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Results for “Magnesium Deficiency”

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PubMed1997

Ex vivo study of the increased sensitivity to NO of endothelium-denuded thoracic aortas isolated from dietary magnesium-deficient rats.

The mechanisms underlying the enhanced relaxant responses to sodium nitroprusside (SNP) associated with magnesium (Mg) deficiency were examined using endothelium-denuded thoracic aortas isolated from rats with dietary Mg deficiency. This enhancement of SNP-induced relaxation was abolished or depressed in the presence of methylene blue (a guanylate cyclase inhibitor). The relaxant responses to 8-bromo cyclic GMP (8-Br cGMP; a membrane-permeable cGMP) of thoracic aortas isolated from Mg-deficient rats were enhanced like those to SNP. These enhanced relaxant responses were depressed by tetraethylammonium (a non-specific K+ channel blocker). Charybdotoxin, a large conductance Ca2+-activated K+ (K[Ca]) channel blocker, inhibited 8-Br cGMP-induced relaxations of aortas from Mg-deficient and control rats. Apamin, a small conductance K(Ca) channel blocker, inhibited 8-Br cGMP-induced relaxations of aortas from Mg-deficient, but not control rats. The relaxant responses to cromakalim (an ATP-sensitive K+ channel opener) of the two groups were not significantly different. These ex vivo results show that dietary Mg deficiency in rats leads to increased sensitivity to NO of endothelium-denuded thoracic aortas in vitro and K(Ca) channel activation via cGMP may be involved in this enhancement.

Animals↗
PubMed2003

Corneal changes in magnesium-deficient rats.

PURPOSE: The purpose of the current study is to investigate the cornea in magnesium (Mg) deficiency and elucidate the local function of trace elements. METHODS: After delivery, mother Wistar Kyoto rats were fed a low Mg diet containing 0.1 mg Mg/100 g diet with all other nutrients and distilled and deionized water. Infant rats were suckled by their mothers for 21 days and then fed the same Mg-deficient diet. Control mother rats were fed commercial rat pellets containing 24 mg Mg/100 g diet and all other nutrients. The corneas were examined by electron microscopy at 6 weeks of age. RESULTS: In the Mg-deficient rats, serum Mg levels were significantly lower and calcium (Ca) levels higher than in the control rats. The corneas of Mg-deficient rats showed decreased microvilli and microplicae in the epithelial cells of the most superficial layer, increased mitochondria with abnormal shapes in the basal cells in the epithelium, condensed chromatin in the nuclei of the basal cells, and high density deposits and macrophage-like cells in the subepithelium of the stroma. Mg-deficient rats had pentagonal and square endothelial cells. CONCLUSION: Since Mg2+ has biologic functions including structural stabilization of protein, nucleic acids, and cell membranes, Mg deficiency may induce changes in the corneal surface and nuclei of corneal epithelial and endothelial cells. These disturbances may interfere with protection from infections, foreign bodies, dryness, and direct exposure to air. Thus, Mg is essential for the cornea to maintain normal structure and function.

Animals↗
PubMed1990

1,25 Dihydroxycholecalciferol and the genesis of hypocalcaemia in magnesium-deficient chicks.

The role of 1,25 dihydroxycholecalciferol (1,25 DHCC) in the genesis of hypocalcaemia of magnesium (Mg) deficiency was studied in chicks fed control or Mg-deficient diets with varying calcium (Ca) content. In one study, Ca and Mg deficiencies were induced simultaneously whereas in a second study, exposure to low dietary Ca followed induction of Mg deficiency. In both studies, Mg-deficient chicks fed adequate dietary Ca were hypocalcaemic yet had normal circulating 1,25 DHCC, whereas Mg-deficient chicks fed low dietary Ca maintained normocalcaemia and had increased 1,25 DHCC. Bone Ca content, which was raised in Mg-deficient chicks fed adequate Ca, decreased in association with increased 1,25 DHCC and normalization of plasma Ca during exposure to low dietary Ca. The results suggest that the inappropriately normal 1,25 DHCC observed in conventional Mg deficiency may contribute to the pathological hypocalcaemia. In addition, these studies indicate that hypomagnesaemia per se does not limit 1,25 DHCC production during Mg deficiency.

Animals↗
PubMed2002

Stress protein expression cDNA array study supports activation of neutrophils during acute magnesium deficiency in rats.

Recent studies underline the importance of the immunoinflammatory processes in the pathology of acute magnesium (Mg)-deficiency. The aim of this study was to assess the effect of acute experimental Mg-deficiency in the rat on neutrophil activity. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 days. In this experiment, we measured neutrophil respiratory burst by chemiluminescence; then, to examine the molecular events associated with acute Mg-deficiency, we applied cDNA array technology to define the transcription response in neutrophils of Mg-deficient rats in comparison with controls. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of neutrophils. Moreover, as shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared to neutrophils from control rats. Moreover, the chemiluminescence of neutrophils from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. Using cDNA array which includes 207 known rat genes of stress proteins, 102 genes were found to be expressed in neutrophils. Among expressed genes, 78 per cent of genes were found to be expressed more than twofold in neutrophils from Mg-deficient rats compared to control rats. Acute Mg-deficiency was characterized by an induction of genes encoding for proteins involved in apoptosis, heat shock proteins, protein belonging to the cytoskeleton, proteins implicated as stress response regulators and effectors and enzyme implicated in thromboxane synthesis. Then, this experimental strategy allowed to identify a series of genes implicated in the immunoinflammatory process of Mg-deficiency.

