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PubMed2002

Magnesium deficit and sudden infant death syndrome (SIDS): SIDS due to magnesium deficiency and SIDS due to various forms of magnesium depletion: possible importance of the chronopathological form.

Sudden Infant Death Syndrome (SIDS) might be due to the fetal consequences of a Mg maternal deficiency, which might be prevented by simple atoxic nutritional Mg intake by the mother. Various stresses in the pregnant women or in the infant may transform a simple Mg deficiency into Mg depletion which may not be cured by nutritional Mg supplement, but requires a correction of its causal dysregulation. Beside the well established risk factors in baby care and in the environment, it is important to stress the possible role of a primary hypofunction of the biological clock. This may be treated by darkness therapy: total light deprivation at night for the infant and atoxic nutritional Mg supplement for the pregnant women. The place in the prevention of SIDS of Mg therapy for the infant and of the use of melatonin, L-tryptophan and taurine is now uncertain yet.

Adult↗
PubMed1997

Magnesium deficiency increases ketamine sensitivity in rats.

PURPOSE: Inhibition of the NMDA receptor likely contributes to ketamine's neurodepressive properties. Magnesium also inhibits the NMDA receptor by binding to a site associated with the ketamine-binding domain. Electrophysiological studies suggest that magnesium prevents ketamine from binding to the NMDA receptor and thereby prevents ketamine inhibition. We undertook an in vivo study to determine if magnesium deficiency was associated with an increased sensitivity to ketamine. METHODS: Weanling rats were maintained on a Mg(2+)-deficient or control diet for 14 days. In Study I, rats were anaesthetized then sacrificed and the Mg2+ concentrations in the brain and plasma were measured. In a second prospective study, experimental animals were rendered hypomagnesaemic and the potency of 125 mg.kg-1 ip ketamine was evaluated. Animals were then were fed a Mg(2+)-containing diet and ketamine sensitivity was re-examined 14 days later. RESULTS: The Mg(2+)-deficient diets rendered the rats hypomagnesaemic as indicated by the brain and plasma concentration of Mg2+. In Study 2, the time to loss of righting reflex was shorter; 1.9 +/- 0.3 min (n = 12) and 2.6 +/- 0.2 min (n = 16, P < 0.05), whereas the latency to toe pinch was prolonged: 25.0 +/- 5.8 min (n = 12) vs 3.1 +/- 2.1 min (n = 16, P < 0.05) in the Mg(2+)-deficient compared with age-matched control animals, respectively. The hypomagnesaemic animals had a higher death rate following ketamine injection. The increased sensitivity to ketamine was no longer apparent when the animals were re-tested following replenishment of Mg2+. CONCLUSION: Hypomagnesaemia is associated with an increased sensitivity to ketamine.

Anesthetics, Dissociative↗
PubMed1993

Erythema formation in magnesium-deficient albino rats. A non-invasive model for the screening of anti-inflammatory agents and oral mineral supplements.

The enteral bioavailability of magnesium firmly bound to a fire-proof, inert SiO2-Al2O3 matrix (ground magnesia boats) was studied in magnesium-deficient albino Sprague-Dawley rats, with and without blocking gastric hydrochloric acid secretion with omeprazole. Magnesium was absorbed, although to a small degree, also at anacidity. Pronounced erythema, developing after only some days in hypomagnesemic hypercalcemic rats, are proposed as a non-invasive model for the screening of antiinflammatory substances. Using this model significant protective effects were proven for cromoglycate, polyenthylene glycol 400, and omeprazole; the latter, however, seems more likely to act via a magnesium-sparing mechanism.

Animals↗
PubMed1975

Influence of magnesium deficiency on horse foal tissue concentraion of Mg, calcium and phosphorus.

