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PubMed1991

Effect of magnesium-deficient diet on cation transport in pregnant rabbits.

The imbalance of cation transport is considered to play an important role in the development of hypertension, and this also applies to hypertension during pregnancy. Magnesium (Mg) is one of the factors that regulate cation transport across the cell membrane. We therefore studied the effect of a magnesium-deficient diet on the activity of erythrocyte Na/K-ATPase and Mg-ATPase from six pregnant rabbits and compared the results to those obtained from six controls on a normal diet. None of the rabbits on the deficient diet developed hypertension or intrauterine growth retardation; nevertheless the activity of both enzymes was significantly reduced compared to the group on the normal diet. Since the reduced activity of these enzymes can determine sodium or calcium retention in the cell, Mg deficiency could be the basis of the onset of some forms of hypertension in pregnancy.

Animals↗
PubMed1977

Serum and duodenal alkaline phosphatase levels in fed and fasted magnesium deficient rats.

Rats depleted of magnesium for 13 days were killed after 18 to 20 hours of fasting or 2 hours after consumption of a standard-sized meal. Serum and duodenal alkaline phosphatase (AP) were reduced in fasted magnesium depleted rats compared to pair-fed and ad libitum-fed controls. With refeeding, serum alkaline phosphatase levels rose significantly in all groups, but the levels in refed Mg deficient rats remained below serum levels of fasted control rats. Inhibition of AP activity with L-phenylalanine and urea suggested that the differences in AP levels of fasted and fed rats were mainly due to enzymes of intestinal origin. Intestinal AP levels increased after feeding in all groups, but were proportionately greatest in Mg depleted rats. The pattern of serum and duodenal AP in fed and fasted rats and the results of polyacrylamide disc gel electrophoresis (PADGE) in duodenal AP extracts suggest that Mg depletion alters the release of AP into the blood that normally occurs in response to feeding.

Alkaline Phosphatase↗
PubMed2003

Comparison of a short irradiation (50 sec) by different wavelengths on audiogenic seizures in magnesium-deficient mice: evidence for a preventive neuroprotective effect of yellow.

Audiogenic seizures triggered by an acoustic stimulus of determined frequency and amplitude have been described in many laboratory animals in many circumstances including magnesium deficiency. This model, recently validated, was used, in DBA/2 mice, to study the preventive neuroprotective effect of 6 wavelengths of the visible spectrum used in Chromatotherapia* (lambda(max) 440, 484, 528, 572, 616 and 660 nm) at low irradiance. Each short illumination lasted 50 seconds and was followed by 20 minutes of darkness. It appeared that yellow fully protected 16 out of 17 mice from seizure occurrence. Green allowed the survival of 69% of mice but did not protect them from seizure occurrence. On the contrary, the other four colors (orange, red, purple and blue) failed to protect the mice and showed a tendency to accelerate their death. White color was not protective but allowed the difficult survival of 30% of mice. Darkness had no protective effect. These results even though surprising open a great field of investigation.

Acoustic Stimulation↗
PubMed2003

Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors?

African-Americans are known to be disproportionately impacted by many chronic diseases such as diabetes, hypertension, cardiovascular, and renal disease. Lower levels of dietary and serum magnesium have been associated with an increased prevalence of hypertension, insulin resistance, and diabetes. Studies suggest a greater prevalence of occult magnesium deficiency among African-Americans compared to other populations. This increased prevalence of hypomagnesemia may contribute to increased insulin resistance leading to accelerated atherosclerosis and premature death. Trials that correct magnesium status/levels among African-Americans, whether through dietary intervention or direct magnesium replacement/supplementation need to be completed to characterize this relationship more completely.

Adult↗
PubMed1980

Magnesium deficiency produces spasms of coronary arteries: relationship to etiology of sudden death ischemic heart disease.

Isolated coronary arteries from dogs were incubated in Krebs-Ringer bicarbonate isolation and exposed to normal, high, and low concentrations of magnesium in the medium. Sudden withdrawal of magnesium from the medium increased whereas high concentrations of magnesium decreased the basal tension of the arteries. The absence of magnesium in the medium significantly potentiated the contractile responses of both small and large coronary arteries to norepinephrine, acetylcholine, serotonin, angiotensin, and potassium. These data support the hypothesis that magnesium deficiency, associated with sudden death ischemic heart disease, produces coronary arterial spasm.

Acetylcholine↗
PubMed2000

Ultrastructure of Achilles tendons of rats treated with ofloxacin and fed a normal or magnesium-deficient diet.

