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PubMed1980

Calcium homeostasis and bone pathology in magnesium deficient rats.

Calcium homeostasis and bone pathology were studied in weanling rats fed a low (70 ppm) magnesium diet for 2-21 days. The rats developed significant, progressive hypercalcemia after 6 days on the diet. The increase in blood calcium was accompanied by progressive hypoactivity of the parathyroid gland (PTG), as determined by histologic and morphometric analyses. Thus hyperactivity of the PTG could not have been responsible for the hypercalcemia observed. Histologic examination of femora and humeri from magnesium-deficient rats showed progressive subperiosteal hyperplasia, consisting of undifferentiated osteoprogenitor cells and fibrous tissue, after 7 days of deficiency. The presence of unmineralized osteoid tissue in the metaphyses indicated that mineralization was not proceeding normally. The alterations in differentiation of osteoprogenitor cells, together with the failure of mineralization, resulted in significantly lower rates of bone formation (as measured by fluorochrome labeling) in the magnesium-deficient rats. Basophilic cementing lines and inactive osteocytes in the cortices of bones from magnesium-deficient rats indicated that bone resorption was also severely reduced in magnesium deficiency. We postulate that bone magnesium depletion (66% by day 21) has a direct negative effect on osteoblastic and osteocytic activity, and may explain, in part, the decreased responsiveness of bone to parathyroid hormone (PTH) that has been observed in magnesium-deficient animals.

Animals↗
PubMed1987

[Studies on histamine containing cells in the spleen of the magnesium-deficient rats].

When young Wistar rats (body wt. 50 g) were maintained on a magnesium-deficient diet (0.001% Mg) for eight days, the splenic weight and histamine content increased about 2-fold and 30-fold, respectively, compared with those of the control rats. There was no significant difference in the number of splenic mast cells between the magnesium-deficient and control rats. More neutrophilic, eosinophilic and basophilic granular cells were found in the spleen cells isolated from the magnesium-deficient rats than in those from the control rats. Of the isolated cells from magnesium-deficient rats, 7.6% were basophilic granular cells; however, no basophilic granular cells were observed in the spleen cells isolated from the control rats. In the cytochemical study, the yellowish fluorochrome formed by the interaction of o-phthalaldehyde and histamine was found in basophilic granular cells. These results suggest that the increase in the histamine content of the spleen of magnesium-deficient rats is related to the increased number of basophilic granular cells.

Animals↗
PubMed1985

Enhanced incidence of isoproterenol-induced ventricular fibrillation in the magnesium-deficient rat.

The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations.

Animals↗
PubMed1996

Changes in the haemostatic profile during magnesium deficiency in swine.

Epidemiological studies of populations living in areas of low magnesium (Mg) intake have consistently shown a higher cardiovascular morbidity. Several hypotheses have been advanced to explain the cardioprotective properties of magnesium. Few studies, however, have analysed the relation of magnesium to haemostasis. The overall purpose of this project was to assess the association between certain haemostatic variables and magnesium deficiency. This experiment was designed to assess the effect of magnesium deficiency on various haemostatic variables which may relate to cardiovascular morbidity. Twelve female Yorkshire swine were fed for seven weeks on an Mg-sufficient or an Mg-deficient diet. Blood samples were obtained at baseline and after the termination of feeding in order to evaluate platelet aggregability and concentrations of antithrombin-III (AT-III), protein C, total protein S, fibronectin, endothelin-1 (ET-1), as well as the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1 alpha). In animals on an Mg-sufficient diet, there were no significant differences in any of the investigated haemostatic variables. In the Mg-deficient group, a significant decrease in serum magnesium was noted after the feeding period (from 2.0 +/- 0.1 to 1.3 +/- 0.1; P < 0.01). Mg-deficient swine showed significant increases in ADP-induced (33.3 per cent and 59.6 per cent) and collagen-induced (36.6 per cent) platelet aggregation, and decreased plasma antithrombin-III (17.7 per cent) and protein S (14.4 per cent) when compared to baseline. Plasma concentrations of TxB2 (28.7 per cent), protein C (57.2 per cent), and ET-1 (74.9 per cent) were dramatically increased. There were no significant differences in plasma fibronectin and 6-keto-PGF1 alpha levels in the magnesium-depleted animals. We conclude that magnesium deficiency is associated with significant proaggregatory and coagulation alterations. This may contribute to the increased cardiovascular morbidity found in magnesium-deficient populations. The beneficial effects of magnesium supplementation in an expanding array of clinical conditions including cardiovascular disease may, in part, be related to the improved haemostatic profile in such patients.

