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PubMed1986

Plasma catecholamines in acute magnesium deficiency in weanling rats.

A controlled study was conducted to quantitate plasma catecholamines in magnesium-deficient weanling rats experiencing the seizure-shock episode. Eighty-four male Sprague-Dawley rats each weighing 35.6 +/- 0.3 g (mean +/- SEM) were fed purified diets to which was added 150 mg magnesium/100 g (Mg-150) or no magnesium (Mg-0). Studies were conducted between d 5 and 8. Plasma and bone magnesium and calcium were measured by atomic absorption spectrophotometry, and plasma catecholamines by radioenzymatic assay using 3H. Compared with Mg-150 rats, the Mg-0 rats showed reduced weight gain (P less than 0.001); reduced plasma magnesium (P less than 0.001) and reduced bone magnesium (P less than 0.001) with no corresponding changes in calcium concentration; and a 25% mortality by d 8. Pair-feeding and 80-dB noise provoked no changes in plasma catecholamines in Mg-150 rats, but both strychnine-induced seizures in Mg-150 rats and seizures induced by 80-dB noise in Mg-0 rats were accompanied by massive increases in plasma catecholamines. In contrast, 80-dB noise in Mg-0 provoked a massive increase in plasma catecholamines (P less than 0.001). However, gross pulmonary pathology developed only in Mg-0-shocked rats, not Mg-150-shocked animals. The study provides no evidence for a role of catecholamines in the pathogenesis of Mg-0 shock. The weanling rat displayed the ability to release massive quantities of three catecholamines during the final stages of acute magnesium deficiency and to normalize the plasma catecholamine levels within 16 h after seizure shock.

Animals↗
PubMed1992

Magnesium deficiency and diabetes mellitus. Causes and effects.

A large body of evidence demonstrates the prevalence and adverse clinical consequences of magnesium deficiency in patients with diabetes mellitus. It would be prudent for physicians who treat these patients to consider magnesium deficiency as a contributing factor in many diabetic complications and in exacerbation of the disease itself. Repletion of the deficiency or prophylactic supplementation with oral magnesium may help avoid or ameliorate such complications as arrhythmias, hypertension, and sudden cardiac death and may even improve the course of the diabetic condition.

Arrhythmias, Cardiac↗
PubMed1987

Effects of iron-, manganese-, or magnesium-deficiency on the growth and morphology of Euglena gracilis.

Iron-, manganese-, or magnesium-deficiency has been induced in Euglena gracilis. Each arrests cell proliferation, decreases the intracellular content of the deficient metal, and increases that of several other metals. Light and electron microscopy of stationary phase cells reveal that Fe-deficient (-Fe) cells are similar in size and shape to control organisms. Magnesium-deficient (-Mg) cells, however, are larger, and approximately 14% are multilobed, containing 2 to 12 lobes of equal size emanating from a central region. Individual (-Mg) cells and each lobe of multilobed cells contain a single nucleus. Manganese-deficient (-Mn) organisms are morphologically more heterogeneous than (-Fe) or (-Mg) cells. Most are spherical and larger than controls. Approximately 15% are multilobed but, unlike (-Mg) cells, contain lobes of unequal size with either zero, one, or several nuclei present in each. Nuclei of (-Mn) cells differ in size and shape from those of control, (-Fe), or (-Mg) cells. All three deficient cell types accumulate large quantities of paramylon. Other cytoplasmic structures, however, appear normal. Addition of Fe, Mn, or Mg to the respective deficient stationary phase cultures reverses growth arrest and restores normal morphology. The results suggest that Fe-, Mn-, and Mg-deficiencies affect different stages of the E. gracilis cell cycle.

Cell Nucleus↗
PubMed1985

Magnesium deficiency in a medical ICU population.

The serum magnesium level was measured in 94 consecutive patients admitted to the medical ICU of Los Angeles County/University of Southern California Medical Center over a 2-month period. Sixty-five percent of patients with serum creatinine concentrations of 1.1 mg/dl or less were hypomagnesemic. Of these, one third had hypocalcemia that was corrected with magnesium supplementation. Physicians should be alert to the high incidence of magnesium deficiency in critically ill patients.

