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PubMed1995

Magnesium deficiency induces joint cartilage lesions in juvenile rats which are identical to quinolone-induced arthropathy.

Quinolones accumulate in cartilage, and because they form chelate complexes with divalent cations, they possess the potential to induce a deficiency of functionally available magnesium. To test the hypothesis that quinolone-induced arthropathy is caused (or aggravated) by magnesium deficiency in cartilage, we induced magnesium deficiency by feeding juvenile rats a magnesium-deficient diet for 9 days and treated the rats with single oral doses of ofloxacin (0, 100, 300, 600, or 1,200 mg/kg of body weight) during this period. Additional groups of juvenile rats on a normal diet were treated with ofloxacin correspondingly. Typical cartilage lesions (e.g., swollen matrix, cleft formation) were found in knee joints of all magnesium-deficient rats, including those without ofloxacin treatment. Lesions in these groups were not distinguishable from lesions induced by a single dose of 600 mg of ofloxacin per kg of body weight or higher in rats on a normal diet. Ofloxacin levels in plasma after 600 mg/kg of body weight were approximately 10-fold higher than those in humans during therapy with this quinolone. Lesions in rats treated with ofloxacin plus magnesium deficiency were more pronounced than those in rats with normal magnesium concentrations. After intake of a magnesium-deficient diet for 9 days, the magnesium concentration in serum (mean +/- standard deviation) was 0.18 +/- 0.05 mmol/liter (control on normal diet, 0.82 +/- 0.10 mmol/liter). Magnesium concentrations in bone (femur) and cartilage (processus xiphoideus) samples were 64.7 +/- 10.5 and 14.3 +/- 3.9 mmol/kg of dry weight, respectively, which corresponded to approximately 50% of the concentrations measured in controls on a normal diet. It was concluded that quinolone-induced arthropathy is probably caused by a deficit of available magnesium in joint cartilage due to the formation of quinolone-magnesium chelate complexes. If juvenile patients must be treated with quinolones for serious infections, it seems prudent to ensure that these patients do not have a disturbed magnesium balance.

Animals↗
PubMedDate not supplied

Comparative evaluation of ultrastructural changes in articular cartilage of ofloxacin-treated and magnesium-deficient immature rats.

Ultrastructural changes in immature articular cartilage were studied after treatment of 5-wk-old rats with ofloxacin-a fluoroquinolone-and in magnesium deficiency. Magnesium deficiency was induced by feeding a magnesium-deficient diet for 9 days; the condition was confirmed by measuring the concentrations of the mineral in plasma, bone, and cartilage samples of the animals by atomic absorption spectrophotometry. Oral administration of single doses of 600 or 1,200 mg ofloxacin/kg body weight and magnesium deficiency were sufficient to induce gross structural cartilage defects. Alterations observed on the ultrastructural level showed striking similarities in magnesium-deficient rats and in rats treated with single doses of 600 mg ofloxacin/kg body weight. Typical observations were (a) bundle-shaped, electron-dense aggregates on the surface and in the cytoplasm of chondrocytes, (b) detachment of the cell membrane from the matrix and necrotic chondrocytes, (c) reduction of the extracellular matrix, and (d) swelling of cell organelles such as mitochondria. These findings further substantiate the histological finding that quinolone treatment and a dietarily induced magnesium-deficiency induce indistinguishable pathological conditions in immature joint cartilage, and they suggest that quinolone-induced arthropathy is probably caused by a reduction of functionally available magnesium (ionized Mg2+) in cartilage (42). Furthermore, they provide a basis for aimed studies with human cartilage samples from quinolone-treated patients that might be available postmortally or after hip replacement surgery.

Aging↗
PubMed1985

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

Calcifediol↗
PubMed1988

Intracellular magnesium deficiency and effect of oral magnesium on blood pressure and red cell sodium transport in diuretic-treated hypertensive patients.

