calciotropic hormones and bone morphology have not yet been studied. To rectify this, groups of normally fed male rats were subjected to distal (n=11), proximal (n=12) or total (n=12) colectomy. Sham-operated rats (n=12) served as controls. At 112 (+/-2) days after colectomy the following changes were noted: (1) weight gain was delayed; (2) faecal excretion of calcium and phosphorus was normal, whereas that of magnesium was increased; (3) intestinal calcium secretion and absorption of calcium and phosphorus were normal, but magnesium absorption was decreased; (4) urinary excretion of magnesium was also decreased, that of phosphorus was increased, and that of pyridinium and deoxypyridinium tended to be high; (5) the serum levels of ionized magnesium, total calcium, 25-hydroxyvitamin D and parathyroid hormone were normal, while that of 1,25-dihydroxyvitamin D was markedly elevated; and (6) bone magnesium and phosphorus content were decreased, but bone calcium was normal, and thus the bone calcium/phosphorus ratio was high. These abnormalities were associated with moderate metabolic acidosis, as reflected by high urinary ammonium, low citrate and low total CO(2), but normal blood gases. Significant structural abnormalities of bone were not detectable, but trabecular bone tended to show rarefication. Distal colectomy had the least effect, whereas proximal and total colectomies had a distinct effect, on these parameters. It is concluded that colectomy in the rat causes: (1) a syndrome of magnesium deficiency of intestinal origin, compensated metabolic acidosis, urinary phosphorus loss, and high circulating 1,25-dihydroxyvitamin D levels, with the degree depending on the extent of surgical resection; and (2) brittle bones, a feature characteristic of low bone magnesium and more generalized magnesium deficiency. The mechanisms leading to this syndrome are unknown, but altered tissue levels of magnesium and phosphorus may play a key role.

Acid-Base Equilibrium↗
PubMed1990

Magnesium deficiency in two hypertensive patient groups.

Magnesium (Mg) deficiency can contribute to cardiac dysrhythmias and may predispose to ischemic heart disease. Most diuretic agents cause loss of Mg, but serum levels may be normal despite cellular depletion. We studied the clinical characteristics of hypertensive patients treated for at least 6 months with either hydrochlorothiazide (HCTZ) or a single nondiuretic drug. To evaluate Mg status in our patients, we measured the percentage retention of a parenterally administered Mg load as an accurate indicator of functionally available total body Mg. Serum lipid, blood chemistry, and serum Mg values were obtained, and cardiac exercise testing and Holter monitoring were done. Levels of potassium were lower, but those of serum Mg were higher with HCTZ treatment despite double the Mg load retention. The Mg load retention data indicate relative Mg depletion in the HCTZ-treated group. Eighty percent of all patients studied had abnormal retention of Mg, even though their serum levels were normal. A percentage Mg load retention determination is needed to assess accurately Mg status.

Antihypertensive Agents↗
PubMed1993

Physiological correlates of abnormal behaviors in magnesium-deficient rats.

In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions.

Acoustic Stimulation↗
PubMed1981

Ultrastructure of the seminiferous tubules in magnesium-deficient rats.

The ultrastructure of the seminiferous tubule in the testis of magnesium-deficient rats is described. The boundary tissue was normal. Cells in the basal compartment were shrunken with large intercellular spaces except where desmosome-like junctions occurred. Cellular relations in the intermediate and adluminal compartments appeared normal but the SER in spermatids was less organised than in the control. There is extensive vesiculation of th SER in Sertoli cells. The role of the Sertoli cell in the maintenance of differences in the ionic compartments of the extratubular and intratubular milieu is discussed.

Animals↗
PubMed1978

Barbiturate withdrawal and magnesium deficiency in mice.

C57BL/6J male mice rendered physically dependent on phenobarbital exhibited significantly lower whole-brain and serum-magnesium concentrations than did control mice. The symptoms of phenobarbital withdrawal were remarkably similar to those seen in magnesium-deficient mice exposed to a low-magnesium diet without drug exposure. These findings suggest that brain magnesium deficits produced by chronic phenobarbital withdrawal could contribute to the observed phenobarbital withdrawal syndrome. Administration of MgSO4 during withdrawal significantly reduced the incidence of tonicclonic and lethal tonic seizures.

Animals↗
PubMed2006

Magnesium deficiency enhances hydrogen peroxide production and oxidative damage in chick embryo hepatocyte in vitro.

Magnesium deficiency and oxidative stress have been identified as correlative factors in many diseases. The origin of free radicals correlated with oxidative damage resulting from Mg-deficiency is unclear at the cellular level. To investigate whether hydrogen peroxide (H2O2) is associated in the oxidative stress induced by Mg-deficiency, the effect of Mg2+ deficiency (0, 0.4, 0.7 mM) on the metabolism of H2O2 was investigated in cultured chick embryo hepatocytes. After being cultured in the media with various concentrations of Mg2+ for 1, 2, 4, 6 and 10 days, parameters of H2O2 production, catalase activity, lipid peroxidation, intracellular total Mg and cell viability were analyzed. Results demonstrated that long-term incubation of chick embryo hepatocyte in extracellular Mg2+-deprivative and Mg2+-deficient (0.4 mM) states significantly enhanced the production of H2O2 (approximately twofold, respectively) and lipid peroxidation in the cell cultures, while decreasing the cell viability. Additionally, the reversing action of Mg2+ re-added to 1.0 mM and the partial reversing action of dimethylthiourea suggested that (i) [Mg2+]e deficiency induced the increase of H2O2 production, (ii) [Mg2+]e deficiency decreased catalase activity in chick embryo hepatocyte in vitro, subsequently causing oxidative stress and cell peroxidative damage.

