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PubMed1995

Magnesium deficiency in rats induces a rise in plasma nitric oxide.

Magnesium deficiency in rats leads to an oxidative stress involving an increased production of radical oxygen species. The present study was designed to examine the effect of experimental magnesium deficiency on plasma nitric oxide (NO) level and nitric oxide synthases (NOS) activities in rats. The data show that the concentration of NO is markedly increased in plasma of magnesium-deficient rats. This rise in plasma NO results from activation of inducible nitric oxide synthase (iNOS) rather than of the constitutive form (cNOS) of the enzyme. These data are in agreement with previous observations indicating that inflammation occurs during magnesium-deficiency and provide an additional cause of oxidative lesions through formation of peroxynitrite from nitric oxide and superoxide anion.

Animals↗
PubMed1988

Canine renal and systemic hemodynamic measurements after 4 weeks of a magnesium deficient diet.

To probe renal hemodynamic measurements in relation to simultaneous systemic hemodynamic measurements in normal, adult, conscious dogs on a magnesium-deficient diet, 6 experimental animals were given 4 weeks of a magnesium-deficient diet compared to 9 animals whose dietary magnesium was normal. Systemic hemodynamics were estimated using a thermodilution catheter, and renal hemodynamics were estimated by standard renal clearance techniques. Electrolytes and hormones were also surveyed in these same animals at the time of hemodynamic measurements. Heart rate was significantly higher in magnesium-deficient dogs, but there were no other systemic hemodynamic differences between the two groups of dogs. Renal blood flow, effective renal plasma flow, and urinary osmolality were significantly higher in the magnesium-deficient animals. Whole-blood ionized calcium and potassium, serum magnesium, and fractional excretion of magnesium were lower in the magnesium-deficient dogs. We conclude that the renal circulation is more sensitive than the systemic circulation to disturbances in magnesium balance. Disturbances of other electrolytes accompanying magnesium deficiency were also confirmed.

Animals↗
PubMed1982

End-organ response to adrenocorticotropin, thyrotropin, gonadotropin-releasing hormone, and glucagon in hypocalcemic magnesium deficient patients.

We have evaluated the responsiveness of hypocalcemic magnesium-deficient patients to ACTH, TRH, gonadotropin-releasing hormone, and glucagon as determined by the rise in serum cortisol, TSH, LH, and plasma cAMP concentrations, respectively. It was previously been shown that the hypocalcemia of magnesium deficiency is secondary to impaired secretion of parathyroid hormone (PTH) along with renal and skeletal resistance to the action of PTH. Since PTH secretion and action are though to be effected through the intermediary action of cAMP, and magnesium is a required cofactor for adenylate cyclase, defective generation of cAMP could account for the observed defects in PTH secretion and action. Other hormonal systems requiring the intermediary action of cAMP may be similarly affected by magnesium deficiency. The results of the present study, however, demonstrate normal responsiveness of the adrenal cortex, thyrotrophs, gonadotrophs, and liver to their respective trophic hormones in hypocalcemic magnesium-deficient patients. The reason why these responses are intact while PTH secretion and action are impaired is unknown but may be accounted for by differing magnesium requirements of the adenylate cyclase complex in these tissues.

Adrenocorticotropic Hormone↗
PubMed1990

Magnesium deficiency in patients on home enteral nutrition.

Home enteral nutrition (HEN) is an established method of long term nutritional support. Many patients receiving HEN have Crohn's disease complicated by intestinal failure and malnutrition, including magnesium deficiency. It is unknown if HEN can correct magnesium deficiency or if patients on HEN can become magnesium deficient. We measured total magnesium intake in nine patients receiving HEN, and assessed their magnesium status. Two patients had magnesium intakes below the recommended dietary allowance of 15 mmol/day. Four patients (44%) had biochemical evidence of magnesium deficiency, although no patient had clinical signs of magnesium deficiency. Several magnesium deficient patients used a liquid feed which had a low magnesium content. Patients on HEN should have their magnesium status checked regularly and may require magnesium supplements.

Journal Article↗
PubMedDate not supplied

Magnesium deficiency in alcohol addiction and withdrawal.

The earliest description of clinical magnesium deficiency was reported in 1934. In 1954, Flink reported alcoholism as a cause of magnesium deficiency. This has been confirmed by low serum and tissue levels, balance studies, low exchangeable 28Mg and parenteral Mg retention tests. Alcohol causes urinary Mg wastage, but other mechanisms related to alcoholism contribute to the magnesium deficiency including malnutrition, gastrointestinal losses, phosphate deficiency, acidosis and/or alkalosis, vitamin D deficiency and free fatty acidemia associated with alcohol withdrawal. Mg replacement therapy is recommended to prevent some of the serious sequelae of magnesium deficiency.