The effects of magnesium supplementation were tested in 20 patients with essential hypertension receiving long-term thiazide diuretic treatment (Th group) and 21 age-matched untreated patients (EHT group). Intra-erythrocyte cations, water content and the ouabain-sensitive sodium efflux rate constant were measured. The Th group received magnesium supplementations as MgO (600 mg Mg/day) for 4 weeks. In the Th group intra-erythrocyte magnesium and the sodium efflux rate constant were lower and red cell sodium was higher than in the EHT group. During magnesium supplementation, there were significant decreases (p less than 0.01) in intra-erythrocyte sodium content and mean blood pressure, and increases (p less than 0.005) in red cell magnesium content and the sodium efflux rate constant. These effects of magnesium were more evident in 9 patients who were unresponsive to diuretic therapy, a definite reduction in mean blood pressure, from 104.8 +/- 2.7 mmHg to 94.4 +/- 2.2 mmHg (p less than 0.001), being observed. In the remaining 11 patients, however, blood pressure remained unchanged. The sodium efflux rate constant was positively correlated with red cell magnesium content and negatively correlated with sodium content (r = 0.61, p less than 0.005 and r = -0.57, p less than 0.01, respectively). These results indicate that long-term diuretic treatment may give rise to intracellular magnesium deficiency and a suppression of cell membrane active sodium transport. The results also suggest that oral magnesium may decrease intracellular sodium, possibly through the activation of Na-K-ATPase, which in turn may contribute to the reduction in blood pressure. Therefore, magnesium supplementation may be a worthwhile additional therapy for diuretics.

Administration, Oral↗
PubMed1975

The skin in magnesium-deficient rats.

The cutaneous vasodilatation occuring in the early stages of dietary deficiency of magnesium has been investigated in rats. While the time of onset of erythema varies in proportion to the weight of the animal, the duration is not related to weight. In severe states of vasodilatation, the skin is thickened and infiltrated with mononuclear cells, apparently derived from the blood. Intact sympathetic and sensory innervation are not necessary for the development of vasodilatation in the skin. Neither can the genesis of the erythema be attributed to degranulation of mast cells. From consideration of this and other investigations, it is concluded that the cutaneous abnormalities of magnesium-deficient rats cannot be due directly to hypomagnesaemia.

Animals↗
PubMedDate not supplied

Oral versus intravenous magnesium supplementation in patients with magnesium deficiency.

The efficacy of oral magnesium supplementation in correcting magnesium deficiency was examined in a group of 40 elderly patients with suspected magnesium deficiency. The patients were randomized in a double-blind, placebo-controlled fashion to oral magnesium-lactate-citrate for 6 weeks. Magnesium status was assessed by an intravenous magnesium-loading test at baseline and after treatment. For comparison, another group of 23 patients received 30 mmol magnesium sulfate intravenously daily for 7 days. A group of 30 patients without known predisposition to magnesium deficiency and a group of 27 young healthy subjects served as controls. The initial magnesium-loading test in the placebo group reduced magnesium retention from a mean 41% (95% confidence intervals 34-49) to 22% (15-29) (p less than 0.01). In the group receiving oral magnesium supplementation for 6 weeks, magnesium retention decreased from 39% (31-47) to 10% (2-18) (p less than 0.01), which was significantly better than with placebo treatment (p less than 0.01). The magnesium retention after oral magnesium supplementation was comparable to that observed after parenteral administration of magnesium for 7 days, 6% (-4 to 16), and to that in the reference groups of patients 4% (-2 to 10) and healthy control subjects 3% (-2 to 8). The study suggests that the bioavailability of orally given magnesium-lactate-citrate is satisfactory, and that oral administration of magnesium for 6 weeks may restore magnesium depots in patients with magnesium deficiency.

Administration, Oral↗
PubMed1985

Elevated circulating immunoreactive calcitonin in the magnesium-deficient normocalcemic rat.