Animals↗
PubMed1996

Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload.

The mineral imbalances in magnesium-deficient rats with dietary iron overload were studied. Forty-four male Wistar rats were divided into six groups and fed six diets, two by three, fully crossed: magnesium adequate or deficient, and iron deficient, adequate, or excess. The concentrations of iron, magnesium, calcium, and phosphorus in tissues of the rats were measured. The results were as follows: (1) The excess iron intake reinforced the iron accumulation in liver and spleen of magnesium deficient rats; (2) The saturation of iron binding capacity was enormously elevated in the magnesium deficient rats fed excess iron; and (3) Dietary iron deprivation diminished the degree of calcium deposition in kidney of magnesium deficient rats. These results suggest that magnesium-deprived rats have abnormal iron metabolism losing homeostatic regulation of plasma iron, and magnesium deficient rats with dietary iron overload may be used as an experimental hemochromatosis model.

Analysis of Variance↗
PubMed2004

Physiological characterisation of magnesium deficiency in sugar beet: acclimation to low magnesium differentially affects photosystems I and II.

Magnesium deficiency in plants is a widespread problem, affecting productivity and quality in agriculture, yet at a physiological level it has been poorly studied in crop plants. Here, a physiological characterization of Mg deficiency in Beta vulgaris L., an important crop model, is presented. The impact of Mg deficiency on plant growth, mineral profile and photosynthetic activity was studied. The aerial biomass of plants decreased after 24 days of hydroponic culture in Mg-free nutrient solution, whereas the root biomass was unaffected. Analysis of mineral profiles revealed that Mg decreased more rapidly in roots than in shoots and that shoot Mg content could fall to 3 mg g(-1) DW without chlorosis development and with no effect on photosynthetic parameters. Sucrose accumulated in most recently expanded leaves before any loss in photosynthetic activity. During the development of Mg deficiency, the two photosystems showed sharply contrasting responses. Data were consistent with a down-regulation of PSII through a loss of antenna, and of PSI primarily through a loss of reaction centres. In each case, the net result was a decrease in the overall rate of linear electron transport, preventing an excess of reductant being produced during conditions under which sucrose export away from mature leaf was restricted.

Adaptation, Physiological↗
PubMed1990

Magnesium deficiency.

Over the past 40 years, human magnesium deficiency has become recognized as a world-wide clinical problem. In 1926, Leroy (1), demonstrated the absolute need of magnesium for growth and life in mice, and the need for magnesium in plants was demonstrated in 1860. Although clinical deficiency was first reported in 1934, it was not until the 1950s that interest in clinical magnesium deficiency developed rapidly. Before the 1950s, textbooks of medicine, pediatrics and biochemistry did not mention magnesium disturbances. In this paper I shall emphasize the recognition and treatment of magnesium deficiency by giving details of the setting, i.e. illnesses, the multifaceted manifestations, the laboratory findings and safe protocols for treatment.

Animals↗
PubMed1989

[Selected organopathies caused by experimental magnesium deficiency].

A role of enzyme mediated metabolic processes is discussed. Unfavourable effect of magnesium deficiency on the functioning of various organs may lead to extensive and irreversible morphological changes of focal character. Basing on the results of several experiments and own experience, the author discusses an effect of low-magnesium diet on histological, histochemical, and microscopic lesions to the myocardium, skeletal musculature, liver, and pancreas. Magnesium deficiency predisposes to myocardial necrosis which simulates electrolyte-steroid-cardiomyopathy by necrosis (ESCN). Low-magnesium diet decreases resistance of the animals to various types of stress such as: cooling, immobilization, and noise. Insignificant degree of the lesions to skeletal musculature produced by magnesium deficiency and no progress in these lesions during the experiment may depend upon relatively stable magnesium reserve in the muscles. Low-magnesium diet increases the number of so-called Ito cells in the liver. It is probable that these cells together with hepatocytes contribute to the formation of collagen fibres. Magnesium deficiency may lead to the abnormal digestion of nutrients in the pancreas, interfering with exocytosis of zymogen granules. Supplementation of the diet with magnesium may prevent various organopathies.