Alcohol Withdrawal Delirium↗
PubMed1976

The activity of certain hydrolases of rat erythrocytes in experimental magnesium deficiency.

In rats with induced syndrome of chronic magnesium deficiency, occurrence of haemolytic anaemia in conjuction with a shortening of the erythrocyte survival time and marked reticulocytosis among other symptoms became noticeable. In the present experiment the authors undertook to study the behaviour of the lysosomal enzymes in the erythrocytes of magnesium-deficient rats. In these animals anaemia and reticulocytosis as well as a marked increase in the percentage of the erythrocytes showing positive reactions to the acid phosphatase and beta-glucuronidase tests developed. It seems likely that the positive lysosomal reactions were obtained with younger blood cells which did not stain with brilliant cresyl blue but still retained single lysosomes in their cytoplasm. This assumption was confirmed by ultrastructural studies which demonstrated the presence of siderosomes inside both the reticulocytes and the mature erythrocytes. The changes in the percentages of reticulocytes and enzyme-positive erythrocytes were independent of the histological structure of the experimental rat's thymus. In the reticulocytes as well as in the mature erythrocytes, the noteworthy presence of degenerated mitochondria containing electron-dense material seems to be a morphological sign of impairment of the magnesium-deficient rat's erythrocytes.

Acid Phosphatase↗
PubMed1985

Influence of magnesium deficiency on liver collagen after carbon tetrachloride or ethanol administration to rats.

The effects of magnesium deficiency on liver collagen after the administration of a hepatotoxic substance were investigated. Rats, fed a control or magnesium-deficient diet (0.040 g/kg), received six CCl4 or mineral oil injections administered at 2-d intervals starting from the first day of diet treatment. They were killed 3 or 12 d after the last injection. Between postinjection d 3 and 12, no change of magnesium concentration in liver was observed in the deficient rats. Three days after the end of treatment liver calcium in the magnesium-deficient CCl4-treated rats was higher than in any other group. Liver collagen of untreated control rats and untreated magnesium-deficient rats was not significantly different. In control and magnesium-deficient animals receiving CCl4 treatment, the liver collagen levels were significantly higher than in untreated rats. The magnesium-deficient rats receiving CCl4 have higher liver collagen than the controls receiving CCl4. In a second experiment the effect of suboptimum intake of magnesium (0.120 g/kg) combined with the ingestion of ethanol was studied in rats given a solution of ethanol in water for 55 d as their only source of fluid. Mortality occurred in the magnesium-deficient rats receiving ethanol, and body weights of these rats were lower than those of animals in the other three groups. The collagen concentration in liver was higher in magnesium-deficient rats consuming ethanol than in any other group. The synergistic action between magnesium deficiency and ethanol therefore appears to be analogous to that observed with CCl4.

Animals↗
PubMed1996

Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats.

To investigate the manganese status in magnesium deficiency, 40 male Wistar rats, 3 wk old, were divided into two groups and fed a magnesium deficient diet or a normal synthetic diet for 2 wk. Dietary magnesium depletion decreased magnesium levels in brain, spinal cord, lung, spleen, kidney, testis, bone, blood, and plasma, while it elevated the magnesium level in liver. In magnesium-depleted rats, calcium concentration was increased in lung, liver, spleen, kidney, and testis, while it was decreased in tibia. In magnesium-depleted rats, manganese concentration was decreased in plasma and all tissues except adrenal glands and blood. Dietary magnesium depletion diminished pyruvate carboxylase (EC 6.4.1.1) activity in the crude mitochondrial fraction of liver. Positive correlation was found between the liver manganese concentration and the pyruvate carboxylase activity. In the magnesium-depleted rats, glucose was decreased while plasma lipids (triglycerides, phospholipids, and total cholesterol) were increased. These results suggest that dietary magnesium deficiency changes manganese metabolism in rats.

Animals↗
PubMedDate not supplied

[Current concepts in the pathogenesis of gestosis with special reference to magnesium deficiency].

Particular investigations and hints from the literature led to suggest that Magnesium deficiency in pregnancy plays a role in the development of pregnancy-induced hypertension as well as gestosis or pre-eclampsia. The integration of the already known facts about the physiopathology of Magnesium deficiency to those of the pathogenesis of gestosis led to the concept of a gestosis model which is based on Magnesium deficiency. In this way Magnesium deficiency represents the cause of (essential) gestosis. Further investigations should be done in this direction.