Fluoroquinolones can cause tendinitis and tendon rupture. However, toxicological as well as clinical information on quinolone-induced tendopathy is scarce. We performed extensive electron microscopic studies with Achilles tendon specimens from ofloxacin-treated rats. The drug was given at a dose of 1,200 mg/kg (body weight) orally. Juvenile Wistar rats received one or three oral doses each of 1,200 mg of ofloxacin/kg (body weight)/day. Three days after treatment, the tenocytes of their Achilles tendons showed degenerative alterations, such as multiple vacuoles and vesicles in the cytoplasm that had developed due to swellings and dilatations of cell organelles. Other indications of cell degradation were the occurrence of cell debris and cell detachment from the extracellular matrix accompanied by a loss of cell-matrix interaction. The tenocytes of juvenile Wistar rats that had been treated at day 36 with a single oral dose of 1,200 mg of ofloxacin/kg (body weight) and sacrificed either 3 or 6 months later exhibited similar degenerative alterations. The number of degenerative alterations of tenocytes after ofloxacin treatment was considerably higher in rats that had received a magnesium-deficient diet than in rats with normal magnesium status. Of the adult rats that had been treated once, 5 times, and 10 times with ofloxacin and killed 1 day later, only those with the 10-times treatment showed a significantly increased number of degeneratively altered tenocytes. In summary, effects observed in tendons show similar pathological features as described earlier in cartilage, indicating that quinolone-induced arthropathy and quinolone-induced tendopathy probably are different clinical manifestations of the same toxic effect on cellular components of connective tissue structures.

Achilles Tendon↗
PubMed2005

A novel assay of cell rubidium uptake using graphite furnace atomic absorption: application to rats on a magnesium-deficient diet.

The [Na,K]ATPase or sodium pump (SP) is a ubiquitous membrane cation transport system. Because of its potential participation in the pathophysiology of essential hypertension and cataract formation, the SP is under active investigation to detail its function and control. In this paper, we describe a novel, nonradioactive method of measuring SP ion transport activity in intact red blood cells (RBCs) using graphite furnace atomic absorption measurement of rubidium ion (Rb) uptake. This method provided sensitivity comparable to radioactive techniques, as assessed by experiments with human red blood cells (RBC) and ouabain, a known SP inhibitor, but this analytical approach eliminates the use of radioisotopes common to other Rb uptake assay methods. As a demonstration of its broader utility, the assay was used to assess the effects of dietary magnesium intake on SP-mediated ion transport in the RBCs of diet-controlled rats. Rats on 7 weeks of a magnesium-deficient (MgD) diet showed significant reductions in serum magnesium concentration, although levels remained in the lower region of the reference interval for healthy, magnesium replete animals. Red cell Rb uptake was significantly reduced in cells from the magnesium-restricted animals, demonstrating the sensitivity of Rb uptake to reduced magnesium intake, despite serum levels that fell within the reported normal range, and the utility of this Rb uptake assay in measuring physiological changes in SP function.

Animals↗
PubMed2004

Experimentally induced prolonged magnesium deficiency causes osteoporosis in the rat.

Background: It has been shown that prolonged daily peroral magnesium (Mg) administration, as tabs of Mg(OH)(2), used as the only treatment in postmenopausal osteoporosis, causes a significant increase in BMD. Objective: In order to obtain definitive evidence of causality of magnesium deficiency in the etiology of osteoporosis, we spent 1 year examining rats given a daily Mg-deficient diet (200 ppm) and compared them with rats given a Mg-adequate diet (2000 ppm). Methods: Sixteen female Sprague-Dawley rats, mean weight 110 (S.D. 23) g, were divided into two groups and randomly assigned to a semisynthetic diet that differed only in Mg content. Urine samples were collected every 3 months and blood was collected at the end of the trial. After the animals were sacrificed, the L3-L5 vertebrae and the femoral regions were examined for bone density (BMD) using dual energy X-ray absorptiometry. The femoral bones were examined for bone fragility and the tibiae by histomorphometry, and the mineral content of the bones was estimated. Results: The mean BMD of L3-L5 vertebral bone was significantly higher in group A (adequately nourished) than in the Mg-deficient group B (p=0.035, one-tail); in addition, the BMD of the femural region was significantly higher in group A (p=0.045, one-tail). The bending stiffness of the femur was slightly higher in group A than in group B; however, after correction to diminish the influence of the difference in bone dimensions between the two groups, femur rigidity (i.e., the loss of elasticity) in group B became significantly higher than that in group A (p=0.024). The force needed to break the bone was significantly higher in group A than in group B (p=0.024) and it remained higher 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) clearly showed the presence of osteoporosis. On microscopy, focal osteoporosis of the metaphyseal spongious bone was observed in the bone rendered Mg-deficient. Conclusions: Because osteoporosis is characterized by lowering of BMD, increased bone fragility, and altered bone architecture, our study showed that maintaining rats for 1 year on a Mg-deficient diet gives rise to the appearance of osteoporosis.

