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PubMed1990

Historical review of the effects of marginal intake of magnesium in chronic experimental magnesium deficiency.

After the discovery of magnesium as an essential nutrient in 1926, research focused upon the identification of effects of an acute deficiency state and determination of the requirement for the mineral for normal growth and reproduction. In this early work, marginal intakes of magnesium were reported to result in alterations of tissue composition. Since the 1970s, research has shown that the ability to adapt to a marginal intake of magnesium, which is commonplace in developed countries, is limited. In fact, a low intake of the mineral for an extended period of time may be associated with abnormalities in reproduction, growth, and development and may be a factor in the pathogenesis of disorders of neuromuscular, cardiovascular, renal, and immune function. Problems related to the use of pharmacological agents or to trace metals, such as aluminium, may be worsened in the presence of a low intake of magnesium. Evidence presented illustrates that, although physical signs of magnesium deficiency may be absent, that is to say in cases of latent clinical forms, a marginal dietary inadequacy of the mineral over a long period of time could result in significant problems.

Animals↗
PubMed1994

Magnesium deficiency: pathophysiologic and clinical overview.

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.

Animals↗
PubMed1989

Effect of magnesium deficiency on interleukin production by Fisher rats: effect of interleukins on reduced in vitro lymphocyte responses to concanavalin A and lipopolysaccharide.

The ability of rats fed a magnesium-deficient diet to produce interleukins (ILs) and the effect of ILs on in vitro lymphocyte mitogenesis have been studied in rats. Lack of magnesium resulted in a lower number of plastic-adherent spleen cells and in a reduction of IL-1 production. IL-2 production was not significantly affected, indicating differential sensitivity of T cells to magnesium deficiency. The diminished mitogenic response of splenocytes to concanavalin A (Con-A) was restored by the addition of IL-1 supernatant, while the addition of IL-2 supernatant and recombinant IL-2 resulted in significantly greater enhancement of proliferation in response to Con-A, compared with that of control spleen cells. The fact that recombinant IL-2 restored the T-cell responses to Con-A indicates that the active factor in the IL-2 supernatant is IL-2.

Animals↗
PubMed1976

Effect of magnesium deficiency on nonspecific excitability level (NEL) and audiogenic seizure susceptibility.

Magnesium deficiency in weanling rats caused an increase in NEL and in audiogenic seizure susceptibility. These behavioral effects were apparent after eight days of magnesium restriction and could be reversed by dietary rehabilitation. Serum magnesium declined rapidly from 1.87 +/- 0.10 mEq/L to 0.91 +/- 0.24 mEq/L in two days. Cerebrospinal fluid (CSF) magnesium decreased gradually from 1.86 mEq/L, becoming significantly lower (1.44 +/- 0.23 mEq/L) after eight days. When deficient rats were injected IP with MgCl2, raising the serum magnesium concentration to 6.6 mEq/L, NEL decreased to normal while audiogenic seizure susceptibility remained. Both NEL and audiogenic seizure susceptibility in rats reflect central nervous system magnesium concentration, except when serum magnesium concentration is very high. Very high serum magnesium concentration lowers NEL but does not reduce audiogenic seizure susceptibility if CSF magnesium is low.

Animals↗
PubMed1978

Effect of magnesium deficiency and food restriction on the immune response in young mice.

Similar batches of five-week-old C57 Bl/6 mice were given either a magnesium-deficient diet (4mg Mg/100 g), or a control diet (40 mg/100 g). Control diet intake was either ad libitum or reduced. After immunization with SRBC (sheep red blood cells), the immune response was studied by estimating the number of spleen AFC (antibody-forming cells) capable of lysing SRBC, and by a cytoadhesion test to determine the number of RFC (rosette forming cells). Limitation of the control diet slowed the growth rate in mice. Whenever food intake was reduced from 4g/day to 2.9 or 2.6g/day, the AFC response intensified but the RFC response remained similar. Food limitation might therefore mainly affect immature IgM producing cells with a high dividing rate. Magnesium deficiency produced a drastic fall in the primary and secondary immune responses, as measured by the number of spleen AFC. The number RFC was also much lower in the spleen of deficient animals. Consequently, the spleen immune system is deeply affected by this deficiency.