1. The effects of feeding with a purified magnesium-deficient diet (--Mg, 7-8 mg Mg/kg) on horse foal blood serum and tissue concentrations of Mg, calcium and phosphorus were studied, and the results compared with histopathological findings. 2. Serum concentrations of Ca and P were unaffected by feeding with the --Mg diet, whereas serum Mg concentrations decreased from a mean initial (day o) concentration of 0.78 mmol/l to 0.53 mmol/l 7 d after foals were placed on the -Mg diet, and then continued to decrease at a slower rate. 3. Aorta concentrations of Ca and P, but not Mg, were positively correlated with the period of time foals were given the -Mg diet, verifying histopathological findings. Results for both aorta Ca and P analyses and histopathological studies indicated that mineralization of the aorta began approximately 30-35 d after foals were placed on the -Mg diet. 4. Feeding with the -Mg diet had no significant, analytically detectable effect on brain, liver, kidney, lung, spleen, skeletal or cardiac muscle concentrations of Ca, P or Mg, although microscopic evidence of mineralization was seen in some of these tissues from foals given the Mg diet for 71-180 d. 5. A significant negative correlation was found between bone ash concentrations of Mg (rib, metacarpus and metatarsus) and the length of time foals were fed on the Mg diet. Bone ash concentrations of Ca and P were, however, unchanged. 6. Low serum Mg values and negative correlations between the bone ash concentration of Mg and the period of time foals were fed on the -Mg diet supplemented with 390 mg. Mg as MgO/kg were interpreted as suggesting that either this level of Mg supplementation is marginal for the growing foal, or that the Mg in MgO is not readily available to the growing foal.

Animal Nutritional Physiological Phenomena↗
PubMed2000

Regional brain monoamine concentrations and their alterations in bovine hypomagnesaemic tetany experimentally induced by a magnesium-deficient diet.

Monoamines are important brain neurotransmitters. An investigation was carried out to determine if hypomagnesaemic tetany was associated with alterations in regional brain monoamine concentrations in bovines. The results, established in cows with normal magnesium status, demonstrated that regional differences existed in the distribution and concentration of brain monoamines in the adult bovine, which were similar to those in other species. In magnesium-deficient cows, severe hypomagnesaemia and lowered cerebrospinal fluid (CSF) magnesium concentrations were associated with significant alterations in monoamine concentrations in some brain regions. Alterations in 3,4-dihydroxyphenylalanine (DOPA) and dihydroxyphenylacetic acid (DOPAC) concentrations in the corpus striatum, and dopamine (DA) in the cerebral cortex and cerebellum were recorded. These regions play an important role in both voluntary and involuntary motor function, and therefore these alterations may play a role in the aetiology of hypomagnesaemic tetany. However, there was no significant change in DA concentrations in the corpus striatum (the main dopaminergic region in the brain) associated with hypomagnesaemia. In addition, a significantly lower norepinephrine (NE) concentration in the corpus striatum of hypomagnesaemic animals was also recorded. Norephinephrine is generally excitatory and therefore lowered NE concentrations would be expected to result in depression rather than stimulation of motor function.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Depressed antioxidant defense in rat heart in experimental magnesium deficiency. Implications for the pathogenesis of myocardial lesions.

Magnesium (Mg) deficiency has been shown to produce myocardial lesions in different experimental models. Based on several lines of evidence, it has been proposed that oxidative injury to the cardiac muscle may explain the pathobiology of such lesions. In pursuance of this postulation, the present study examined the effect of dietary deficiency of Mg on the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase, in rat heart. This article reports a significant lowering of the activity of both these enzymes in the cardiac tissue in Mg-deficient rats. Since depressed antioxidant defense in the heart may enhance myocardial susceptibility to oxidative injury, the observation is of possible relevance to the pathogenesis of cardiac lesions in Mg deficiency.

Animals↗
PubMed1977

Magnesium deficiency in embryos of Xenopus laevis.

Embryos of Xenopus laevis reared in media with various low (less than or equal to 10(-5) M) magnesium ion concentrations will exhibit differing degrees of a potentially lethal magnesium starvation syndrome depending on the ion concentration and rearing temperature. The higher the rearing temperature or the lower the magnesium ion content of the medium the more severely the syndrome will be expressed. (Normal development can be expected at temperatures 13-30 degrees C and magnesium ion concentrations greater than 10(-5)M to 10(-2) M.). The magnesium deficiency syndrome in Xenopus embryos is described in detail and compared with the normal and anucleolate conditions. The deficiency condition becomes manifest after hatching as retarded growth and differentiation with progressive paralysis and edema. At the same time alterations are observed in the pattern of soluble proteins. The use of magnesium ions as a probe for investigating developing systems is discussed.

Age Factors↗
PubMed1977

[Control of glycolysis in magnesium deficiency: studies on intact red cells and hemolysates].