Animals↗
PubMed1994

Calcium and oxalate uptake by the renal brush border membrane vesicles in magnesium-deficient rats.

Calcium and oxalate uptake by renal brush border membrane vesicles (BBMV) was examined in magnesium-deficient and pair-fed control rats. Uptake studies were carried out by rapid filtration technique and rate of influx of calcium and oxalate as a function of extravesicular concentration (0.1 nM--1.0 mM) examined. Calcium uptake by renal BBMV exhibited saturable kinetics while oxalate uptake followed a biphasic transport mechanism showing saturable kinetics at low oxalate concentrations and passive diffusion at higher concentrations. In magnesium deficiency the kinetics of calcium and oxalate uptake by renal BBMV remained unaltered but the rate of uptake was significantly enhanced at all the extravesicular concentrations studied. Double reciprocal plot for calcium uptake showed no change in Vmax but a decrease in Km (2.08 mM) in magnesium--deficient rats as compared to pair-fed controls (Km = 5.00 mM). Similar plot for oxalate uptake showed an increase in Vmax (7.69 nmoles/8 min/mg protein) in magnesium deficient group as compared to pair-fed controls (5.55 nmoles/8 min/mg protein), while Km remained unchanged. The results of the present study indicate high risk of calcium oxalate stone formation in magnesium--deficient rats due to hyperabsorption and retention of calcium and oxalate by the renal tubular brush border membrane.

Animals↗
PubMedDate not supplied

Magnesium-deficient myocardium demonstrates an increased susceptibility to an in vivo oxidative stress.

Previous studies in our laboratory have indicated free radical participation in magnesium deficiency cardiomyopathy. In this study, we examined the capacity of the magnesium-deficient animals to withstand an in vivo oxidative stress. Syrian hamsters were placed on either magnesium-deficient diet or a magnesium-supplemented control diet. Animals from each group also received vitamin E. After 14 days some of animals were given the catecholamine isoprenaline; 2 days later the animals were killed. The severity of the isoprenaline-induced injury was assessed by a morphometric analysis. The isoprenaline-induced injury was dramatically increased in the magnesium-deficient animals. The addition of vitamin E reduced the severity of the injury by 81% in these animals, indicating that the injury process was primarily due to an oxidative mechanism. These data show that magnesium deficiency increases the susceptibility of the cardiovascular system to oxidative stress.

Animals↗
PubMed1984

Metabolic activity of liver mitochondria from magnesium-deficient rats.

Comparisons were made between the metabolic activities of whole mitochondria and intact mitochondrial inner membrane preparations from magnesium-deficient and control rats in a basic medium without exogenous magnesium. Magnesium deficiency partially uncoupled oxidative phosphorylation in whole mitochondria and completely uncoupled it with inner membrane preparations. Addition of 1 mM MgCl2 to the medium prevented the total uncoupling of inner membranes and gave ADP:O values similar to those obtained with whole mitochondria from magnesium-deficient rats. No impairment in proton extrusion by intact inner membranes or in ATPase activity by either intact or fragmented inner membranes was detected during magnesium deficiency, but there was evidence of increased membrane permeability to the inward movement of protons. It is concluded that magnesium deficiency probably increases the permeability of the mitochondrial inner membrane and this weakens the coupling between oxidation and phosphorylation.

Adenosine Triphosphatases↗
PubMed1993

Intestinal absorption of calcium and oxalate in magnesium-deficient rats.