Previous studies indicate that magnesium, like calcium, stimulates the release of calcitonin (CT) from the thyroid gland. On the other hand, C-cell hyperplasia has been noted in magnesium-deficient dogs and rats. To explore further possible interrelationships between magnesium and CT, 21-day-old Sprague-Dawley male rats fed a control diet (0.043% Mg and 0.47 Ca) were match-fed with rats given either a control low calcium diet (0.043% Mg and 0.15% Ca) or a low magnesium-low calcium diet (0.001% Mg and 0.15% Ca). The low calcium content in the magnesium-deficient diet prevented the development of hypercalcemia characteristic of the magnesium-deficient rat. After 17 days, animals were killed by decapitation. Blood was obtained from some animals in the basal state and in other animals 1 min postpentagastrin or 1 min postmagnesium chloride infusion. No significant difference was found in the serum calcium level in the three groups, while the mean serum immunoreactive CT (iCT) level was significantly higher in magnesium-deficient rats both before and after pentagastrin. An acute iv infusion of MgCl2 resulted in significant increases in serum iCT in both the control and magnesium-deficient animals. The results of this study demonstrate that basal serum iCT levels and their response to pentagastrin are increased in magnesium-deficient, normocalcemic animals. The further increase in serum iCT after magnesium infusion in magnesium-depleted animals appears paradoxical and indicates that the relationship between extracellular magnesium and iCT release is not a simple feedback mechanism. It is possible that the increase in circulating iCT may be a response to extracellular-intracellular differences in magnesium concentration. Alternatively, the increased C-cell activity may be secondary to some unknown metabolic alteration induced by magnesium deficiency, rather than to magnesium deficiency per se.

Animals↗
PubMed1986

Magnesium deficiency in alcoholism.

Significant magnesium deficiency occurs in chronic alcoholism. The evidence depends on a number of related lines of evidence: hypomagnesemia, a number of clinical symptoms in common with patients with nonalcoholic causes of magnesium deficiency, induction of magnesium excretion by alcohol ingestion (167-260% of control values), positive magnesium balance on alcohol withdrawal (average 1.15 meq/kg), decreased exchangeable magnesium (28Mg, mean deficit 1.12 meq/kg), a mean deficit of 11.4 meq/kg of fat-free dry weight of muscle of alcoholic patients, and hypocalcemia responsive only to magnesium therapy. When alcohol is withdrawn, free fatty acids rise sharply and plasma magnesium falls. Respiratory alkalosis occurs abruptly also on alcohol withdrawal. The alkalosis and rise of free fatty acids with concomitant fall of magnesium produces an acute instability of the internal milieu and could result in acute symptoms. There also are a number of nutritional deficiencies which need to be cared for, but magnesium, thiamine, and other B vitamins need to be administered immediately. Potassium and phosphorus should be supplied when they are low.

Alcoholism↗
PubMed1996

[Diagnosis of magnesium deficiency in intensive care patients].

AIM: Magnesium deficiency was investigated in critically ill patients, comparing measurements of plasma concentrations with the results obtained by the magnesium tolerance test. DESIGN AND METHODS: 20 critically ill patients (5 females, 15 males) between the ages of 27 and 86 were investigated. Magnesium plasma concentrations were determined before the magnesium tolerance test according to Ryzen was performed. For this purpose, magnesium sulfate (0.1 mmol/kg) was infused intravenously over four hours. Renal magnesium excretion was measured in the 24 h urine beginning at the start of the infusion. Magnesium concentrations in plasma and urine were determined using atomic absorption spectrophotometry. MAIN RESULTS: In 12 patients magnesium plasma concentrations were decreased to 0.58-0.79 mmol/l. 6 patients showed values within the normal range of 0.80 to 1.0 mmol/l. In 2 patients the plasma concentration was increased to 1.07 and 1.27 mmol/l. Parenteral magnesium tolerance testing revealed a considerable magnesium deficiency by retention of 65-100% of the loading dose in 14 of the 20 patients. The remaining 6 patients retained 23-48% of the loading dose, thus demonstrating a moderate magnesium deficiency. CONCLUSION: Determination of magnesium plasma concentration appears suitable as an informative preliminary survey, since low values are reliable indicating a magnesium deficiency. However, this study confirms that normal magnesium plasma concentrations do not exclude a considerable magnesium deficiency, which is more sensitively determined by the magnesium tolerance test.