The behaviour of glycolytic flux and glycolytic metabolic concentrations was studied under conditions of magnesium deficiency. The Mg-deficiency was produced in whole animals (rats) by feeding a diet almost completely free of Mg and in hemolysates of men by the addition of a chelating agent. The results show that the decrease of the free Mg-level is diminished by partial destruction of ATP and 2,3-DPG. The analysis of the control strength of the overall flux leads to the conclusion that the decrease of the glycolytic rate is caused by an inhibition of the hexokinase-phosphofructokinase-control system. The decrease of the MgATP-Complex and free Mg++-level explains the diminished phosphorylation of glucose by the hexokinase. The ATP-inhibition of the phosphofructokinase is amplified by a small increase of free ATP-concentration and a simultaneous decrease of the Fru-6P-level. The increase of the PEP-level is caused by the diminished free Mg++ and MgATP-complex and does not demonstrate a larger control strength of the pyruvate kinase.

Adenosine Diphosphate↗
PubMed1980

Magnesium deficiency allergy-like crisis in hairless rats: a suggested model for inflammation studies.

Two groups of rats, one hairy and one hairless, received either a magnesium deficient diet (4 mg Mg/100 g diet) or a control diet (40 mg/100 g diet). After four days, an easily observable redness of the skin occurred in the hairless deficient group, progressing from the tail to the forehead, and later a hyperemia of the ear and dermatosis which increased with scratching appeared in both deficient groups. The clinical signs were more acute in the deficient hairless group. Histamine, total white blood cells and eosinophil counts increased in both deficient groups during the allergy-like crisis. Then, these factors tended to normal values. After three weeks on a diet an enlargement of the spleens was observed, but not of the thymus in both deficient groups. There was a large difference in the histamine content of the spleen between the deficient and control hairless groups: the values obtained were 4 350 ng and 166 ng per 100 g tissue respectively.

Animals↗
PubMed1983

Fasting and ketogenic diet effects on audiogenic seizures susceptibility of magnesium deficient rats.

Because fasting and ketogenic diets decrease seizure susceptibility in epileptics, their anticonvulsant effects were studied using sound-induced seizures in the magnesium-deficient rat. Fasting markedly depressed seizure incidence and severity but did not affect latency (sec to seizure onset). High-fat diet increased incidence of audiogenic seizures and seizure severity, and decreased latency. Gavage of medium chain triglyceride, beta-hydroxybutyrate or glucose did not affect seizure incidence, seizure severity or latency. Nonspecific excitability level was not associated with treatment nor with seizure incidence, severity or latency time.

Acoustic Stimulation↗
PubMed2006

Magnesium deficiency augments myocardial response to reactive oxygen species.

Magnesium (Mg) deficiency and oxidative stress are independently implicated in the etiopathogenesis of various cardiovascular disorders. This study was undertaken to examine the hypothesis that Mg deficiency augments the myocardial response to oxidative stress. Electrically stimulated rat papillary muscle was used for recording the contractile variation. Biochemical variables of energy metabolism (adenosine triphosphate (ATP) and creatine phosphate) and markers of tissue injury (lactate dehydrogenase (LDH) release and lipidperoxidation), which can affect myocardial contractility, were assayed in Langendorff-perfused rat hearts. Hydrogen peroxide (100 micromol/L) was used as the source of reactive oxygen species. The negative inotropic response to H2O2 was significantly higher in Mg deficiency (0.48 mmol Mg/L) than in Mg sufficiency (1.2 mmol Mg/L). Low Mg levels did not affect ATP levels or tissue lipid peroxidation. However, H2O2 induced a decrease in ATP; enhanced lipid peroxidation and the release of LDH were augmented by Mg deficiency. Increased lipid peroxidation associated with a decrease in available energy might be responsible for the augmentation of the negative inotropic response to H2O2 in Mg deficiency. The observations from this study validate the hypothesis that myocardial response to oxidative stress is augmented by Mg deficiency. This observation has significance in ischemia-reperfusion injury, where Mg deficiency can have an additive effect on the debilitating consequences.

Adenosine Triphosphate↗
PubMed1994

Mechanisms of the enhanced contractile response to phenylephrine in thoracic aorta isolated from rats with dietary magnesium deficiency.