To examine the contribution of exogenous calcium and oxalate in magnesium deficiency, intestinal absorption of both calcium and oxalate was studied by preparing brush border membrane vesicles (BBMV). Purity of the BBMV was ascertained biochemically by enrichment of the marker enzyme alkaline phosphatase by 14-fold with a concomitant 90 per cent decrease in the basolateral marker enzyme Na+/K(+)-ATPase in the purified membrane preparation as compared to the respective homogenate in both the groups. Uptake studies were carried out by a rapid filtration technique. The kinetics were studied by measuring the rate of influx as a function of concentration (0.1-1.0 mM). BBMV from both the groups showed a linear positive relationship between the uptake rate and the concentration for both calcium and oxalate, thereby demonstrating that calcium and oxalate are transported through intestinal microvillus membrane by a simple passive diffusion process. However, the rate of uptake of calcium and oxalate was significantly higher in the magnesium-deficient group as compared to the pair-fed control group, as shown by the increase in the slope line for both calcium and oxalate (for calcium, control = 3.88, deficient = 5.86; for oxalate, control = 4.41, deficient = 7.20). Analysis of the lipid composition of the BBM revealed a significant decrease in the cholesterol content (P < 0.01) with a concomitant increase in the triglycerides (P < 0.01) and total fatty acid content (P < 0.001) in the magnesium-deficient group. Thus the results indicate that, although the mechanism of translocation of calcium and oxalate in the intestine is similar in the two groups, magnesium deficiency leads to hyperabsorption of both the ligands through alterations in the lipid composition of the membrane, thereby increasing the risk of stone formation.

Animals↗
PubMed2003

Structural alterations of the vascular wall in magnesium-deficient mice. A possible role of gelatinases A (MMP-2) and B (MMP-9).

Vascular alterations during magnesium deficiency have long been known but the implicated mechanisms have so far been poorly documented. In this preliminary assay, we compared the thoracic aortic histology in Swiss OF1 mice fed a severe magnesium-deficient diet (50 +/- 5 ppm) for 42 days to that of controls fed a standard diet (1700 +/- 100 ppm magnesium). It appeared (eosin-haematoxylin coloration) that, in magnesium-deficient mice, the aortic wall was thinner than in controls. Specific colorations of the two of main fibers vascular tissue (collagens and elastin) showed severe structural alterations of both components. These changes were consecutive to the expression of matrix metalloproteinases (MMP) -2 and -9 which were present as zymogens (inactive forms) in controls and supposed to be present in their active and inactive forms in magnesium-deficient mice (zymography). These changes which have not been reported so far would explain, at least in part, the sensitivity of magnesium-deficient mice to various stress or xenobiotics.

Animals↗
PubMedDate not supplied

Propranolol reduces cardiomyopathic injury induced by magnesium deficiency.

We have previously established a link between magnesium-deficiency-induced cardiomyopathy and free radical injury. In the present study, golden Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group received either d,l-propranolol or d-propranolol (the non-beta-blocking form). After 14 days, the animals were sacrificed and their hearts isolated for morphological and morphometric analyses. Hematoxylin/eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Propranolol reduced both the density of lesions, from 0.32 to 0.06 lesions/mm2 (p < 0.01), and the area fraction of lesions, from 9.8 x 10(-4) to 2.5 x 10(-4) lesion area/mm2 (p < 0.01). In addition, d-propranolol was virtually equipotent to d,l-propranolol, indicating that part of the protective effect of propranolol, in this model, was attributable to its antioxidant properties.

Animals↗
PubMed1994

Enhanced contractile response to phenylephrine and increased density of [3H]PN200-110 binding sites in thoracic aorta isolated from dietary magnesium-deficient rats.

The present study was undertaken to examine whether the enhanced contractile response to phenylephrine observed in thoracic aorta isolated from dietary magnesium-deficient rats depends on an increased density of alpha 1-adrenoceptor or calcium channels. Adult male Wistar rats were fed with a magnesium-deficient diet (0.001 per cent magnesium) for 30 days with control groups (0.07 per cent magnesium). The contractile response to phenylephrine was significantly inhibited by nifedipine in both aortas without endothelium, and the degree of the inhibition was significantly greater in magnesium-deficient rats than in controls. Membranes were isolated from both thoracic aortas without endothelium, and the binding of [3H]PN200-110 or [3H]prazosin to the membranes was studied. A single binding site for [3H]PN200-110 or [3H]prazosin was evident for both membranes with high affinity. Dietary magnesium-deficiency increased significantly the maximal number (Bmax) of [3H]PN200-110 binding sites, but not Bmax of [3H]prazosin, and did not alter the binding affinity of both ligands. These results suggest that increased density of calcium channels participates in the enhanced contractile response to phenylephrine in thoracic aortas isolated from dietary magnesium-deficient rats.

