Magnesium Treatment Research Articles

Recovery and reuse of chromium from tannery wastewaters using Turbinaria ornata seaweed

AbstractBrown seaweed (Turbinaria spp) was pre‐treated with sulfuric acid, calcium chloride and magnesium chloride and tested for its ability to remove chromium from tannery wastewater. Protonated seaweeds gave better uptake of chromium compared with calcium and magnesium treatments. Chromium uptake was optimal at pH 3.5. Turbinaria weed exhibited maximum uptake of about 31 mg of chromium for one gram of seaweed at an initial concentration of 1000 ppm of chromium. Freundlich and Langmuir adsorption isotherm models were used to describe the biosorption of chromium(III) by Turbinaria spp. The chromium‐loaded seaweed was reused as a reductant in the preparation of the tanning agent basic chromium sulfate (BCS). Leathers made from this tanning agent had properties comparable to conventionally processed chrome‐tanned leathers. Copyright © 2004 Society of Chemical Industry

Intravenous administration of magnesium is only neuroprotective following transient global ischemia when present with post-ischemic mild hypothermia

We hypothesized that post-ischemic hypothermia plays an important role in magnesium mediated neuroprotection following global cerebral ischemia. To test this hypothesis, we subjected rats to 8 min of global cerebral ischemia and magnesium treatment with and without post-ischemic body temperature maintenance. In Group 1, rats received an intravenously administered loading dose (LD) of 360 μmol/kg MgSO 4 immediately before ischemia followed by a 48-h intravenous infusion (IVI) at either 60, 120 or 240 μmol/kg/h. Animal body temperature was kept at 37±0.2 °C during ischemia and between 36.6 and 37.8 °C for 6 h after ischemia. In Group 2, rats received a 360 μmol/kg MgSO 4 LD followed by a 48-h IVI of either 120 or 240 μmol/kg/h MgSO 4. In this group, body temperature following ischemia was monitored but not regulated. Control animals in Groups 1 and 2 received normal saline. Seven days after ischemia, hippocampal CA1 neurons were histologically examined. All Group 1 MgSO 4-treated and control animals demonstrated less than 6% hippocampal CA1 neuronal survival. In Group 2, the rectal temperature of MgSO 4-treated and control animals spontaneously dropped as low as 35.4 °C during the 6-h post-ischemia monitoring period. In addition, Group 2 animals that received the LD followed by an IVI of 120 or 240 μmol/kg/h MgSO 4 demonstrated 34% ( p<0.05) and 20% ( p=0.936) CA1 neuronal survival, respectively. The CA1 neuronal survival in saline-treated control animals in both groups was less than 6%. Our data demonstrate only the combination of MgSO 4 treatment and post-ischemic mild hypothermia is neuroprotective following global ischemia.

Interference of magnesium on zinc adsorption by pond sediment and on zinc accumulation in a freshwater teleost, Labeo rohita (Hamilton)

Two experiments were conducted to evaluate the interference of magnesium on zinc adsorption in freshwater fish pond sediment and zinc accumulation in the freshwater teleost Labeo rohita (Hamilton). The study demonstrated that increasing the concentration of magnesium as magnesium sulfate from 100 to 400mgkg–1 decreased the adsorption of zinc in sediment. The maximum adsorption was found at a concentration of 100mgkg–1 of Mg2+ and the minimum with 400mgkg–1 of Mg2+. This study also demonstrated that the exposure of fish to 0.25mgL–1 of zinc as zinc sulfate with different concentrations of magnesium (100, 200, 300, and 400mgL–1) for 14d resulted in the minimum accumulation of zinc in L. rohita (2.97mgkg–1 dry weight) at 200mgL–1 of Mg2+, while the maximum accumulation (8.47mgkg–1 dry weight) occurred with no magnesium treatment.

A molecular basis for the efficacy of magnesium treatment following traumatic brain injury in rats.

