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PubMed1987

Neurological consequences of magnesium deficiency: correlations with epilepsy.

1. The plasma calcium and magnesium concentrations of sheep have been manipulated by feeding liquid diets with various calcium and magnesium concentrations. 2. When the magnesium status of the diet was low, both plasma calcium and magnesium concentrations declined, but the decline in calcium was much more rapid and extensive when the content of calcium in the diet was also low. This loss of calcium control in magnesium deficiency was attributed to end-organ resistance to parathyroid hormone. 3. Correlation between plasma and CSF calcium and magnesium concentrations indicated that convulsions occurred when CSF magnesium and plasma calcium concentrations declined. 4. The neurological mechanisms likely to be responsible for the induction of these convulsions are discussed and the factors precipitating convulsions in magnesium deficiency and epilepsy are compared.

Animals↗
PubMed1992

Erythrocytes from magnesium-deficient hamsters display an enhanced susceptibility to oxidative stress.

Previous studies in our laboratory have indicated a role for free radical participation in magnesium deficiency cardiomyopathy. We have demonstrated the ability of various antioxidant drugs and nutrients to protect against magnesium deficiency-induced myocardial injury. In this study, we have examined erythrocytes from normal and magnesium-deficient animals and compared their susceptibility to an in vitro oxidative stress. Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group also received vitamin E in doses of 10 and 25 mg as subcutaneous implants. Erythrocytes obtained after 14 days on the diet were exposed to an exogenous hydroxyl (.OH) radical generating system (dihydroxyfumarate not equal to Fe3+ ADP) at 37 degrees C for 20 min. Erythrocyte crenation was observed and quantified by scanning electron microscopy. Lipid peroxidation, hemolysis (%), and intracellular glutathione levels were determined. In addition, serum lipid changes and membrane phospholipids were characterized. Our data demonstrate that erythrocytes from magnesium-deficient animals are more susceptible to free radical injury, supporting our hypothesis that magnesium deficiency reduces the threshold antioxidant capacity.

Adenosine Diphosphate↗
PubMed1986

Alteration of prostanoid metabolism in rats with magnesium deficiency.

Plasma and tissue concentrations of prostanoids PGE2, PGF2 alpha. 6-keto-PGF1 alpha (a stable metabolite of prostacyclin) and TXB2 (a stable metabolite of thromboxane A2) were measured in normal and magnesium-deficient rats. The mean values for prostanoids in plasma were significantly higher in magnesium-deficient rats than in normals (515 +/- 43 vs 296 +/- 31 pg/ml for 6-keto-PGF1 alpha, p less than 0.01, 3700 +/- 322 vs 346 +/- 33 pg/ml for TXB2, p less than 0.001 and 1234 +/- 132 vs 434 +/- 51 pg/ml for PGE2, p less than 0.001). Tissue levels of prostanoids were also significantly higher in magnesium-deficient rats as compared to normals. The increased synthesis of prostanoids is apparently linked to enhanced influx and translocation of Ca++ into the cells. If the adenylate cyclase is inhibited in magnesium deficiency, the lowered c-AMP will permit a high cyclooxygenase activity and a drastic increase in TXB2. It is possible that the changes in prostaglandin synthesis in magnesium deficiency are linked to the development of different diseases.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Effects of magnesium deficiency on parturition and uterine involution in the rat.

The effects of moderate magnesium deficiency on the outcome of pregnancy, the process of parturition and uterine involution, were studied in successive experiments using Sherman rats. Females were fed purified diets containing 0.110 or 1.500 g Mg/kg throughout pregnancy and lactation. This magnesium deficient diet decreased the plasma magnesium but did not affect the number of pregnant rats or the weight of females at parturition. There was no change in the weight and size of litter. The number of still births was not significantly increased. The parturition process was observed; abdominal contractions were less obvious in deficient animals than in controls, and they were often not noticeable. Parturition was slightly lengthened in deficient rats. The major effects of magnesium deficiency occurred during lactation when the dam lost weight and the growth of her young was reduced. The uterine weight and its collagen content was higher and the collagen solubility was lower in the deficient rats than in controls between 2 and 10 days post partum. The delay in uterine involution could be prevented by provision of a magnesium supplement after parturition.

Animals↗
PubMed1979

Metabolic performance and GI function in magnesium-deficient rats.