Adult↗
PubMed1990

Relation of cardiovascular disease to potassium and magnesium deficiencies.

Potassium and magnesium deficiencies, particularly those induced by conventional loop and thiazide diuretic therapy, have been linked in clinical studies to an increased frequency in serious arrhythmias and mortality in acute myocardial infarction. Magnesium repletion has been shown not only to increase magnesium levels, but also to increase muscle potassium and to decrease the frequency of ventricular ectopic beats. Potassium replenishment alone may have a detrimental effect in magnesium-depleted patients. The potassium-sparing diuretic spironolactone (Aldactone) has been shown to spare both potassium and magnesium, and may therefore be a more appropriate diuretic therapy in patients at cardiovascular risk.

Heart Failure↗
PubMed2002

Assessment of the relationship between hyperalgesia and peripheral inflammation in magnesium-deficient rats.

Magnesium-deficient rats develop simultaneously a significant lowering of nociceptive threshold and a generalized inflammation. We investigated the relationship between these two phenomena by testing drugs that are able to suppress the inflammation in this model. In weaning rats fed a magnesium-depleted diet for ten days, the nociceptive threshold was assessed by the paw pressure test and the inflammation by a clinical score. A non-steroidal anti-inflammatory drug (piroxicam); antagonists of H1 and H2 receptors (astemizole and cimetidine. respectively); a glucocorticoid (dexamethasone); an inhibitor of mastocyte degranulation (cromoglycate); and estradiol benzoate were used to block the inflammatory response. Dexamethasone and estradiol significantly suppressed the inflammation (p < 0.001 vs control group). Cromoglycate showed a delayed anti-inflammatory effect (p < 0.01 vs control group on D10). The combination of astemizole and cimetidine partially blocked the inflammation process, whereas astemizole and piroxicam were without effect. Regardless of the effect of the test drugs on inflammation, no change in the time course of hyperalgesia was observed. These data support the view that hyperalgesia induced by the magnesium-depleted diet is not a consequence of the inflammatory process.

Animals↗
PubMed1995

The bioavailability of magnesium in spinach and the effect of oxalic acid on magnesium utilization examined in diets of magnesium-deficient rats.