Magnesium ions have been shown to be a promising treatment for brain lesions caused by traumatic brain injury (TBI), as well as for the associated acute neurodegeneration and progressive functional deficits. This study investigated the effects of magnesium on the expression of the cell death/survival related proteins following TBI. Male Sprague-Dawley (SD) rats (n = 66, 280-320 g body weight) were subjected to sham surgery alone (n = 14), or to the surgery followed by a lateral fluid percussion brain injury of moderate severity (n = 52, 2.4-2.7 atm). The injured rats were randomly treated with an intravenous bolus of magnesium chloride (n = 26, 125 micromol) or saline vehicle (n = 26). The coronal brain sections were quantitatively analyzed for cell apoptosis and the expression of p53-related proteins, Bcl-2, cyclin D1 and PCNA at 1, 2, and 4 days post-injury by immunohistochemistry or in situ hybridization. Tissue damage was observed primarily in the ipsilateral cortex of the injured region with the induction of apoptosis and p53 mRNA level at 2 days after TBI. The expression of p53 and responding proteins (p21(WAF1/CIP1), Mdm2 and Bax) showed a temporal pattern similar to the apoptotic events in the time course experiments. They were induced in the early time points of days 1-2, decreasing by day 4 after TBI. In contrast, the expression of the cell survival related proteins - Bcl-2, cyclin D1, and PCNA - was most significant at day 4 post-injury, when the rate of apoptosis decreased. Magnesium treatment resulted in a reduction in apoptosis and expression of p53-related proteins. However, it had only a slight additive effect on the expression of the survival related proteins in the same time-course. These results provide a molecular basis for the efficiency of magnesium in treating TBI-induced tissue damage.

Magnesium sulfate fails to reduce infarct volume following transient focal cerebral ischemia in rats

Studies on the neuroprotective effect of magnesium treatment in animal models of focal and global cerebral ischemia have produced inconsistent results. Nevertheless, two magnesium acute stroke phase III trials (IMAGES and FAST-MAG) have either been completed or are planned. Therefore, we decided to re-evaluate the efficacy of magnesium following focal cerebral ischaemia in rats. Two experiments were carried out in two independent laboratories based in Australia. Both used the intraluminal thread method to induce focal cerebral ischemia in the rat. In the Perth study the middle cerebral artery (MCA) was occluded for 45 min and body temperature was controlled during and after ischemia. In the Canberra laboratory the MCA was occluded for 2 h and body temperature was only controlled during surgery. Three different doses (180, 360, or 720 μmol/kg) of MgSO4 in the Perth study and two different MgSO4 doses (370 or 740 μmol/kg) in the Canberra study were intravenously or intra-arterially administered immediately before ischemia. Control animals were given an equal volume of normal saline just before ischemia in both studies. Twenty-four or 72 h post-ischemia, infarct volume was determined following 2′,3′,5′-triphenyl-2H-tetrazolium chloride (TTC) staining. No significant differences (P>0.05) in total, cortical and striatal infarct volumes between saline and MgSO4 treated animals were observed in either study. We conclude MgSO4 does not reduce infarct volume when administered before focal cerebral ischemia in rats.

Antidepressant- and anxiolytic-like activity of magnesium in mice

The antidepressant- and anxiolytic-like effects of magnesium, an N-methyl- d-aspartate (NMDA) glutamate receptor inhibitor, were studied in mice using the forced swim test and elevated plus-maze test, respectively. The doses of 20 and 30 mg Mg/kg, reduced immobility time in the forced swim test exerting antidepressant-like activity. In the elevated plus-maze test, magnesium at the same doses produced anxiolytic-like effect. The doses of magnesium active in both tests did not affect locomotor activity. To evaluate the tolerance to these effects, we also performed experiments on the following acute/chronic magnesium treatment schedule: chronic saline and saline challenge at 0.5 h before behavioral experiments or serum magnesium determination (S+S), chronic saline and magnesium challenge (S+Mg), chronic magnesium and saline challenge (Mg+S), chronic magnesium and magnesium challenge (Mg+Mg). The antidepressant- and anxiolytic-like effect of magnesium was demonstrated in groups treated acutely and chronically with magnesium (Mg+Mg), but not in the Mg+S group. Moreover, these effects seem to be connected with at least 58% increase in serum magnesium concentration. The results indicate that magnesium induces the antidepressant- and anxiolytic-like effects without tolerance to these activities, which suggests a potential antidepressant and anxiolytic activity of magnesium in these disorders in humans.