Journal Article↗
PubMed1990

Cardiotoxicity in magnesium-deficient rats fed cadmium.

We studied the cardiotoxicity in magnesium (Mg)-deficient male rats fed 50 micrograms/g Cd for 45 consecutive days. Cd at a low concentration (0.28 ppm) in the heart induced cardiotoxic effects manifested by a decrease of the heart rate and weight and histopathological changes in the presence of Mg deficiency through Cd supplementation to a normal diet did not induce any cardiotoxic effect. Cardiac output (CO) did not increase in response to the decrease in the total peripheral resistance (TPR) in the Mg-deficient rats fed Cd, suggesting that supplementation of Cd to the Mg-deficient diet may lead to a decrease in the myocardial contractile function. However, supplementation of Cd to Mg-deficient diet also alleviated myocardial necrosis and Ca overload observed in the heart of Mg-deficient rats. The present data suggest that Cd ameliorates Ca overload in the heart of Mg-deficient rats but also may inhibit the release of Ca2+, which is a major determinant of the level of contractile force.

Animals↗
PubMed1988

Keratoconus, magnesium deficiency, type A behavior, and allergy.

The etiology of keratoconus is still unknown. This project was designed to study, in a group of keratoconic patients and a control group, the following: clinical, endocrinological, immunological, psychological, and ophthalmological factors. We found mean serum magnesium deficiency and type A behavior to be significantly more common in keratoconic patients than in a control group of patients. In addition changes in gluco-mineral corticoids, changes in glucose metabolism, edema of allergic origin, and genetic factors may collaborate in the development of keratoconus. All these factors could affect the osmotic mechanism of the cornea: Na-K and/or Ca ATPase, the collagen structure by alteration of the adenylate cyclase activity, and other mechanisms. This study suggests an association between keratoconus, magnesium depletion, and type A behavior, which together constitute a new clinical syndrome and confirm an association between keratoconus and atopy.

Adult↗
PubMed1976

Changes in the alkaline phosphatase (EC 3.1.3.1) and inorganic pyrophosphatase (EC 3.6.1.1) activities of rat tissues during magnesium deficiency. The importance of controlling feeding pattern.

1. The adoption of a meal-eating pattern of feeding by rats altered the alkaline phosphatase (EC 3.1.3.1) activity in serum and liver. It was therefore necessary to regulate the feeding pattern of both magnesium-deficient rats and control animals receiving a Mg-adequate diet in order to study the effect of the deficiency. 2. Mg deficiency decreased the activities of alkaline phosphatase and inorganic pyrophosphatase (EC 3.6.1.1) in serum, kidney and tibia, but increased them in spleen. 3. Addition of a standard concentration of exogenous Mg to tissue extracts usually increased the activity of corresponding enzymes from Mg-deficient and control rats by the same proportion, indicating that the main effect of the deficiency was on the amount of enzyme present rather than on the efficiency of its operation. 4. Certain quantitative differences in the response to exogenous Mg and the activity ratio, alkaline phosphatase:inorganic pyrophosphatase were found between tissues from Mg-deficient and control rats. The significance of these are discussed in relation to the association of the two enzymic activities with the same protein molecule, and the possible occurrence of isoenzymes.

Alkaline Phosphatase↗
PubMed1985

Magnesium deficiency in human subjects--a personal historical perspective.

Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.

Adolescent↗
PubMed1975

[Bartter's disease associated with hypercorticism, phosphate and magnesium deficiencies and familial renal tubular disease].

A new case of Bartter's syndrome is described. There is a context of other cases of familial renal tubular disease with a sex-linked heredity. In this case, the Bartter's syndrome is associated with magnesium deficiency and hypomagnesemia, with a ricket and severe phosphate deficiency, and finally with an hypercorticism. The basal secretion rate of cortisol agree with a Cushing's syndrome. This hypercorticism is corrected by aminogluthetimide. The influence of the hyperreninism on the hypercorticism is discussed.

Adrenocortical Hyperfunction↗