Animals↗
PubMed1993

Plasma esterase activities in rats fed magnesium-deficient diets.

In a study with rats it was determined whether dietary magnesium concentration affects plasma esterase activities. The feeding of a diet with 0.01% (w/w) instead of 0.04% magnesium reduced plasma magnesium concentration by 50%. Plasma total esterase, arylesterase and butyrylcholinesterase activities were significantly decreased in the magnesium-deficient rats. In rats fed a diet containing 0.02% magnesium, plasma magnesium concentration was lowered by 30%, and group mean plasma total esterase activity was decreased, but not the activities of arylesterase and butyrylcholinesterase.

Animals↗
PubMed1978

The postmortem diagnosis of magnesium deficiency: studies in an animal model for the human infant.

Weanling rats were studied as a model for the human infant to determine the optimal tissue in which to assess the status of magnesium after death. Control rats were fed laboratory chow or purified diets that provided a surfeit of magnesium and accommodated a normal rate of growth. Other rats were fed diets that resulted in two degrees of magnesium deficiency: one that might result in spontaneous death within one week, and the other, within two weeks. These times may correlate with six months and one year in the human infant, the period during which the sudden infant death syndrome usually occurs. There was no consistent difference between the magnesium concentration found in the vitreous humor, liver, heart, or skeletal muscle of magnesium-deficient and control rats. However, bone accurately reflected the level of dietary magnesium. There was a significant difference between the magnesium concentration of the anterior and posterior halves of the ribs, indicating irregular distribution of magnesium within the bone. Significant differences were found in the magnesium concentrations of different bones from the same animals. Therefore one entire bone, such as the sternum or the rib, should be studied. The need to match control and study subjects for age was apparent.

Animals↗
PubMed2002

Protective effect of calcium deficiency on the inflammatory response in magnesium-deficient rats.

BACKGROUND: Previous studies indicated that dietary Mg-deficiency in rats results in a marked pro-inflammatory effect. Since magnesium (Mg) frequently acts as a natural calcium (Ca) antagonist, the possibility exists that the pro-inflammatory effect of Mg-deficiency may be a consequence of a reduced extracellular Mg(2+)/Ca(2+) antagonism. AIM OF THE STUDY: Thus, the aim of the study was to assess whether dietary Ca-deficiency improves the abnormal inflammatory response of Mg-deficient rats. MATERIALS AND METHODS: Weaning male Wistar rats were randomly divided into 4 groups according to the dietary Mg and Ca as follows: Mg-adequate Ca-adequate (control), Mg-adequate Ca-deficient, Mg-deficient Ca-adequate, Mg-deficient Ca-deficient. Animals were fed the appropriate diets for 8 days. RESULTS: Mg-deficient Ca-adequate rats as compared to controls displayed the usual decrease in plasma Mg, whereas the plasma Ca concentration was unaffected. The classical symptoms of inflammation including hyperemia, increased number of blood leukocytes and increased spleen weight were observed. In addition, these animals also showed an increase in heart lipid peroxidation and in plasma triglyceride concentration. In Mg-deficient rats, Ca-deficiency induced hypocalcemia and offered a significant protection against the pro-inflammatory effect of Mg-deficiency. This was evidenced by lower inflammation scores, prevention of leukocytosis and of spleen enlargement. The protective effects of Ca-deficiency on the inflammatory response in Mg-deficiency was accompanied by significant reduction in lipid peroxidation and by a normalization of plasma triglyceride concentration. CONCLUSION: All together, the results suggest that Ca is implicated in the inflammatory response of experimental Mg-deficiency and that oxidative stress and hypertriglyceridemia are the results of the acute phase response following Mg-deficiency in rats.

Animals↗
PubMed1994

Ferrylmyoglobin formation induced by acute magnesium deficiency in perfused rat heart causes cardiac failure.