Animals↗
PubMed2004

Magnesium deficiency in sugar beets alters sugar partitioning and phloem loading in young mature leaves.

Magnesium deficiency has been reported to affect plant growth and biomass partitioning between root and shoot. The present work aims to identify how Mg deficiency alters carbon partitioning in sugar beet (Beta vulgaris L.) plants. Fresh biomass, Mg and sugar contents were followed in diverse organs over 20 days under Mg-sufficient and Mg-deficient conditions. At the end of the treatment, the aerial biomass, but not the root biomass, of Mg-deficient plants was lower compared to control plants. A clear inverse relationship between Mg and sugar contents in leaves was found. Mg deficiency promoted a marked increase in sucrose and starch accumulation in the uppermost expanded leaves, which also had the lowest content of Mg among all the leaves of the rosette. The oldest leaves maintained a higher Mg content. [14C]Sucrose labelling showed that sucrose export from the uppermost expanded leaves was inhibited. In contrast, sucrose export from the oldest leaves, which are close to, and export mainly to, the roots, was not restricted. In response to Mg deficiency, the BvSUT1 gene encoding a companion cell sucrose/H+ symporter was induced in the uppermost expanded leaves, but without further enhancement of sucrose loading into the phloem. The observed increase in BvSUT1 gene expression supports the idea that sucrose loading into the phloem is defective, resulting in its accumulation in the leaf.

Base Sequence↗
PubMed1993

Effect of acute magnesium deficiency on the masking and unmasking of the proton channel of the uncoupling protein in rat brown fat.

The short term regulation of heat production in brown adipose tissue mitochondria (BAT) of acutely Mg-deficient rats was demonstrated by comparing several parameters of mitochondrial energization. Mg deficiency in vivo had absolutely no effect on the BAT uncoupling protein concentration (UCP) which was only modified by thermal conditions. The same high concentration was observed 10 d cold exposed control and Mg-deficient rats. Four days of warm re-exposure at thermal neutrality led to a moderate 26 per cent decrease with both diets which was not modified by cold stress for 1 h. Proton conductance. CmH+, and proton motive force, delta p, were calculated from membrane potential and respiration rate measurements. The same high level CmH+ was observed in cold exposed rats with both diets. Compared to warm re-exposed control rats, CmH+ was threefold higher in the corresponding Mg-deficient group which indicated a much lower masking of the proton channel of UCP with the Mg-deficient diet. This difference was not dependent on the presence of magnesium in vitro. The basal CmH+, independent of UCP, was not altered by magnesium deficiency. These results emphasize that acute regulation of thermogenic BAT activity through the masking and unmasking process is altered when magnesium supply is limited in vivo.

Adipose Tissue, Brown↗
PubMed1982

Magnesium deficiency contributing to ventricular tachycardia. Two case reports.

Two cases of ventricular tachycardia (VT), possibly caused by magnesium deficiency, are presented. Skeletal muscle biopsies and blood samples were taken before and after magnesium infusions. These infusions resulted in a significant retention of magnesium, and the VT attacks vanished permanently in one case and temporarily in the other.

Aged↗
PubMed1990

Association of magnesium deficiency with the blood pressure-lowering effects of calcium.

The role of dietary calcium and magnesium in the development of hypertension was studied in nine groups, each consisting of nine spontaneously hypertensive rats aged 8-31 weeks. The animals were fed AIN 76A semi-purified diets varying in calcium (0.075, 0.5 and 2.5%) and magnesium (0.01, 0.05 and 0.75%) concentrations according to a 3 x 3 factorial design. Dietary calcium and systolic blood pressure were inversely related, significantly (P less than 0.05) after 12 weeks. Total and ultrafilterable serum calcium concentrations were also significantly negatively correlated with blood pressure (r = -0.46; P = 0.001 and r = -0.57; P = 0.001, respectively). Repeated measures analysis of variance indicated that dietary magnesium had no effect on systolic blood pressure, and no calcium x magnesium interaction on blood pressure was observed. Signs of magnesium deficiency, calcium deposits in the kidneys, and histological lesions were observed in groups on a high-calcium diet receiving normal and low levels of magnesium. Thus a lowering of blood pressure by calcium supplementation, without concomitant magnesium supplementation, was accompanied by biochemical and histological abnormalities in this animal model.

Animals↗
PubMed1991

Magnesium deficiency as a cause of acute intractable seizures.

Clinical and experimental investigations have shown that magnesium depletion causes a marked irritability of the nervous system, eventually resulting in epileptic seizures. Although magnesium deficiency as a cause of epilepsy is uncommon, its recognition and correction may prove life-saving. Two case reports are presented which emphasize the importance of recognizing hypomagnesaemia in patients with acute intractable seizures.

Adult↗
PubMed1993

[The oral magnesium loading test for detecting possible magnesium deficiency].

In 26 top sportsmen (volleyball players, rower) aged 15-18 years the serum magnesium level and urinary Mg excretion before and after oral administration of 5 g Mg lactate was assessed (oral magnesium load test). In 11 sportsmen (42.3%) a low percentage of excretion of administered Mg was found, suggesting magnesium deficiency, irrespective of the basal serum Mg levels. After subsequent 10-day Mg supplementation 6 volleyball players responded by a markedly lower retention after an identical Mg load, again without marked changes of the serum Mg level. The authors consider the magnesium load test a more sensitive indicator of latent Mg deficiency than the serum Mg level which is maintained at a relatively stable level and declines only in severe deficiency. The test assumes normal renal function and intestinal absorption.

Administration, Oral↗