A quantitative evaluation of the mass balance and GI motor effects of dietary magnesium deficiency in the adult male Sprague-Dawley rat is described. Seventy-seven animals were used. Both sham control and experimental groups were maintained on a commercial stock laboratory diet ad libitum for 30 days, after which the experimental rats were switched for 30 days to magnesium-deficient diet ad libitum, containing a magnesium concentration of 16.2 ppm. Ten rats were used to determine the acetylcholine responsiveness of duodenal muscle segments in vitro. In all cases, the segments from the deficient rats were hyperresponsive to a fixed acetylcholine dose. Forty-six rats were used to determine the average intestinal transit rate, which increased significantly in 30-day magnesium-deficient rats. A final series employed 21 rats who were housed in individual metabolic cages. After 5 days on the deficient diet, the average daily fecal pellet counts and fecal weights were significantly reduced. It is concluded that chronic magnesium deficiency is associated with altered GI motor function in the adult male rat.

Animals↗
PubMed1994

Magnesium deficiency prolongs myocardial stunning in an open-chest swine model.

The effect of magnesium deficiency on postischemic myocardial dysfunction (myocardial stunning) in an open-chest swine model was studied. Twelve swine were assigned either to low magnesium diet or control diet. Myocardial stunning was assessed by measuring regional wall thickening by epicardial Doppler before and after brief occlusion (8 min) of the left anterior descending coronary artery. Serum magnesium levels decreased significantly in the experimental group only. Glutathione levels were 42.6% lower in the magnesium deficient swine than in controls. Stunning time was significantly prolonged from 32.8 +/- 3.1 min in the control group to 43.8 +/- 4.6 min in the hypomagnesemic swine. In conclusion, magnesium deficiency is associated with prolonged recovery from myocardial stunning.

Animal Feed↗
PubMed1988

Magnesium deficiency exacerbates and pretreatment improves outcome following traumatic brain injury in rats: 31P magnetic resonance spectroscopy and behavioral studies.

The biochemical mechanisms mediating delayed or secondary tissue injury after central nervous system trauma remain speculative. We have demonstrated previously that traumatic brain injury in rats causes a rapid decline in tissue intracellular free magnesium [Mg]f and total magnesium [Mg]t concentrations, which were significantly correlated with injury severity. In order to examine the relationship between magnesium and traumatic brain injury, we assessed whether (1) magnesium deficiency exacerbates or (2) magnesium treatment improves posttraumatic outcome following fluid-percussion brain injury (2.0-2.4 atm) in rats. Animals placed on magnesium-deficient diet for 14 days showed a 15% decrease in brain [Mg]f as measured by phosphorus (31P) magnetic resonance spectroscopy (MRS). Magnesium deficiency significantly exacerbated neurologic dysfunction and increased mortality following injury when compared to normally fed saline-treated controls. Conversely, pretreatment with magnesium sulfate (0.1 mEq) 15 min before brain injury prevented the fall in [Mg]f observed by 31P MRS in saline-treated animals and significantly improved both cellular bioenergetic state and chronic posttraumatic neurologic outcome. These combined observations suggest that alterations in brain [Mg]f after trauma may play a role in the pathophysiology of traumatic brain injury.

Animals↗
PubMed1972

Magnesium deficiency in patients on long-term diuretic therapy for heart failure.

Magnesium levels in serum, erythrocytes, skeletal muscle, and bone were measured in 10 patients with valvular heart disease who had received diuretic therapy for heart failure for an average of 3.3 years. Five patients were found to have diminished values for skeletal muscle, indicating significant magnesium deficit. Values for erythrocytes were low in only two of the five patients, and none had low values for serum ultrafiltrate and bone: Magnesium replacement therapy restored skeletal muscle values to normal. Clinical features consistent with the presence of magnesium deficiency were found in all five magnesium-deficient patients. These features were, with few exceptions, corrected by magnesium replacement. The latter also corrected low skeletal muscle potassium values present in all five patients with low skeletal muscle magnesium, four of whom showed clinical features of digoxin poisoning before magnesium therapy was given. Concomitant secondary aldosteronism, inadequate dietary intake, and digoxin therapy had probably augmented the magnesium loss due to diuretic therapy.

Adult↗
PubMed1976

Effect of fluoride on the mobilization of skeletal magnesium and soft-tissue calcinosis during acute magnesium deficiency in the rat.