Spinach was evaluated for its bioavailability of magnesium in the experiment with magnesium-deficient rats. The effect of oxalic acid on absorption of dietary magnesium was also examined in the same experiment. After there were significant differences in the body weight of the rats between the control group and the magnesium-deficient group, and after the number of dead rats increased, the magnesium-deficient rats were divided into six groups. They were pair-fed for 8 days on the magnesium-deficient diet, magnesium-deficient diet supplemented with raw powdered spinach (R-sp), boiled powdered spinach (B-sp), or fried powdered spinach (F-sp), control diet supplemented with oxalic acid (Ox-C), and control diet (+Mg). On the 10th day, there was no significant difference in the food intake of the rats between the control group and magnesium-deficient group. However, the body weight, and body weight gain of the rats increased more significantly in the control group than in those of the magnesium-deficient group. Also, the contents of calcium and phosphorus in the liver and kidneys, and serum calcium content increased significantly in the magnesium-deficient rats compared with those of the control rats. However, the serum magnesium content decreased significantly in the magnesium-deficient rats. An especially large amount of calcium was accumulated in the kidneys of the magnesium-deficient rats. At the end of the experimental period, there were no significant differences in the food intake, body weight and body weight gain of the rats among the control group and each of the spinach-added groups. The body weight and body weight gain of the Ox-C rats decreased significantly in comparison with those of the control group and each of the spinach-added groups. Although, there were no significant differences in the concentrations of serum minerals (Mg, Ca and P) among each of the groups, kidney magnesium, calcium and phosphorus, and liver magnesium and phosphorus were significantly higher in each of the spinach added groups than those of the control, Ox-C and +Mg groups. A large amount of calcium was accumulated in the kidneys of the rats fed on the R-sp, B-sp, F-sp and Ox-C diets. However, the kidney calcium of each of the spinach-added groups markedly decreased in comparison with kidney calcium of the magnesium-deficient rats on the 10th day, when the magnesium-deficient rats were separated. There was no significant difference in the magnesium content of the left tibiae among each of the spinach-added groups. Also, the magnesium contents of the left tibiae of each of the additional groups did not reach the level of those of the control rats. The contents of calcium and phosphorus of the left tibiae were not significantly different among any of the groups except for both the R-sp and Ox-C groups, and decreased significantly in the R-sp and Ox-C groups compared with those of the other groups. A highly positive correlation between bone calcium and bone strength was not observed in this study; the breaking force of the left femurs of the B-sp and F-sp rats increased significantly in comparison with that of the Ox-C group. The rate of magnesium absorbed by the rats receiving the control, R-sp, B-sp, F-sp, Ox-C, and +Mg diets was 88.9, 80.2, 88.4, 90.4, 88.1, and 87.7%, respectively. The rate of apparent absorption of calcium from the control, Mg-deficient, R-sp, B-sp, F-sp, Ox-C and +Mg diet was 87.0, 84.1, 57.3, 66.4, 66.2, 53.3 and 83.5%, respectively. The data indicate that oxalic acid remained in spinach after cooking of boil or frizzle was not deleterious to magnesium availability, and that spinach is one of the most promising sources of magnesium.

Animals↗
PubMed1998

Early morphological and immunological alterations in the spleen during magnesium deficiency in the rat.

Dietary magnesium deficiency in rodents, and especially in rats, causes inflammation and leads to alterations in the immune response. One of the characteristics of magnesium deficiency in the rat is a marked enlargement of the spleen. Considering the importance of the spleen for the immune response, in this study we have evaluated histological, cytological and immunological changes in this organ of rats in early stages of this deficiency. For this purpose, male weaning Wistar rats were pair-fed with either control or magnesium-deficient diet, for 2, 4 or 8 days. Results indicate that after 8 days on the deficient diet rats presented clinical signs of inflammation, splenomegalia and leukocytosis. As shown by histometrical analysis, both the red and white spleen pulps of deficient rats displayed an increased incidence of polymorphonuclear leukocytes and macrophages in all studied stages of deficiency. Concomitantly, the relative number of lymphocytes decreased. This observation was confirmed by the analysis of the cell suspension obtained from the spleen. The greater number of adherent cells in the cell suspension from deficient rats provides an additional confirmation of the increased number of macrophages in the spleen of these rats. Analysis of lymphocyte populations demonstrated a reduced proportion of CD5+ and CD8+ cells after 8 days of deficiency. The reduction in the number of CD8+ cells in deficient rats could be related to the observed decrease in IFN-gamma concentration in the spleen homogenate. In short, this study shows that magnesium deficiency causes early cytological and immunological modifications in the spleen which appeared before macroscopical changes in this organ and before clinical symptoms of inflammation. These changes could be related to the altered immune response of deficient animals.

Animals↗
PubMed1975

Ultrastructural changes of the hypothalamo-hypophysial neurosecretory system in the magnesium deficient rats.

A magnesium deficient diet caused transient but marked degenerative changes in the rat hypothalamo-hypophysial neurosecretory system which strongly resembled in many ultrastructural respects those induced by a prolonged administration of aldosterone as previously reported by us. The possible mechanism for this selective alteration in the neurosecretory neurons has been briefly discussed with regard to aldosterone secretion.

