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PubMed1988

Adaptation to low dietary calcium in magnesium-deficient rats.

To determine if adaptation to low calcium (Ca) diets is impaired by magnesium (Mg) deficiency, weanling rats were pair-fed control (700 mg Mg/kg diet) or low Mg (70 mg Mg/kg diet) diets containing 5000 mg Ca/g diet for 7 or 10 d. Half of the animals from each group were then killed; the remainder continued on their previous Mg intakes and were subjected to low (500 mg Ca/kg diet) dietary Ca for 7 or 15 d. After 10 d of Mg deficiency, rats fed adequate Ca were hypomagnesemic and hypercalcemic, relative to controls, and had elevated circulating parathyroid hormone (PTH) but normal 1,25-dihydroxycholecalciferol (1,25-DHCC). After 7 d of low dietary Ca, there were no significant differences in plasma Ca, 1,25-DHCC or PTH between control and Mg-deficient rats despite a 50% reduction in plasma Mg in the latter group. After 15 d of low Ca stress, control rats remained normocalcemic, but Mg-deficient rats developed relative hypocalcemia despite similar, high circulating levels of PTH. Plasma 1,25-DHCC in the hypocalcemic, Mg-deficient rats was significantly lower than that of control rats also exposed to low dietary Ca, suggesting an impairment in 1,25-DHCC production during chronic Mg depletion. Significantly elevated renal Ca content was present in the Mg-deficient rats, which was unrelated to dietary Ca and preceded the development of hypocalcemia. The results indicate that both the duration of Mg deficiency and the Ca content of the experimental diet are important determinants of an animal's ability to maintain Ca homeostasis during Mg depletion.

Adaptation, Physiological↗
PubMed1997

Effect of magnesium deficiency on vitamin B2 and B6 status in the rat.

OBJECTIVE: The present study was undertaken to investigate the effect of dietary magnesium (Mg) deficiency on vitamin B2 (riboflavin) and B6 (pyridoxine) status in rats. METHODS: We fed Wistar rats an Mg-deficient diet (56 mg magnesium per kg food) for 70 days. On days 21, 35 and 70 we measured Mg and manganese (Mn) in plasma and whole blood, alkaline phosphatase in plasma, erythrocyte glutathione reductase activity coefficient (AC-EGR) for riboflavin status, and erythrocyte aspartase transaminase activity coefficient (AC-EAST) for vitamin B6 status. RESULTS: Intake of the Mg-deficient diet significantly decreased plasma and whole blood levels of Mg and plasma alkaline phosphatase activity on all sampling days. The Mg deficit had no effect on plasma concentrations of Mn, but significantly increased whole blood levels of this element on days 35 and 70. The Mg-deficient diet had no effect on AC-EGR, and thus appeared not to affect riboflavin status. However, AC-EAST was significantly increased on day 70, implying that the animals were at risk for vitamin B6 deficiency. CONCLUSION: Mg deficiency impairs vitamin B6 status by depleting intracellular Mg and thus inhibits the activity of alkaline phosphatase, a metalloenzyme required for the uptake of pyridoxal phosphate by tissues. Although part of the intraerythrocyte loss of Mg is countervailed by Mn, which can act as a substitute activator of alkaline phosphatase, the degree of compensation is insufficient to fully offset the decrease in activity caused by Mg depletion.

Alkaline Phosphatase↗
PubMed1975

[Neuromuscular and phlebothrombotic clinical aspects of primary magnesium deficiency].

The symptomatology of the neuromuscular hyperexcitability due to magnesium deficit is non-specific. An analysis of its diagnostic criteria and of the etiological and physiopathological problems is made. The description of a phlebothrombosis syndrome due to primary magnesium deficit must lead to an investigation of the part played by this ionic disturbance in various thrombogenic conditions which may induce a leakage of this ion. Practical data related to the problems raised by the administration of oral magnesium therapy.

Anxiety↗
PubMed1986

Magnesium deficiency in IDDM related to level of glycosylated hemoglobin.