The oxidation states of intracellular myoglobin and cytochrome oxidase aa3 were monitored by reflectance spectrophotometry in isolated perfused rat hearts subjected to an acutely magnesium deficient environment. After exposure to low extracellular [Mg2+]o (i.e., 0.3 mM) for 30 min, more than 80% of the oxymyoglobin converted to its deoxygenated form. The level of reduced cytochrome oxidase aa3 also increased about 80% in low [Mg2+]o. The deoxymyoglobin was converted further to a species identified as ferrylmyoglobin by its reaction with Na2S to form ferrous sulfmyoglobin which was optically visible. This process, set into motion by acute Mg deficiency, resulted from a direct accessibility of the exogenous peroxide to the cytosolic protein. The results suggest that a pathway leading to cardiac tissue damage, induced by magnesium deficiency, is probably involved in the generation of a ferrylmyoglobin radical which could be prevented by addition of ascorbate, which is known to be a one-electron reductant of this hypervalent form of myoglobin. In further studies, we also investigated whether addition of different concentrations of ascorbic acid (AA) to the perfusate could enhance myocardial function after exposure to low [Mg2+]o perfusion. Four concentrations of AA (0.5, 1, 5, 10 mM) were tested, and the results indicate that they exert their effects in a concentration-dependent manner; 1 mM AA was the most effective dose in improving aortic output in a Mg-deficient heart. Ferrylmyoglobin formation was found to be formed considerably before intracellular release of either creatine phosphokinase or lactic dehydrogenase. These studies may have wide implications as a new mechanism by which low extracellular Mg2+ can induce myocardial injury and subsequent cardiac failure.

Animals↗
PubMed1972

Evidence for parathyroid failure in magnesium deficiency.

Serum immunoreactive parathyroid hormone (IPTH) was low to nondetectable in spite of hypocalcemia in a patient with chronic magnesium deficiency. The administration of magnesium led to parallel increases in serum IPTH, serum calcium, and renal phosphate clearance. These findings support the view that magnesium depletion may result in impaired synthesis or release of parathyroid hormone in man, or both.

Adult↗
PubMed1975

The effects of magnesium deficiency on the host response to intramuscular bone matric implanted in the rat.

HCl-demineralized mid-diaphyseal allogeneic segments of tibia were implanted in the lumbar muscles of rats fed either a magnesium-deficient or a magnesium-supplemented diet for one week prior to implantation and for three weeks thereafter. Histological studies, histochemical mucopolysaccharide determinations, tests for protease content of undemineralized bone tissue, and microradiography showed that in the normal hosts mostly trabecular bone grew into the heterotopic site, whereas in the deficient rats a large fibrous covering formed about the implant and in many instances cartilage was present in multiple locations under the fibrous coat. In some instances cartilage wedges, not preceded by multinucleated giant cells (matrixclasts), invaded the implant. This fibrocartilaginous response to an exogenous inductor resembled the modified growth pattern of bone recently reported in magnesium-deficient rats.

Animals↗
PubMed1996

Functional alterations in sarcoplasmic reticulum membranes of magnesium-deficient rat skeletal muscle as consequences of free radical-mediated process.

Free radical-induced physiopathologies are generally thought to be mediated by membrane injuries. Using a pro-oxidant model induced by dietary magnesium deficiency, we have recently shown that skeletal muscle lesions occurred with a rise in the calcium level and enhanced free radical production. In this study, we investigated the physicochemical and biochemical properties of sarcoplasmic reticulum membranes isolated from hind limb muscles of weanling male rats pair fed magnesium-deficient or control diets for 12 d. The calcium-induced calcium efflux from preloaded vesicles was increased in membranes isolated from Mg-deficient rat muscle. In agreement with this latter observation, we demonstrated increased ryanodine binding affinity of the calcium channel. The Ca2(+)-ATPase activity of the pump was shown to be reduced. The viscosity state of the membranes, assessed by 1,6-diphenyl-1,3,5-hexatriene fluorescence anisotropy, was significantly increased in Mg-deficient membranes. Moreover, these membranes demonstrated an increased content of protein carbonyls as compared with controls. These functional as well as structural changes are closed to those described in sarcoplasmic reticulum membranes oxidatively modified in vitro. Together, these data fitted well with the concept that free radical-induced membrane damages resulting in calcium overload may be at the origin of skeletal muscle lesion during Mg-deficiency.