The mechanisms underlying the enhanced contractile response to phenylephrine (PE) and increased susceptibility to nifedipine of de-endothelialized thoracic aorta isolated from rats with dietary magnesium deficiency (Mg-deficient rats) were examined by functional and radioligand binding studies. Enhanced PE-induced contractions and increased susceptibility to nifedipine in Mg-deficient rats were not observed in the presence of 10 microM H7. PE significantly decreased the KD value without changing Bmax in the binding of [3H]PN200-110 to de-endothelialized aortic strips. The KD value obtained in the Mg-deficient rats was significantly smaller than that in the controls. Nifedipine displaced the binding of [3H]PN200-110 concentration-dependently, and the pKi value in Mg-deficient rats was significantly larger than that in the controls. A combination of PE and H7 abolished this difference. These results indicate that the modulation of L-type Ca2+ channels via the stimulation of alpha 1-adrenoceptors may be involved in the enhancement of vasoconstriction and increased susceptibility to nifedipine in aortas isolated from Mg-deficient rats. The H7-sensitive mechanisms may play an important role in these phenomena.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Hypothesis: new concepts concerning the pathophysiology of the sudden infant death syndrome due to magnesium deficiency shock.

There appear to be many contributing factors to sudden infant death syndrome (SIDS). One final common pathway that may explain some cases of SIDS is presented as a hypothesis: SIDS occurs as a shock-like event in a stressed infant with congenital or acquired magnesium deficiency with respect to calcium, or with genetically determined high magnesium requirements. Increased calcium and stress-related catecholamines favour platelet aggregation and release of mediators, chief of which appears to be thromboxane A2 (TXA2). TXA2, a major vasoconstrictor, bronchoconstrictor, and platelet aggregator is relatively unopposed during shock by prostacyclin, a vasodilator, bronchodilator, and platelet disaggregator which normally counterbalances its effects. The shock episode is self-limited. Infants who recover have suffered an apparent life threatening event (ALTE); those who die have insufficient pathology to explain the cause of death; the diagnosis is SIDS.

Humans↗
PubMed2000

Priming with magnesium-deficient media inhibits preadipocyte differentiation via potential upregulation of tumor necrosis factor-alpha.

The effect of priming stromal-vascular cells in primary cultures with magnesium-deficient (MgD) media on preadipocyte differentiation was studied. Cultures were derived from dorsal subcutaneous fat tissue of young pigs and maintained 3 d in serum-free control or MgD Dulbecco's modified Eagle's medium, 3 d in 10% fetal bovine serum and dexamethasone, and 6 d in insulin. At d 12 of culture, immunocytochemical and glycerophosphate dehydrogenase assays indicated depressed adipocyte differentiation in the MgD groups. Cultures were enriched for preadipocytes up to 50% of total cells. On the third day of treatment with control and MgD medium, total cell lysates were isolated and 50 microg of them were run on two-dimensional gel electrophoresis. The separated proteins from both treatment groups showed similar patterns. However, spots of proteins with predicted molecular weight in the range of 25.8-37.4 kDa and pI of 5.39-5.85 were sixfold denser from the MgD 10 groups than from the controls. These proteins migrate similarly to tumor necrosis factor-alpha (TNF-alpha). The amount of TNF-alpha in cell lysates from the MgD group was about 2.35 times greater than controls determined by TNF-alpha-ELISA. It is likely that proteins upregulated by MgD medium are TNF-alpha isoforms.

Adipocytes↗
PubMedDate not supplied

Magnesium deficiency affects the pentylenetetrazol-induced convulsions in magnesium-deprived rats.

A group of 11 young albino rats was fed with a Mg2+ free diet. After a few days, the animals showed typical signs of Mg2+ deficiency, consisting in skin vasodilation, red conjunctiva and hair loss. Pentylenetetrazol (50 mg/kg i.p.) injected in these rats, 6 and 12 days after the beginning of the diet, elicited a more severe convulsive activity compared with that shown by a control group of 12 rats. These results suggest that a Mg2+ deficiency, though not necessarily responsible for the convulsive activity, may contribute to facilitate an epileptic episode or may lead to more severe convulsions. The possibility of a more powerful activation of the NMDA receptors in Mg2+ deficiency is discussed.

Animals↗