Animals↗
PubMed2003

Magnesium deficiency reveals the neurotoxicity of delta-9-tetrahydrocannabinol (THC) low doses in rats.

In the present study, muricide behaviour (MB) was studied in Long Evans rats in various situations. The MB pattern of each experimental group was compared, in 6 successive assays 1 hr-delayed to that of natural killer rats (NK). The percentage of NK rats was 11% in the strain used. In the 11 mg THC/kg b.w. treated naive rats, a significant additional percentage of rats (59%) became muricidal. The durations of the 3 MB phases were significantly increased as a result of an increased aggressiveness in the 1st assay but returned progressively to NK values on the 6th assay, in parallel with the physiological elimination of THC. This result indicates a true killing training in those non killer rats that became muricidal under THC. A severe magnesium deficiency induced by a 50 ppm magnesium-deficient diet induced 100% MB whereas a 150 ppm magnesium deficiency did not induce additional MB. In the severe deficiency, the MB pattern was rather similar to that of NK with the exception of the attack on the living mouse which was doubled probably because of magnesium-induced hyperexcitability responsible for a lower attack efficiency. In both 50 but also 150 ppm magnesium-deficient rats, a single injection of THC at low doses (2, 4 or 8 mg THC/kg b.w.) which is without aggressive effect in control rats, induced a 100% MB, the pattern of which was all the more severe as the magnesium deficiency was important or the THC dose higher. The pattern showed an important decrease in the two first phases and a dramatic increase in the attack on the dead mouse, suggesting that the combination of both treatments provoked severe central damage with a compulsive killing behavior. Consequently, it appears that a magnesium deficiency, even a moderate one, may aggravate the neurotoxicity of THC at low doses and, reciprocally, that low doses of THC may reveal the potential neurotoxicity of a moderate magnesium deficiency.

Aggression↗
PubMed1996

Relation between severity of magnesium deficiency and frequency of anginal attacks in men with variant angina.

OBJECTIVES: We evaluated whether the severity of magnesium deficiency was correlated with the frequency of attacks of variant angina. BACKGROUND: Magnesium deficiency may be associated with the development of variant angina. However, the relation between the activity of variant angina and magnesium deficiency remains to be elucidated. METHODS: We assessed the body magnesium status of 18 men with variant angina: Group 1 (> or = 4 attacks/week, n = 7) and Group 2 (< 4 attacks/week, n = 11). Concentrations of magnesium were determined in serum, urine, mononuclear cells and erythrocytes, and the 24-h magnesium retention rate was determined. RESULTS: Group 1 showed a higher 24-h magnesium retention rate (mean +/- SEM 63.5 +/- 7.6% vs. 24.9 +/- 2.7%, p < 0.01) and a lower intracellular concentration of magnesium in mononuclear cells and erythrocytes than did Group 2 (respectively, 156.3 +/- 13.5 vs. 212.1 +/- 6.9 fg/cell, p < 0.01; and 3.5 +/- 0.5 vs. 5.2 +/- 0.4 fg/cell, p < 0.05), demonstrating the presence of magnesium deficiency in Group 1. The 24-h magnesium retention rate and intracellular concentrations of magnesium in mononuclear cells and erythrocytes correlated well with the frequency of anginal attacks (r = 0.78, p < 0.01; r = -0.78, p < 0.01; r = -0.62, p < 0.01, respectively) for all patients. CONCLUSIONS: Data suggest that the magnesium status of men with variant angina is closely related to disease activity.

Aged↗
PubMed1975

Effect of magnesium deficiency and parathyroid hormone on cyclic AMP metabolism in rat renal cortex.

The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex. Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.

Adenylyl Cyclases↗