California↗
PubMed1983

[Changes in the suppressive activity of splenic lymphocytes of mice induced in vitro by sodium periodate during magnesium deficiency].

Male DBA/2 Mice were kept on a magnesium deficient diet or a control diet. The antibody response of spleen cells, after in vitro immunization with Sheep red blood cells (SRBC) was determined comparatively in the two groups of Mice, from the 19th to the 22nd day of the diet. The effect of sodium periodate treatment on the induction of in vitro antibody suppressor cells was also studies. This treatment activated suppressor cells towards anti-SRBC response in the control group, but not in the Mg-deficient group (P less than 0.002). A greater sensitivity of periodate induced T suppressor cells to Mg deficiency is suggested by the present results.

Animals↗
PubMed1993

[Characteristics of the audiogenic convulsive crisis in mice made sensitive by magnesium deficiency].

Mice of the OF1, C57BL/6, AKR, C3H/He, DBA/2, BALB/C, B6D2F1 and CBA strains are susceptible to audiogenic seizures after 40 or 20 days of acute magnesium deficiency. The duration of the various phases of the audiogenic seizure response (at 100 dBA) (wild running latency period, convulsions latency period and the clonic and tonic convulsions) among these mice was measured. Using the Kruskall-Wallis test, no difference was recorded using these measurements and those obtained for genetically audio-susceptible animals. This shows that acute magnesium deficiency-induced audiogenic seizures develop in exactly the same way as in genetically audio-susceptible animals (21-days-old DBA/2 mice). Lower intensity (60 and 80 dBA) produced only audiogenic seizures in magnesium deficient mice. Repeated auditory stimulation caused an increase in the number of lethal seizures. Sound-induced seizures in magnesium deficient mice provide a sensitive screening test for anti convulsive drug, and for drugs use in magnesium depletion.

Acoustic Stimulation↗
PubMed2004

Prolonged magnesium deficiency causes osteoporosis in the rat.

BACKGROUND: Peroral magnesium (Mg) administration, used as the only treatment in postmenopausal osteoporosis, has been shown to cause a significant increase of BD. OBJECTIVES: To gauge the role of magnesium deficiency in the etiology of osteoporosis, we compared rats fed a Mg deficient diet daily with rats fed a Mg adequate diet over a period of one year. METHODS: Sprague-Dawley female rats (mean weight 110, SD 23 g) were divided into two groups of 8 and randomly assigned to an identical semisynthetic diet, containing either 2000 ppm (group A) or 200 ppm Mg (group B). Urine samples were collected every 3 months and blood samples at end of trial. After sacrifice, L3-L5 vertebrae and the femoral regions were examined for bone density (BD) using dual energy X-ray absorptiometry. The femurs were examined for bone fragility, the tibias by histomorphometry and the mineral contents of the bones was estimated. RESULTS: The mean BD of L3-L5 vertebral bone (BDL) was significantly higher in group than in the Mg deficient group B (p = 0.035, 1 tail). The BD of the femoral region (BDF) was also significantly higher in group A (p = 0.045, 1 tail). The stiffness of the femur, as determined by resistance to bending, was slightly greater in group A than in group B, but after correction to diminish the influence of the difference in bone dimensions in the two groups, the stiffness (ie loss of elasticity) in group B became significantly greater than that in group A (p = 0.024). The force needed to break the bone (F-max) was significantly higher in group A, than in group B (p = 0.024) and remained so after correction, although no longer significantly. In Group B, the diminution of the trabecular bone volume, in relation to tissue volume (BV/TV) and the increase in the degree of trabecular interconnection (TBPf) indicated osteoporosis, and focal osteoporosis of the metaphyseal spongy bone was seen on microscopy. CONCLUSION: Experimentally induced prolonged Mg deficiency causes osteoporosis in rats.

Absorptiometry, Photon↗
PubMed1994

Effect of dietary magnesium deficiency with/without cholesterol supplementation on phospholipid content in liver, plasma and erythrocytes of rabbits.