Animals↗
PubMed2002

Intestinal and renal handling of oxalate in magnesium-deficient rats. Evaluation of intestinal in vivo 14C-oxalate perfusion.

OBJECTIVE: To clarify in vivo, using isolated small intestinal loops perfused with radioactive 14C-oxalate, whether intestinal hyperabsorption or reduced secretion is important in magnesium deficiency (MgD), as this is a potential cause of calcium oxalate urolithiasis. MATERIALS AND METHODS: Twenty-four Sprague-Dawley rats were either fed a standard diet (control, 12 rats) or a magnesium-deficient diet (MgD, 12 rats) for 19 weeks. One hour before the animals were killed, a defined length of a small intestinal loop was isolated and filled with 5 mL of 0.9% NaCl and a defined amount of intravenous 14C-oxalate applied. Using this method it was possible to determine the secretion of unlabelled oxalate into the intestinal lumen, from the specific activity in plasma. RESULTS: Plasma oxalate levels doubled under MgD; urinary calcium and phosphorus also increased significantly, while urine oxalate tended to decrease. The secretion of oxalate into the intestinal lumen of MgD animals increased significantly, by five times that of the control. The relative supersaturation for calcium oxalate remained constant. Elementary analysis of renal tissue showed an increase in calcium and phosphorus under MgD, in the sense of nephrocalcinosis, but no concretions were detected (no nephrolithiasis). CONCLUSION: In contrast to earlier studies, there is no evidence that hyperoxaluria is responsible for the possible development of urolithiasis in MgD. This was confirmed by calcium phosphate deposits in renal tissue, even though there was no evidence of oxalate urolithiasis. The increase in plasma oxalate seems to be completely compensated by strongly increased oxalate secretion into the intestinal lumen.

Animals↗
PubMed2002

Increased phagocytosis and production of reactive oxygen species by neutrophils during magnesium deficiency in rats and inhibition by high magnesium concentration.

Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0.8 v. 8.0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.

Animals↗
PubMed1983

Review article. Magnesium deficiency provoked by diuretics.

Many diuretics cause hypermagnesiuria which may lead to magnesium deficiency, presenting as hypomagnesaemia, cardiac arrhythmias and tetany. Loop diuretics cause hypermagnesiuria mainly through direct blockade of magnesium reabsorption at the loop of Henle. Distal tubular diuretics block magnesium reabsorption at the distal convoluted tubule and also reduce magnesium reabsorption at the loop of Henle by an indirect mechanism.

Diuretics↗
PubMed1983

The effect of magnesium deficiency and excess on bovine coronary artery tone and responses to agonists.

1 The hypothesis that magnesium deficiency, linked to the magnesium content of drinking water, induces major tone increases in coronary arteries and enhances their responses to vasoactive agents to an extent sufficient to explain sudden death associated with ischaemic heart disease was examined in an in vitro preparation. 2 The spontaneous tone of cattle coronary arteries was not increased during a 30 min exposure to Mg2+-deficient Krebs until the mineral was omitted entirely from the bathing medium, and even then the observed increase was small. Only in strips maintained under extremely deficient conditions for a prolonged period, namely Mg2+ concentration of 0.2 mM and 0.0 mM for 3 h, was tone substantially greater than in controls in standard (1.2 mM) Mg2+-Krebs. 3 Responses to acetylcholine and to noradrenaline were not increased in Mg2+-free Krebs but those to potassium and to 5-hydroxytryptamine were enlarged over the lower parts of their concentration-response curves. Responses to potassium and to 5-hydroxytryptamine were also examined in Krebs containing very low concentration of Mg2+ (0.4 and 0.2 mM) and only modest increases in contraction size were detected. Increases in the Mg2+ concentration of the Krebs (to 4.8 mM) depressed responses to potassium and 5-hydroxytryptamine. 4 It is concluded that Mg2+ deficiency must be nearly complete (0.4-0.0 mM) to induce even moderate tone increases in coronary vessels, or to sensitize them to agonist responses, and that there is no reason to link marginally subnormal Mg2+ levels, occasionally reported in humans with heart disease, to marked changes in coronary dynamics.

Acetylcholine↗