To investigate the effect of fluoride on the mobilization of skeletal magnesium and on kidney calcification during magnesium depletion, male Holtzman rats were fed a magnesium-sufficient diet (400 ppm of magnesium) and drinking water containing either 0, 50 or 100 ppm of fluoride for a 20-day period prior to the initiation of magnesium deficiency. The high fluoride regimen resulted in a 100-fold increase in the fluoride content of the skeleton. On day 20 magnesium depletion was initiated by feeding the animals a diet containing 12 ppm of magnesium. Over a 4-week period of magnesium deprivation, a 26% decrease of the total magnesium in the humeri was observed. Fluoride exerted a significant effect in retarding the mobilization of skeletal magnesium. Four weeks of magnesium deficiency was associated with a decreased rate of skeletal mineral accretion and with an increase in the kidney calcium content. The decreased rate of mineral accretion was accentuated by the administration of fluoride during the deficiency state. While fluoride exerted an initial protective effect on calcinosis of the kidneys, the overall effect of the administration of fluoride during magnesium deficiency was to promote calcification of the kidneys rather than to prevent it.

Animals↗
PubMed1985

Magnesium deficiency and myocardial infarct size in the dog.

Although epidemiologic data suggest a relation between myocardial infarction death rates and dietary intake of magnesium, there are no experimental studies reflecting such a phenomenon. It is now reported that beagle dogs kept on a severely magnesium-deficient diet for 100 days develop a larger infarct than do control animals. Control animals were either kept on the same diet as experimental animals with supplementary magnesium, or were fed standard dog chow. The control groups were indistinguishable and were therefore pooled. Infarction was produced by occlusion of the left anterior descending coronary artery for 1 hour followed by 4 hours of reperfusion. Slices of ventricular myocardium, 5 mm thick, were made from the apex to the base. Ischemic muscle, considered to be the muscle at risk, was delineated by a microsphere-autoradiographic method, and necrotic muscle was delineated by tetrazolium stain. Involved areas were measured by planimetry, and these integrated to produce the volume. The volumes of muscle made ischemic were similar in the experimental and control groups. The volumes of necrotic muscle, however, were less in the control than in the experimental animals. The ratio of necrotic muscle volume to the volume of muscle at risk was greater in the experimental animals than in the control animals by a factor of almost two (p less than 0.004). These experiments indicate that, under the conditions used here, animals fed a magnesium-deficient diet develop a larger infarct than do control animals. This could occur either through decreased postocclusion collateral flow or increased vulnerability of the ischemic muscle in magnesium-deficient animals. Although these experiments cannot rule out an effect on postocclusion collateral flow, they do suggest that electrolyte abnormalities related to magnesium deficiency are of such a character as to increase myocardial vulnerability to injury.

Animals↗
PubMed1992

Effect of magnesium deficiency on 15-hydroxyeicosatetraenoic acid in cultured human umbilical arterial endothelial cells.

Effects of magnesium deficiency on the production of 15-hydroxyeicosatetraenoic acid (15-HETE) and cytosolic free calcium concentration in human umbilical arterial endothelial cells were studied by radioimmunoassay. 15-HETE release by endothelial cells incubated with normal magnesium media (900 microM Mg2+) for 24 h was 2.2 +/- 0.3 ng/mg protein. 15-HETE release gradually increased in proportion to decrease of magnesium. Low magnesium media (180 microM Mg2+) caused an increase in 15-HETE release in a time-dependent manner. Cytosolic free calcium concentration of endothelial cells in normal magnesium media fluctuated between 129.4 nM and 134.2 nM during a 24 h period. Low magnesium media (180 microM Mg2+) caused a time-dependent rise in cytosolic free calcium concentration which is consistent with a time-dependent increase in H-HETE release. High magnesium medium (1800 microM Mg2+) did not have any effect on cytosolic free calcium concentration or 15-HETE production. In conclusion, 15-HETE release by endothelial cells was stimulated by increase in cytosolic free calcium concentration induced by magnesium deficient media. It is suggested that magnesium deficiency induces atherosclerosis via increase in 15-HETE production.

Calcium↗
PubMed1978

Parathyroid hormone secretion in magnesium deficiency.

The effect of an acute elevation of the serum magnesium concentration on the concentrations of serum immunoreactive parathyroid hormone (IPTH) were studied in hypocalcemic hypomagnesemic patients, hyperparathyroid patients, and normal individuals. Basal serum IPTH concentrations in the hypomagnesemic patients ranged from undetectable to 3 times the upper limit of normal. All hypomagnesemic patients were observed to have an immediate rise in the serum IPTH concentration after magnesium administration regardless of the basal IPTH concentration. In contrast, normal individuals and patients with primary and secondary hyperparathyroidism responded to magnesium administration with either a decrease or little change in the serum IPTH concentration. These date indicate that an acute stimulation of PTH secretion induced by magnesium is characteristic of the magnesium-deficient state. The consistency of this response suggests that impaired PTH secretion is a significant factor contributing to the hypocalcemia of magnesium deficiency.