The effect of magnesium deficiency with/without supplementary cholesterol on phospholipid content in liver, plasma and erythrocytes was investigated in New Zealand White male rabbits. After the rabbits had been fed a low magnesium and/or high cholesterol diet for seven weeks, the phospholipid content in liver, plasma and erythrocytes was measured. Dietary magnesium deficiency produced a marked elevation of total phospholipid and certain individual phospholipids in the rabbit liver. The elevation was accentuated by cholesterol supplementation. In the plasma, a low magnesium intake enhanced plasma phosphatidylcholine, phosphatidic acid, phosphatidylinositol, and sphingomyelin, but an activated conversion from phosphatidylethanolamine to phosphatidylcholine made the increase in phospholipid insignificant. On the other hand, a low magnesium intake restricted the increase in magnitude of phospholipid caused by cholesterol supplementation. In the erythrocytes, total phospholipid, phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine were decreased by a low magnesium and/or a high cholesterol intake. We suggest that the increased contents of total phospholipid and/or certain individual phospholipids in the livers and plasma resulted from the enhanced synthesis of phospholipid in the liver by low magnesium intake. A decreased utilization of food by low magnesium diet limited the magnitude of plasma phospholipid increase produced by cholesterol supplementation.

Animals↗
PubMed1969

Values for tissue magnesium as a guide in detecting magnesium deficiency.

A large-scale survey of the normal magnesium content of various human tissues was carried out to facilitate clinical detection of magnesium deficiency, especially occult deficiency.A review of the literature favours the magnesium content of skeletal muscle as the most reliable index of the body's store of magnesium. There is a significant difference (P < 0.001) in both the serum and erythrocyte magnesium levels between normal pregnant women in the third trimester and the average normal population. The reason for this difference is discussed.

Adult↗
PubMed1991

Captopril protects against myocardial injury induced by magnesium deficiency.

We have previously reported that antioxidant drug intervention protects against magnesium deficiency-induced myocardial lesions. In the present study, Golden Syrian male hamsters were fed either a magnesium-deficient diet or a magnesium-supplemented diet. Animals from each group received sulfhydryl-containing angiotensin converting enzyme inhibitors: captopril, epi-captopril (a stereoisomer of captopril), and zofenopril* (arginine blend of zofenopril containing a free SH group); another group of animals received the non-sulfhydryl-containing angiotensin converting enzyme inhibitor enalaprilat. The animals were killed after 14 days, and their hearts were isolated for morphological and morphometric analyses. Hematoxylin and eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Captopril reduced both the density of lesions, from 0.32 to 0.08 lesions/(mm2) (p less than 0.01), and the area fraction of lesions, from 7.42 x 10(-4) to 2.03 x 10(-4) lesion area/(mm2) (p less than 0.01), as well as the degree of inflammatory infiltration around the blood vessels. Epi-captopril and zofenopril* were virtually equipotent to captopril, but enalaprilat afforded only slight (nonsignificant) protection. These results indicate that a significant component of the protective effect of captopril in this model was attributable to its sulfhydryl moiety, rather than solely due to the inhibition of the angiotensin converting enzyme. These data further support our previous findings of possible free radical participation in cardiomyopathy due to magnesium deficiency.

Analysis of Variance↗
PubMed1990

Magnesium deficiency and blood 2,3-diphosphoglycerate concentrations in sedentary and exercised male Osborne-Mendel rats.

Magnesium deficiency lowers endurance capacity of untrained rats by an as yet unknown mechanism. We tested the hypothesis that low plasma and blood Mg concentrations would reduce blood 2,3-diphosphoglycerate (2,3-DPG) concentrations, thus diminishing the oxygen delivery system of the Mg-deficient rat. Untrained male Osborne-Mendel rats (95 g) were studied at rest or following exhaustive exercise after three weeks of dietary treatment (400 or 100 micrograms Mg/g diet; deionized or high Mg water [greater than 85 micrograms Mg/ml]). Magnesium deficiency resulted in lowered plasma and red blood cell (RBC) Mg concentrations and reduced endurance capacity compared with controls. Magnesium supplementation normalized these parameters. 2,3-DPG was elevated by 10% in rats acutely exercised compared with sedentary rats; however, 2,3-DPG levels were not affected by dietary Mg intake. Acute exercise tended to increase erythrocyte Mg concentrations in control rats and lower erythrocyte Mg levels in deficient rats. In conclusion, the reduced endurance capacity of Mg-deficient rats is not due to impaired 2,3-DPG production.