Evaluation of Red Blood Cell Deformability and Uterine Blood Flow in Pregnant Women with Preeclampsia or IUGR and Reduced Uterine Blood Flow Following the Intravenous Application of Magnesium

Objective: Red blood cell (RBC) deformability is one of the factors determining microcirculation. In preeclampsia (PE) and some cases of intrauterine growth restriction (IUGR), RBC deformability and, consequently, microcirculation appear to be impaired. Magnesium sulfate is administered to reduce the risk of seizures in PE. The aim of our study was to detect the effect of 24‐hour intravenous (IV) magnesium on RBC deformability and on uterine artery blood flow in pregnant patients with preeclampsia or IUGR and pathologic uterine blood flow. Methods: Magnesium IV (1 g/h) was administered to 25 pregnant women with reduced uterine blood flow for a period of at least 24 hours. The RBC deformability was measured by laser diffractoscopy, blood volume flow was measured by uterine artery Doppler. Measurements were taken before the start of magnesium therapy and 24 h later. Magnesium plasma levels were measured at the same time. Results: High plasma levels of magnesium improve RBC deformability from E = 0,109 (SD ± 0.023) to E = 0.115 (SD ± 0.021) after 24 h IV magnesium (p = 0.043). There is no correlation of E to the plasma magnesium level either before or after 24 h magnesium treatment. Blood volume flow in the uterine arteries increased significantly from 5.09 mL/s (SD ± 3.03) to 10.02 mL/s (SD ± 5.86) after 24 h magnesium (p = 0.0002). The differences in the resistance index do not significantly differ from 0 (p = 0.46). Conclusion: A high IV dosage of magnesium over a period of 24 hours dilates the uterine arteries of pregnant women with PE and/or IUGR, reduces uterine blood flow, and improves the deformability of RBC. Both parameters enhance the oxygen supply to the fetus, a critical parameter in these pregnancies. Thus magnesium might not only be effective as phrophylaxis against seizures but also in cases of IUGR with a reduced uterine blood flow. The clinically observed beneficial effect of magnesium in PE could be due to the improved blood supply for the fetus.

Magnesium in treatment of acute myocardial infarction

Magnesium has properties of myocardial cytoprotection, the pathophysiological explanations of which in acute myocardial infarction include prevention of arrhythmia, antiplatelet effect, prevention of reperfusion injury, and coronary vasodilation. Although several studies have evaluated the role of magnesium administration in patients with acute myocardium infarction, the clinical impact of such a therapy in this condition has been controversial, largely as a result of conflicting data from randomized controlled trials. The data available to date do not favor the routine administration of intravenous magnesium in patients with myocardial infarction, but this should not preclude magnesium administration to replenish low serum magnesium concentrations or use of magnesium sulfate for treatment of torsade de pointes in patients with myocardial infarction.