Acid Phosphatase↗
PubMed1976

Teratogenic effects of magnesium deficiency in rats.

The effect of severe magnesium deficiency on plasma magnesium levels in pregnant and nonpregnant rats and on reproduction was investigated. Magnesium deficiency produced a rapid fall in plasma magnesium concentration, in both pregnant and nonpregnant rats. At term, all implantation sites of pregnant rats fed a diet severely deficient in magnesium showed total fetal resorption. When pregnant females were fed the magnesium deficient diet only between days 6 and 14 of gestation, there was a high incidence of resorptions and gross malformations were seen in full term fetuses. The results demonstrate the rapidity of the effects of severe magnesium deficiency in pregnant rats and indicate the importance of the element for embryonic development.

Animals↗
PubMed1993

Protein oxidation in magnesium deficient rat brains and kidneys.

Magnesium deficiency produces a pro-oxidant systemic inflammation in rats. The purpose of these experiments was to determine if and when there is any oxidation of cellular proteins. We have found there is a significant increase in protein oxidation products, protein carbonyls, in both the brain and the kidney within 2 to 3 weeks on a magnesium deficient diet. These changes occur prior to any detectable changes in cellular glutathione, tissue damage or dysfunction. We conclude that oxidation of cellular proteins occur early in magnesium deficiency and may contribute to the tissue damage and loss of function observed in the later stages of the deficiency. This is the first demonstration of the time course of protein oxidation product development in magnesium deficient animals.

Animals↗
PubMed1981

Bone pathology and parathyroid gland activity in hypocalcemic magnesium-deficient chicks.

Growing chicks fed magnesium-deficient (150 ppm Mg) diets for 14 or 21 days developed significant hypomagnesemia and hypocalcemia compared to control chicks fed 1,000 ppm Mg. The hypocalcemia was accompanied by significant parathyroid gland hyperactivity, suggesting that magnesium deficiency did not impair parathyroid gland function. Despite parathyroid gland hyperactivity, however, bone resorption was decreased in the magnesium-deficient chicks, although bone formation was not affected by magnesium depletion. The decrease in bone resorption in the magnesium-deficient chicks was correlated with significant bone magnesium depletion and resulted in increased bone calcium content. These findings suggested that the development of hypocalcemia in magnesium-deficient chicks was related to decreased bone resorption, due to impaired osteocytic function rather than parathyroid gland insufficiency. The results also offer an explanation for the decrease in skeletal responsiveness to PTH which has been reported during magnesium depletion.

Animals↗
PubMed1998

Diminished kidney function and nephrocalcinosis in rats fed a magnesium-deficient diet.

The effect of a magnesium-deficient diet on kidney function was studied in young male rats. The rats were fed a purified diet with a magnesium content of either 20.5 (control diet) or 2.6 mmol/kg (magnesium-deficient diet) for 21 d. In rats fed the magnesium-deficient diet, kidney wet and dry weights were significantly increased, and calcium and phosphorus concentrations in the kidney were significantly higher than in rats fed the control diet. Upon histological examination, an increase in the mesangial matrix of the glomeruli and injury to the brush border of the proximal tubules were observed in rats fed the magnesium-deficient diet. Also, a deposition of calcium was observed in the tubules of the corticomedullary junction and medulla of these rats. Total protein and albumin concentrations in serum were significantly decreased in rats fed the magnesium-deficient diet. Urinary albumin excretion was significantly higher, and N-acetyl-beta-D-glucosaminidase activity in the urine was significantly increased in rats fed the magnesium-deficient diet. These findings indicate diminished glomerular and proximal tubular functions. We suggest that a magnesium-deficient diet not only induces nephrocalcinosis, but it also diminishes kidney function.

Acetylglucosaminidase↗