2,3-Diphosphoglycerate↗
PubMed2001

Role of spinal NMDA receptors, protein kinase C and nitric oxide synthase in the hyperalgesia induced by magnesium deficiency in rats.

1. Magnesium (Mg)-deficient rats develop a mechanical hyperalgesia which is reversed by a N-Methyl-D-Aspartate (NMDA) receptor antagonist. Given that functioning of this receptor-channel is modulated by Mg, we wondered whether facilitated activation of NMDA receptors in Mg deficiency state may in turn trigger a cascade of specific intracellular events present in persistent pain. Hence, we tested several antagonists of NMDA and non-NMDA receptors as well as compounds interfering with the functioning of intracellular second messengers for effects on hyperalgesia in Mg-deficient rats. 2. Hyperalgesic Mg-deficient rats were administered intrathecally (10 microl) or intraperitoneally with different antagonists. After drug injection, pain sensitivity was evaluated by assessing the vocalization threshold in response to a mechanical stimulus (paw pressure test) over 2 h. 3. Intrathecal administration of MgSO4 (1.6, 3.2, 4.8, 6.6 micromol) as well as NMDA receptor antagonists such as MK-801 (0.6, 6.0, 60 nmol), AP-5 (10.2, 40.6, 162.3 nmol) and DCKA (0.97, 9.7, 97 nmol) dose-dependently reversed the hyperalgesia. Chelerythrine chloride, a protein kinase C (PKC) inhibitor (1, 10.4, 104.2 nmol) and 7-NI, a specific nitric oxide (NO) synthase inhibitor (37.5, 75, 150 micromol x kg(-1), i.p.) induced an anti-hyperalgesic effect in a dose-dependent manner. SR-140333 (0.15, 1.5, 15 nmol) and SR-48968 (0.17, 1.7, 17 nmol), antagonists of neurokinin receptors, produced a significant, but moderate, increase in vocalization threshold. 4. These results demonstrate that Mg-deficiency induces a sensitization of nociceptive pathways in the spinal cord which involves NMDA and non-NMDA receptors. Furthermore, the data is consistent with an active role of PKC, NO and, to a lesser extent substance P in the intracellular mechanisms leading to hyperalgesia.

2-Amino-5-phosphonovalerate↗
PubMed2004

Alterations in growth plate and articular cartilage morphology are associated with reduced SOX9 localization in the magnesium-deficient rat.

Insufficient dietary magnesium (Mg) intake has been associated with low bone mass in humans,and recent basic science studies have indicated that this bone loss may be secondary to increased release of substance P and TNFc Much less is known about the effects of low Mg intake on cartilage. We have evaluated growth plate and articular cartilage in rats following a 6 month dietary Mg restriction. Histomorphometry demonstrated significantly decreased distal femur articular cartilage chondrocyte density and decreased tibial growth plate width in experimental animals compared to controls. Growth plates of Mg-restricted animals showed reduced chondrocyte column formation. Extracellular matrix of both articular cartilage and growth plates in experimental animals contained reduced amounts of proteoglycans. Immunolocalization of Sox9 was decreased in both articular and growth plate cartilage in experimental animals compared to controls, suggesting that reduced Mg intake causes cartilage changes that may be secondary to reduced levels of the SOX9 transcription factor.

Animal Feed↗
PubMed1993

1,25-dihydroxycholecalciferol supplementation prevents hypocalcemia in magnesium-deficient chicks.