Magnesium and potassium were analyzed in plasma, erythrocytes, and urine collected during 24 h and in muscle biopsies from 25 subjects with insulin-dependent, type I diabetes mellitus (IDDM). Magnesium was also measured in mononuclear cells. The results were compared with those of 28 healthy controls, and were also correlated with the degree of diabetic control as estimated by analysis of the level of glycosylated hemoglobin (HbA1c). Subjects with IDDM had significantly lower muscle (P less than 0.01) and plasma (P less than 0.001) concentrations of magnesium compared with those of healthy controls. The HbA1c levels correlated significantly with the concentrations of magnesium in muscle (r = -0.62, P less than 0.001), plasma (r = -0.62, P less than 0.001), and mononuclear cells (r = -0.47, P less than 0.05). The results indicate that some patients with IDDM have lowered contents of magnesium in striated muscular and/or plasma, and that those parameters are dependent on the degree of diabetic control.

Adult↗
PubMed1987

Clinical clues to magnesium deficiency.

Two cases of congestive heart failure with coexistent magnesium and potassium depletion are described. The prolonged QTc intervals and ventricular premature beats of the first patient and the idionodal tachycardia of the second patient disappeared only after magnesium repletion, which normalized both extra- and intracellular potassium and magnesium levels. The third patient had a case of urosepsis while on total parenteral nutrition. He developed diarrhea, hypocalcemia, hypokalemia, hypomagnesemia, weakness, muscular fasciculations and athetoid movements. The neurological manifestations were relieved and the biochemical abnormalities normalized only after magnesium repletion.

Aged↗
PubMedDate not supplied

[Magnesium deficiency in patients with HIV-AIDS].

The serum magnesium concentrations are compared between the three clinical classification categories established in 1993 by the Centers for Disease Control (CDC) (infection) by the human immunodeficiency virus) in adults, and its relation with the CD4 lymphocyte count, albumin, and pre-albumin. The serum magnesium concentration is part of the broad analytical screening and it is determined by atomic absorption spectroscopy. The data obtained were analyzed by the statistical program SPSS. The comparisons of the serum magnesium concentrations between the three clinical categories of the CDC were evaluated by an analysis of variance (ANOVA test). Afterwards, and using a regression analysis, the relations between the different variables were evaluated. 35 patients affected by HIV-AIDS were studied, 22 belonging to category A, 3 to category B, and 10 to category C, 29.4% of the patients studied presented hypomagnesemia, with an average serum magnesium level of 17.6 +/- 10.3 mg/l. There is a quadratic relation between the serum magnesium level and the number of CD4 lymphocytes in HIV-AIDS patients studied. A larger number of cases would allow us to conclude whether hypomagnesemia is a factor belonging to the disease, as well showing the possible differences in the magnesium state between the three diagnostic groups studied. Future studies will be necessary to clarify the role of magnesium in the clinical progression of patients infected by HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effects of a dietary magnesium deficiency and excess vitamin D3 on swine coronary arteries.

The effect of a moderate magnesium (Mg) deficiency on coronary arteries of 61 swine, fed various levels of vitamin D3, was studied by light and electron microscopy. The effect of subnormal Mg intake on vitamin D3-induced intimal lesions of the arteries showed a trend towards increased damage. The degree of cell degeneration and intimal thickening, which was induced by high vitamin D intakes, was as great in swine whose diet was low in Mg and moderately high in vitamin D as it was in those on twice as much vitamin D. Also, the degree of arterial calcification was intensified by inadequate Mg intake at the two higher vitamin D intakes. Present findings indicate that suboptimal dietary Mg, in combination with an excess of vitamin D, has an additive effect in the initiation of ultrastructural changes in the coronary arteries. Extension of the study is indicated to ascertain the extent to which further reduction of Mg intake can potentiate vitamin-D-induced coronary lesions.

Animals↗
PubMed2005

Effects of high calcium intake on bone metabolism in magnesium-deficient rats.