Calcium↗
PubMed1995

Possible alterations of the in vivo 1,25(OH)2D3 synthesis and its tissue distribution in magnesium-deficient rats.

In a previous work we showed that a decrease in the free intracellular magnesium produced alterations in the kinetic behaviour of 1 alpha-hydroxylase which reduced the synthesis rate of 1,25(OH)2D3. This in vitro result strongly supports that magnesium deficiency could also induce in vivo failure of the renal enzyme and then a decrease of 1,25(OH)2D3 serum levels. In the present work we have tested the effect of magnesium deficiency on the in vivo transformation of the substrate 3H-25(OH)D3 to 3H-1,25(OH)2D3 as well as the distribution of synthesized hormone among its different target tissues. We found that magnesium deficiency produced a decrease of both the in vivo synthesis of 3H-1,25(OH)2D3 and the binding of the radioactive hormone to bone tissue. These results may explain the different criteria present in the scientific literature concerning the relationships between magnesium status and vitamin D metabolism.

Animals↗
PubMed2001

Magnesium deficiency promotes muscle weakness, contributing to the risk of sudden infant death (SIDS) in infants sleeping prone.

A review was published (1991) of 19 retrospective case-control studies that had investigated the relationship between prone sleeping position (on the stomach) and the sudden infant death syndrome (SIDS). These studies, which had been conducted between 1965 and 1990 in New Zealand, Australia, England, France and the Netherlands, showed an overall higher rate of SIDS in infants who usually slept prone. In those countries, vigorous community intervention to change babies' sleep position away from the prone has resulted in marked declines of 50 per cent or more in the rate of SIDS. Such encouraging reports from many countries prompted the American Academy of Pediatrics to recommend that infants be placed to sleep on their backs to reduce the risk of SIDS. This was followed by a successful campaign in the United States between mid-1994 and 1998. Despite the decreased incidence, SIDS remains the leading cause of death in infants 1 month to 1 year of age of industrialized nations of the world. Studies have been conducted in human infants, mechanical models and animal models to learn the role of risk factors in prone sleeping infants. Soft bedding, thermal stress and biologic risk factors such as impaired ventilatory and arousal responsiveness are among many factors that have been investigated. Hunt states that there is not a single unifying factor that explains increased SIDS in prone sleeping infants. Two major studies conducted in the 1970s showed: (1) muscle weakness in the upper half of the body in infants who subsequently died of SIDS, and (2) shoulder hypotonia in near-miss for SIDS infants. An infant sleeping face-down in the prone position could be jeopardized if he lacked the muscle strength to shift his position or turn his head to rescue himself from a life-threatening situation. In contrast, recent studies in neonates sleeping in the prone position report that normal infants can spontaneously arouse and turn their heads. Some data support the hypothesis that magnesium deficiency contributes to SIDS. Muscle strength is seriously impaired in the young magnesium deficient subject, while magnesium rapidly reverses muscle weakness. In rats, marginal deprivation in dietary magnesium reduces exercise capacity, an early effect of magnesium deficiency which is preventable by consuming magnesium-enriched mineral water. It is concluded that magnesium deficiency is at least one major unifying factor that explains increased SIDS in prone sleeping infants.

Humans↗
PubMed1994

Effects of fructooligosaccharides on the absorption of magnesium in the magnesium-deficient rat model.