To determine the relevance of circulating 1,25-dihydroxycholecalciferol [1,25(OH)2D3] to the pathogenesis of hypocalcemia during magnesium deficiency, growing chicks were pair fed control or Mg-deficient diets with or without 1,25(OH)2D3 supplementation. Within 14 d, chicks fed the Mg-deficient diet without 1,25(OH)2D3 supplementation exhibited hypomagnesemia and hypocalcemia compared to control chicks. 1,25-Dihydroxycholecalciferol supplementation in Mg-deficient chicks elevated plasma 1,25(OH)2D3 twofold and increased plasma calcium to control levels. Supplementation with 1,25(OH)2D3 did not increase plasma Mg concentration in Mg-deficient chicks, indicating that exogenous 1,25(OH)2D3 prevented hypocalcemia in the absence of greater Mg availability. Magnesium-deficient chicks supplemented with 1,25(OH)2D3 had more intestinal calbindin D-28K relative to Mg-deficient nonsupplemented chicks, suggesting that increased absorption of dietary Ca may have contributed to the greater plasma Ca concentration in 1,25(OH)2D3 supplemented Mg-deficient chicks. Although clinical hypomagnesemia has been associated with vitamin D resistance, our data indicate that primary Mg deficiency did not impair target tissue responsiveness to 1,25(OH)2D3, at least at the level of the intestine. Supplementation with 1,25(OH)2D3 did not increase bone Mg concentration and did not alter the characteristic skeletal morphology. It also did not increase bone Ca concentration in Mg-deficient chicks. The data suggest that skeletal alterations during Mg deficiency result from hypomagnesemia per se, rather than hypocalcemia or insufficient 1,25(OH)2D3.

Animals↗
PubMed2001

[Reasons for magnesium deficiency in children with coeliac disease].

UNLABELLED: Magnesium (Mg) deficiency is often noted in patients with coeliac disease (CD). The aim of the study was the analysis of the reasons of this deficiency in children with CD, diagnosed according to ESPGAN criteria. MATERIAL: The study was performed on 41 patients aged 6-18 years adhering to strict gluten-free diet GFD(+) for mean 11 years, with normal small intestine mucosa, and IgAEmA(-), and on 32 patients aged 5-17 years on gluten containing diet, with classical CD, silent CD or after gluten challenge--GFD(-). In this group the villous atrophy of the small intestine and IgAEmA(+) were observed. In 18 of these patients Mg deficiency was found using Mg-loading test (30 mmol/1.73 m2). METHODS: The following parameters were analysed: type of the disease, observance of gluten-free diet, sex, and living place. Mg, Ca, Na, protein, fat, and dietary fiber intake was assessed using food frequency questionnaire method, and steatorrhea using faecal fat excretion (g/24 h). RESULTS: The frequency of Mg deficiency was similar in both sexes, occasionally in children from small towns (4.5%), and more often in children from big cities (31.5%), and village (34.4%). Dietary Mg intake below RDA was observed in 23% of children from GFD(+) group, in 19% from GFD(-) one, and in 17.6% in children with Mg deficiency. Insufficient Mg intake was found in 18.2% of children from small towns, in 17.6% from big cities, and in 12.5% from villages; Ca in 36.6%, 58.8%, and 59.3%, and protein in 18.2%, 35.3%, and in 34.4% respectively. In all groups of children high intake of fat and Na was observed. Dietary fiber intake was within the recommended values. All children with classical CD had increased fat excretion (mean 25.9 g/24 h), in other patients it was within normal values [GFD(+) mean 1.95 g/24 h, in GFD(-) without diarrhoea 1.7 g/24 h. CONCLUSIONS: Magnesium deficiency in children with CD depends on the form of the disease, adhering to GFD, diarrhoea with steatorrhea, and/or low Mg intake with the diet.

Adolescent↗
PubMed1993

Is magnesium content in erythrocytes suitable for evaluating cation retention after oral physiological supplementation in marginally magnesium-deficient subjects?

In this study, the effects of oral magnesium supplementation were evaluated on plasma, erythrocyte, and urinary cation levels. The study was carried out with an open, cross-over and randomized design. Healthy subjects received two sachets per day of magnesium (366 mg Mg2+/d) for two 28 d cycles, separated by a 3-week washout interval. Magnesium concentrations were measured before the supplementation and at weekly intervals during the treatment. Urinary excretion of Mg was significantly increased during supplementation, with no differences among the weeks examined. Only small increases in plasma magnesium occurred, and values returned to the prestudy levels before the end of supplementation. The increase in erythrocyte magnesium, however, was statistically significant; this trend suggests the existence of a saturable mechanisms, which prevents any possible magnesium overload during oral supplementation. We conclude that erythrocytes might be considered a suitable index for evaluating the bioavailability of magnesium salts in marginally magnesium-deficient subjects.

Administration, Oral↗