We examined the effects of high calcium (Ca) intake on bone metabolism in magnesium (Mg)-deficient rats. Male Wistar rats were divided into three groups, with each group having a similar mean body weight, and fed a control diet (control group), a Mg-deficient diet (Mg-deficient group) or a Mg-deficient Ca-supplemented diet (Mg-deficient Ca-supplemented group) for 14 d. Femoral Ca content was significantly lower in the Mg-deficient Ca-supplemented group than in the control group and Mg-deficient group. Femoral Mg content was significantly lower in the Mg-deficient group and Mg-deficient Ca-supplemented group than in the control group. Furthermore, femoral Mg content was significantly lower in the Mg-deficient Ca-supplemented group than in the Mg-deficient group. Serum osteocalcin levels (a biochemical marker of bone formation) were significantly lower in the two Mg-deficient groups than in the control group. As a biochemical marker of bone resorption, urinary deoxypyridinoline excretion was significantly higher in the Mg-deficient Ca-supplemented group than in the control group and Mg-deficient group. The results in the present study suggest that high Ca intake had no preventive effect on alteration of bone metabolism in Mg-deficient rats.

Absorption↗
PubMed1990

A synergism of antigen challenge and severe magnesium deficiency on blood and urinary histamine levels in rats.

The effects of severe and moderate magnesium (Mg) deficiency on blood and urinary histamine were studied in 36 male weanling Sprague-Dawley rats with or without IgE-stimulating antigen challenge. The rats were divided into six groups: two each on 50 (severely deficient), 300 (moderately deficient), and 2000 (control) ppm Mg diets without and with immunization with ovalbumin challenge on days 0, 14, and 29. Unimmunized severely Mg-deficient rats had significantly elevated urinary histamine which returned to normal by 22 days, but whole blood histamine was still significantly elevated at 36 days. Both blood and urinary histamine of immunized severely Mg-deficient rats were significantly higher than those of all the other groups throughout the study, particularly after the antigen challenge. There was a synergism of antigen challenge and severe Mg deficiency on blood and urinary histamine levels. The results suggest that severe Mg deficiency can aggravate diseases which are caused by abnormal histamine release after exposure to an IgE-stimulating antigen.

Animals↗
PubMed2004

Magnesium deficiency alters the threshold for epinephrine-induced arrhythmias during halothane or sevoflurane anesthesia in the rat.

OBJECTIVE: To determine the effect of chronic magnesium (Mg2+) deficiency on the relative arrhythmogenicity of halothane and sevoflurane in the rat. DESIGN: Prospective, randomized, nonblinded study. SETTING: University laboratory. PARTICIPANTS: Male Sprague-Dawley rats (n = 48). INTERVENTIONS: Rats were maintained on a Mg2+-deficient or control diet for 14 days, at which time they were anesthetized with halothane or sevoflurane, a tracheostomy was performed, and the lungs were ventilated to maintain normocapnia. Catheters were inserted into a femoral vein and carotid artery. Lead II of the electrocardiogram was monitored to determine the threshold for epinephrine-induced arrhythmias. MEASUREMENTS AND MAIN RESULTS: Chronic Mg2+ deficiency significantly decreased the dose of epinephrine required for arrhythmias (ADE). The reduction in the ADE was approximately one third during halothane anesthesia (p < 0.05) and one fifth during sevoflurane anesthesia (p < 0.001). Infusion of magnesium sulphate completely reversed the reduction in ADE. In normomagnesemic rats, the halothane ADE was significantly less than the sevoflurane ADE (mean difference = 6.0 microg/kg, 95% confidence interval of the difference = 3.6 to 8.4 microg/kg) (p < 0.005). Mg2+ deficiency significantly attenuated the difference between the halothane ADE and the sevoflurane ADE (mean difference in the Mg2+-deficient group = 0.6 microg/kg, 95% confidence interval of the difference = -0.2 to 1.5 microg/kg). CONCLUSION: Chronic Mg2+ deficiency decreased the threshold for epinephrine-induced arrhythmias and attenuated differences between the arrhythmogenic potential of halothane and sevoflurane, suggesting that arrhythmias are as likely to develop with sevoflurane as with halothane in the presence of coexisting magnesium deficiency and elevated catecholamines.

Anesthesia, Inhalation↗
PubMed1999

Integrins mediate the effects of quinolones and magnesium deficiency on cultured rat chondrocytes.