Female↗
PubMed1978

Effects of magnesium deficiency on duodenal and ileal magnesium absorption and secretion.

Intestinal adaptation by the growing rat to a low-magnesium diet was studied by in situ perfusion of duodenum and ileum in vivo. Rats were fed diets containing either 0.066 or 0.022% Mg for 3 weeks. Magnesium-restricted rats became hypomagnesemic and hypercalcemic. Net magnesium secretion was studied by perfusing an initially magnesium-free saline solution; secretion was higher in duodenum than in ileum, and decreased significantly in the duodenum in response to magnesium restriction. Net magnesium adsorption studied by intraluminal perfusion of 2.5 mM magnesium in saline was greater in duodenum than ileum in rats taking a low-magnesium diet, but duodenal and ileal absorption did not differ in animals taking the normal magnesium diet. Absorption did not adapt significantly to magnesium restriction in either segment. Adaptation of small-intestinal magnesium transport to a low magnesium diet is minimal, consisting mainly of reduced duodenal magnesium secretion.

Animals↗
PubMed1995

The effects of magnesium deficiency on DNA and lipid synthesis in cultured human umbilical arterial endothelial cells.

This study investigated the effects of magnesium deficiency on thymidine incorporation and lipid synthesis in human umbilical arterial endothelial cells. To study [3H]thymidine incorporation, the cells were exposed for 12 to 96 h to experimental media containing decreasing magnesium concentrations of 237, 118 and 5 microM. A magnesium concentration of 949 microM was used as control. At 48 h of exposure to the experimental media, magnesium was restored to 949 microM in half of the magnesium-deficient cultures. To determine [14C]acetic acid distributions among cholesterol, phospholipid and triglyceride, the cells were treated with decreased magnesium media at the levels mentioned above for 12 to 48 h. The results showed that [3H]thymidine incorporation into DNA was inhibited by magnesium deficiency. The inhibition was augmented correspondingly with decreased magnesium concentrations and increased exposure periods. When magnesium in the medium was enhanced to normal level, incorporation was no longer inhibited. Incorporation of [14C]acetic acid into phospholipid was inhibited, its incorporation into triglyceride was stimulated, but its incorporation into cholesterol was not affected by magnesium deficiency. We suggest (i) that with the restoration of adequate magnesium, the inhibiting effect of magnesium deficiency on thymidine incorporation is reversible; (ii) that magnesium deficiency can result in a redistribution of [14C]acetic acid between phospholipid and triglyceride.

Acetates↗
PubMed1988

Disturbances of vitamin D metabolism and action during clinical and experimental magnesium deficiency.

It has been known since the 1920s that magnesium is influential in calcium homeostasis. In the 1970s it was documented that parathyroid secretion and activity may be impaired in magnesium deficiency. In the past two decades a variety of studies have indicated alterations in circulating vitamin D metabolites in humans, although these observations are not entirely consistent. Animal studies have not consistently demonstrated impaired vitamin D metabolism during relatively brief periods of magnesium deprivation, despite in vitro magnesium dependence of 1 alpha-hydroxylase activity. Studies of the administration of active vitamin D metabolites to humans and animals suggest that skeletal resistance to these compounds in magnesium deficiency may, in part, explain their reduced calcaemic effect during magnesium deficiency.

Animals↗
PubMed1975

The effect of magnesium deficiency in mice on serum immunoglobulin concentrations and antibody plaque-forming cells.

Magnesium-deficient mice immunized with SRBC showed a significant decrease (P less than 0.001) in the number of PFC in their spleens compared with mice on a control diet. Serum immunoglobulin concentrations (IgG1, IgG2, IgA and IgM) were determined after 3, 6, 9 and 12 days on the respective diets. The serum IgG2 and IgM concentrations of magnesium- deficient mice were decreased (P less than 0.005) by 6 days and remained at these concentrations until 12 days. The serum IgG1 and IgA concentrations of magnesium deficient animals also decreased (P less than 0.01) by 6 days but returned toward control concentrations at 12 days. Serum magnesium concentrations confirmed the magnesium deficiency of the experimental animals. Therefore, magnesium deficiency has profound immunosuppressive capabilities in mice by significantly reducing the number of antibody synthesizing cells and serum immunoglobulin concentrations.

Animals↗
PubMed1997

Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats.