Magnesium (Mg) is an essential dietary element that plays important roles, acting as a cofactor of many enzymes. Rats fed a Mg-deficient diet have been reported to exhibit auricular and facial peripheral hyperemia and hemorrhage. Moreover, increased intake of calcium (Ca) or phosphorus (P) has been reported to impair apparent absorption of Mg. We tried to induce such typical inflammation in Mg-deficient rats by feeding low-Mg, high-Ca, and high-P diets. Increasing concentrations of Ca or P in the experimental diets significantly decreased the apparent absorption of Mg. And all rats fed the low-Mg (0.25 mg/g diet), high-Ca (10.4 mg/g diet), and high-P (12.0 mg/g diet) diet exhibited auricular and facial peripheral-hyperemia and hemorrhage. Then, we used the low-Mg, high-Ca, and high-P diet to investigate the effects of the fructooligosaccharides (FO) on absorption of Mg and skin inflammation. In the rats fed FO-containing (1 or 5%) diet, apparent absorption of Mg was significantly increased as compared with that of the control (FO 0%) group. In the rats fed a 5% FO-containing diet and sufficient Mg (0.50 mg/g), auricular and facial peripheral hyperemia and hemorrhage were significantly reduced. We concluded that FO increased the Mg absorption in rats fed a low-Mg, high-Ca, and high-P diet. Moreover, FO reduced inflammation in Mg-deficient rats, such as peripheral hyperemia and hemorrhage.

Animals↗
PubMed1977

Cytoenzymatic studies on the lymphocytes of peripheral blood and lymphatic nodes of rats in an experimental magnesium deficiency.

Wistar rats kept on a magnesium deficient diet show several changes in the lymphatic organs as well as some disorders in the function of the immunological system, which appear as an impairment of cellular immunity and also as hypogammaglobulinemia. In the present experiment the level of leuco- and lymphocytosis has been studied. Furthermore, the activity of some lysosomal enzymes in blood lymphocytes, as well as the ability to incorporate labelled leucine shown by lymph nodes lymphocytes of deficient rats have been investigated. The rise in leuco- and lymphocytosis is similar to that reported by other authors. A significant rise in the activity of beta-glucuronidase as well as a considerable drop in the percentage of enzyme-negative lymphocytes have been observed as early as the first week of experiment. Tissue cultures of the lymph nodes, lymphocytes of deficient rats showed significantly lower values of labelled leucine incorporation with respect to the controls; in contrast, after phytohemagglutinin M stimulation the increase of incorporation in the lymphocytes of deficient and control rats was similar. Our findings may be indicative of some disorders in the redistribution of T and B lymphocytes in the blood and tissues of deficient rats. The observed cytochemical changes may be due to the intensification of autophagic processes in the lymphocytes that manifest a diminished ability to synthetize proteins.

Animals↗
PubMed1975

The effects of magnesium deficiency of ketamine sleeping times in the rat.

Young growing rats were maintained on a magnesium deficient diet, and injected with ketamine after 7, 11, 14, and 18 days on the diet. A comparison of the sleeping times, as measured by the loss of the righting reflex after injections of three doses of ketamine, was made with rats similarly maintained on a control diet. Tolerance with successive injections to ketamine, indicated by a decrease in sleeping time, was noted only among the control rats. After 14 and 18 days on the diet, the magnesium deficient rats showed no tolerance to the earlier injections, but their sleeping times were longer than their control counterparts. In rats injected for the first time on day 14 of the diet, the magnesium deficient rats showed significantly longer sleeping times than the control rats; this suggests that the difference in sleeping times between groups is not entirely dependent upon the development of tolerance to the drug seen in the control rats. In addition, a sex difference was noted, with female rats sleeping longer with ketamine than male rats.

Animals↗
PubMed1975

Depressed immune response in the magnesium-deficient rat.

The effects of dietary magnesium on growth, food efficiency, organ development, splenic nucleic acids, and serum antibody were studied in two experiments with male Wistar rats. Diets containing 30% protein from casein were fed ad libitum. Rats were immunized intravenously with sheep red blood cells. Blood was obtained 5 and 9 days after immunization. In experiment 1, a group of weanling rats was fed 10 ppm Mg for 8 days, followed by 142 ppm for 37 days. Group 2 (controls) was fed 480 ppm Mg for 45 days. Group 1 weighed less but had larger spleens, kidneys, and testes relative to body size than did group 2. Nucleic acids per gram spleen were similar in both groups as were serum gamma-globulin and its 19S and 7S components. Antibody log titers for group 1 were 45 and 65% of control agglutinin levels and 44 and 80% of control hemolysin values on days 5 and 9, respectively. In experiment 2,200-g rats were fed 10 (group 3) or 480 ppm (group 4) Mg for 38 days. Most effects of the 10 ppm Mg diet were similar to those seen in magnesium deficiency in experiment 1. Antibody titers for group 3 were 30 and 25% of control agglutinin and 43 and 53% of control hemolysin values on days 5 and 9, respectively. Total serum gamma-globulin and its 19S fraction were similar in both groups, while the 7S fraction of group 3 was only 64% of the control value.

Animals↗