Animals↗
PubMed1978

Barbiturate and amphetamine activity in rats fed a magnesium-deficient diet.

Hexobarbital hypnosis and d-amphetamine toxicity were observed in rats fed a commercially available rat food preparation (lab chow) and in another two groups fed complete nutritionally defined diets with or without magnesium. Neither hexobarbital sleeping time nor hexobarbital blood concentration at awakening were affected after 4, 8 or 12 days of feeding the deficient diet. However, increased sensitivity to d-amphetamine was observed after 11 days of feeding the same magnesium deficient diet to other rats. The LD50 of d-amphetamine in magnesium deficient rats was less than 0.5 that recorded for the groups fed lab chow or the nutritionally defined diet with a magnesium supplement.

Animals↗
PubMed1991

Central nervous system magnesium deficiency.

The central nervous system concentration of magnesium (Mg++) appears to have a critical level below which neurologic dysfunction occurs. Observations presented suggest that the interchange of the Mg++ ion between the cerebrospinal fluid, extracellular fluid, and bone is more rapid and dynamic than is usually believed. This is especially so when the hypertrophied parathyroid gland is associated with significant skeletal depletion of Mg++ as judged by history rather than serum level. Magnesium, much like calcium, has a large presence in bone and has a negative feedback relationship with the parathyroid gland. A decline in central nervous system Mg++ may occur when the skeletal buffer system orchestrated largely by the parathyroid glands is activated by an increase in serum calcium. Observations in veterinary medicine and obstetrics suggest that the transfer of Mg++ from the extracellular fluid into bone during mineralization processes may be extensive. If the inhibition of the hypertrophied parathyroid gland is prolonged and the skeletal depletion of Mg++ extreme, serious neurologic symptoms, including seizures, coma, and death, may occur. Noise, excitement, and bodily contact appear to precipitate neurologic symptoms in Mg+(+)-deficient human subjects as it has been documented to occur in Mg+(+)-deficient experimental animals. The similarity of the acute central nervous system demyelinating syndromes with reactive central nervous system Mg++ deficiency is reviewed.

Adolescent↗
PubMed1996

Renin immunochemistry, sodium excretion and relative heart weight in cyclosporine- or alimentary-induced magnesium deficiency in rats.

Rats were given a magnesium-(Mg) depleted (Mgd), or a Mg-standard (Mgst) or a Mg-enriched (Mge) diet, with 20 mg/kg/day cyclosporine (Cy) or olive oil per os for 90 days (6 groups). Anti-renin antibody was applied and the percent of renin-positive glomeruli (RI) was taken. Sodium excretion (NaU), relative heart weight (HW), as a measure of hypertension, and total femur Mg were measured. Compared to dietary controls, femur Mg was reduced under Cy and Mgd or Mgst indicating Mg deficiency. RI was higher in all Cy groups (p < 0.01), and Nau was lower in Mgd + Cy and in Mgst + Cy (p < 0.01). Correspondingly, HW was found to be significantly higher in Mgd + Cy and Mgst + Cy. In animals under Mge + Cy, there were no differences in NaU and HW compared to controls. The results indicate a relation between Cy-related hypertension and Mg status: Mg deficiency seems to enhance the hypertensive effect of Cy via sodium retention.

Animals↗
PubMed2004

About the misdiagnosis of magnesium deficiency.

The experience of our self-help organisation shows that the reason patients with symptoms of magnesium (Mg) deficiency do not get Mg therapy is acceptance of an inappropriate lower limit of the reference values for serum Mg concentration. The commonly designated low limit of the normal range seems to have been selected from values obtained for symptomatic patients. It is below levels that exist in patients with marginal deficiencies that can predispose to development of pathologic findings, so that the prevalence and importance of this disease is insufficiently considered. The lower reference limit of the normal population is erroneously regarded as a diagnostic criterion that excludes Mg deficiency when the serum level is even slightly above the reference limit that only excludes normality at lower levels. It is a statistical error to use the confidence limits of the normal population as the exclusion limit for those with abnormal Mg status.

Diagnosis, Differential↗
PubMed1992

Magnesium deficiency in vitro enhances free radical-induced intracellular oxidation and cytotoxicity in endothelial cells.

The effect of magnesium (Mg)-deficient culture on endothelial cell susceptibility to oxidative stress was examined. Bovine endothelial cells were cultured in either control sufficient (0.8 mM) or deficient (0.4 mM) levels of MgCl2. Oxygen radicals were produced extracellularly by the addition of dihydroxyfumarate and Fe(3+)-ADP. Isolated Mg-deficient endothelial cells produced 2- to 3-fold higher levels of thiobarbituric acid (TBA)-reactive materials when incubated with this free radical system. Additional studies were performed using digitized video microscopy and 2',7'-dichlorofluorescein diacetate (DCFDA) as an intracellular indicator for oxidative events at the single cell level. In response to the exogenous oxidative stress, endothelial cells exhibited a time-dependent increase in fluorescence, suggestive of intracellular lipid peroxidation. The increase in cellular fluorescence began within 1 min of free radical addition; the Mg-deficient cells exhibited a more rapid increase in fluorescence than that of Mg-sufficient cells. In separate experiments, cellular viability was assessed using the Trypan blue exclusion assay. Mg deficiency increased cytotoxicity of the added oxyradicals, but the loss of cellular viability began to occur only after 15 min of free radical exposure, lagging behind the detection of intracellular oxidation products. These results suggest that increased oxidative endothelial cell injury may contribute to vascular injury during Mg deficiency.

Adenosine Diphosphate↗