Magnesium deficiency has been shown to produce vascular lesions in experimental animals, but the underlying mechanisms of vascular injury are not clear. It has been reported that in rodents, magnesium deficiency enhances circulating levels of factors that promote free radical generation and are mitogenic. In pursuance of these observations, the present study tested the hypothesis that magnesium deficiency may enhance oxidative stress and trigger an accelerated growth response in vivo in the aorta of rats. Oxidative stress was evaluated in terms of levels of thiobarbituric acid-reactive substances in the serum and aorta and activity of superoxide dismutase and catalase in the aorta; fractional rates of collagen synthesis were assessed using [3H]-proline. Serum and tissue levels of magnesium and calcium were determined by atomic absorption spectrophotometry. The present study demonstrated for the first time that magnesium deficiency significantly (P < 0.001) increases levels of thiobarbituric acid-reactive substances in the aorta of rats. Other changes in the aorta of animals on the Mg-deficient diet included a significant reduction (54%, P < 0.001) in the activity of superoxide dismutase and catalase (37%, P < 0.01) and a 19% increase in net fractional rates of collagen synthesis (P < 0.05). While serum magnesium was significantly reduced in these animals (P < 0.001), aortic tissue levels of magnesium in these animals remained unaltered throughout the duration of the study, suggesting the existence of other control mechanisms, apart from reduced tissue levels of magnesium, mediating the observed effects. These findings suggest that magnesium deficiency may trigger a wound healing response, involving oxidative injury and growth stimulation, in the vascular system.

Animals↗
PubMed1980

A biochemical and ultrastructural study of skeletal muscle from rats fed a magnesium-deficient diet.

In order to study changes in skeletal muscle during a magnesium deficiency, serum and muscle tissues were collected from male Sprague-Dawley rats fed either a control or magnesium-deficient diet. The rats were killed on days 7, 10, 14, 17, 19, 21 and 26 of the experiment. Ion concentrations in serum and muscle were determined by atomic absorption spectrophotometry, taurine concentrations of serum and muscle were determined by the Pentz method, and ultrastructural changes in skeletal muscle were detected with the use of the transmission electron microscope. The results indicated an increase in serum taurine which preceded an increase in muscle taurine concentration in rats fed a magnesium-deficient diet. The electron micrographs showed a swelling of mitochondria on day 14 of the deficiency and a total disorganization of the sarcoplasmic reticulum by day 26. In conclusion, in skeletal muscle from rats fed a magnesium-deficient diet, major ultrastructural changes apparently occur after the serum magnesium concentration is reduced and about the same time as muscle taurine concentration becomes elevated. The changes may be initiated by alterations in membrane permeability which may be influenced by taurine, since taurine has been shown to influence ion movement across membranes or membrane stability.

Animals↗
PubMed1994

Effect of various serotoninergically induced manipulations on audiogenic seizures in magnesium-deficient mice.

The aim of our study was to analyse the possible implication of the serotoninergic system in the pathophysiology and the lethality of audiogenic seizures induced by magnesium deficiency, either by decreasing cerebral serotonin (5-HT) levels (p-chlorophenylalanine) or by increasing 5-HT levels in the brain (5-hydroxytryptophan, L-tryptophan, nialamide, fluoxetine). In magnesium-deficient mice, the percentages of audiogenic seizures and of fatal seizures were dependent on the time lapse between the p-chlorophenylalanine (PCPA) injection and the audiogenic test. The percentage was at least 24 h after the injection: in OF1 and C57BL/6 strains, PCPA fully protected the mice from seizure occurrence, whereas it only partially protected the animals of the other strains. 5-Hydroxytryptophan caused a decrease in the audiogenic seizures in magnesium-deficient OF1 mice as well as in control DBA/2 mice. In contrast L-tryptophan did not reduce the number of wild courses or of clonic and tonic seizures in either the magnesium-deficient OF1 strain or control DBA/2 mice. Nialamide and fluoxetine were only effective in decreasing the numbers of clonic and tonic convulsions of the audiogenic seizure without affecting the wild courses. The combination of nialamide and tryptophan caused a cessation of the audiogenic seizure phases in both magnesium-deficient OF1 and control DBA/2 mice. In contrast, the fluoxetine-tryptophan combination did not have the same effect on magnesium-deficient and non-magnesium-deficient mice. This work showed that the serotoninergic system plays a secondary role in the pathophysiology of audiogenic seizures in magnesium-deficient mice rather than in that of genetically audiosusceptible mice.

5-Hydroxytryptophan↗