Chondrocyte-matrix interaction is mediated by a series of adhesion molecules. Both alpha and beta integrin subunits are involved and govern crucial functions of cell adhesion and signal transduction. These molecules modulate proliferation and differentiation, thus establishing cartilage integrity. We studied the influence of magnesium deficiency and quinolone antibiotics (which form chelate complexes with divalent cations) on chondrocytes in vitro in order to assess the role of Mg2+ ions in integrin function and to establish cellular changes mediated via integrin signal transduction. Mg2(+)-free medium and quinolone supplementation was found to decrease chondrocyte attachment to collagen type II-coated coverslips. Adhesion and growth of chondrocytes were reduced in the respective medium. Organisation of cytoskeletal fibers (vimentin) was changed and formation of stress fibers (f-actin) was disturbed. Additionally, rates of cell proliferation declined. These results indicate that quinolone-magnesium complex formation is important for chondrotoxicity of these substances. Cell-matrix detachment and morphological alterations described in vitro may explain the lesions observed in articular cartilage after quinolone administration in vivo. The attachment assay described could serve as a simple test to establish the susceptibility of chondrocytes of different species to different quinolones in use or new ones to be introduced.

Animals↗
PubMed1988

Histamine metabolism and pinnal hyperaemia during magnesium deficiency in rats.

The relation between histamine metabolism and an appearance of pinnal hyperaemia during magnesium (Mg) deficiency, and the effects of some factors on these were studied in 3-week-old Wistar rats. On a Mg-deficient diet (Mg 0.001%), the histamine concentrations in plasma and urine increased after 4-5 d, and reached a maximum after 6-12 d. Pinnal hyperaemia appeared during the same time course. The hyperaemia was reduced by the administration of antihistamines (cimetidine and diphenhydramine). These results indicate that pinnal hyperaemia during Mg deficiency is mediated by histamine. The administration of oestradiol benzoate (0.08 mg/100g body weight subcutaneously once a day for 8 d) and/or gamma-ray irradiation (600 rad/d before experiments) reduced the appearance of pinnal hyperaemia and the increment in the urinary histamine during Mg deficiency. The histamine content increased in the spleen and some tissues after 8 d, but not in the skin, with increasing the activity of histamine synthesis. The treatments mentioned above depressed the increment of histamine content. These results suggest that the pinnal hyperaemia and the increment of the urinary histamine in the Mg-deficient rat are related to the increment of both the histamine synthesis and release.

Amine Oxidase (Copper-Containing)↗
PubMed1995

Changes in tissue calcium and phosphorus content and plasma concentrations of parathyroid hormone and calcitonin after long-term magnesium deficiency in rats.

OBJECTIVE: The present study was undertaken to investigate the effect of dietary magnesium (Mg) deficiency on plasma levels of parathyroid hormone (PTH) and calcitonin (CT), and the changes in tissue calcium (Ca) and phosphorus (P) content. METHODS: Wistar rats were fed an Mg-deficient diet. Plasma levels of PTH and CT, and Ca and P content in plasma, whole blood, skeletal muscle, heart, kidney, femoral bone and brain, were determined after 7, 35, 42, 49, 56, 63 and 70 days. RESULTS: Mg deficiency significantly increased plasma levels of ionic Ca after 1 week of deficiency, and significantly increased total Ca in plasma and whole blood after 5 weeks. Whole blood and plasma levels of P decreased significantly after 8 and 5 weeks, respectively, in comparison with values obtained in pair-fed control rats. Plasma levels of CT were not modified by hypercalcemia and hypomagnesemia. Plasma PTH decreased significantly during the first 3 weeks, then recovered gradually, reaching control values in week 7 and remaining stable thereafter, despite elevated levels of ionic Ca. The Mg-deficient diet led to calcification in skeletal muscle, heart, kidney and femur, detectable as early as week 5. However, P content increased only in kidney after 1 week, decreased in heart and femur after 5 weeks, and did not change in muscle. The Mg-deficient diet did not significantly modify Ca or P content in brain. CONCLUSION: Mg deficiency led to tissue calcification and decreased P levels in blood, heart, and femur. These changes did not affect CT secretion. PTH appeared to be more closely related with hypomagnesemia than with hypercalcemia.

Animals↗