Long-Term Outcome of Intravenous Magnesium Therapy in Thrombolysis-Ineligible Acute Myocardial Infarction Patients

The aim of our study was to analyze the long-term survival and cardiac function in 194 consecutive, thrombolysis-ineligible acute myocardial infarction (AMI) patients receiving 48-hour intravenous magnesium sulfate (22 g) – 96 patients, compared with placebo – 98 patients. After a mean 4.8-year follow-up, all-cause mortality and cardiac mortality were significantly lower in the magnesium compared to the placebo group [(18 vs. 33 patients, p < 0.01) and (12 vs. 30 patients, p < 0.001), respectively]. Rest radionuclide ventriculography tests for left-ventricular ejection fraction (LVEF) were assessed in surviving patients up to completion of follow-up. Magnesium-treated patients had a significantly higher LVEF (0.51 ± 0.10 vs. 0.44 ± 0.14, p < 0.05) and a lower incidence of heart failure compared to placebo-treated patients (12 vs. 3 patients, p = 0.02). Beneficial effects of intravenous magnesium therapy in thrombolysis-ineligible AMI patients appeared to last for at least 4.8 years, concomitant with preserved LVEF, suggesting a favorable role for acute magnesium treatment in these patients.

Effect of magnesium sulphate in experimental spinal cord injury: evaluation with ultrastructural findings and early clinical results

Excitotoxic mechanisms have been implicated in the pathophysiology of spinal cord injury (SCI). The authors have studied the protection against secondary damage to rat spinal cord with magnesium sulphate, a well-known N-methyl- d-aspartate antagonist. Rats were randomly allocated into 5 groups. Group 1 rats were controls and normal spinal cord samples were obtained after clinical examination. 50 g–cm contusion injury was introduced to Group 2. Group 3 was vehicle, 1 cc of physiologic saline was injected posttrauma. Group 4 and 5 were treatment groups and 100 mg/kg and 600 mg/kg of Magnesium sulphate was given immediately after trauma, intraperitoneally. Animals were evaluated with inclined plane, Tarlov motor scale and Basso–Beattie–Bresnahan scale 24 h after SCI. Spinal cord samples for ultrastructural evaluations were obtained following clinical examinations. Magnesium treatment improved neurological outcome. Electron microscopic results showed obvious neuroprotection in the treatment groups. Application of 600 mg/kg of magnesium revealed better ultrastructural findings and clinical results than 100 mg/kg. These findings demonstrated that magnesium sulphate possesses neuroprotection on spinal cord ultrastructure and on functional scores after acute contusion injury to the rat spinal cord.

Effects of Oral Magnesium Therapy on Exercise Tolerance, Exercise-Induced Chest Pain, and Quality of Life in Patients With Coronary Artery Disease

Previous studies have demonstrated that magnesium supplementation improves endothelial function in patients with coronary artery disease (CAD). However, the impact on clinical outcomes, such as exercise-induced chest pain, exercise tolerance, and quality of life, has not been established. In a multicenter, multinational, prospective, randomized, double-blind and placebo-controlled trial, 187 patients with CAD (151 men, 36 women; mean ± SD age 63 ± 10 years, range 42 to 83) were randomized to receive either oral magnesium 15 mmol twice daily (Magnosolv-Granulat, total magnesium 365 mg provided as magnesium citrate) (n = 94) or placebo (n = 93) for 6 months. Symptom-limited exercise testing (Bruce protocol) and responses given on quality-of-life questionnaires were the outcomes measured. Magnesium therapy significantly increased intracellular magnesium levels ([Mg]i) in a substudy of 106 patients at 6 months compared with placebo (35.5 ± 3.7 vs 32.6 ± 2.9 mEq/L, p = 0.0151). Magnesium treatment significantly increased exercise duration time compared with placebo (8.7 ± 2.1 vs 7.8 ± 2.9 minutes, p = 0.0075), and lessened exercise-induced chest pain (8% vs 21%, p = 0.0237). Quality-of-life parameters significantly improved in the magnesium group. These findings suggest that oral magnesium supplementation in patients with CAD for 6 months results in a significant improvement in exercise tolerance, exercise-induced chest pain, and quality of life, suggesting a potential mechanism whereby magnesium could beneficially alter outcomes in patients with CAD.

Effects of temperature, UV-light and magnesium on anthocyanin pigmentation in cocoplum leaves

SummaryThis study aimed to understand factors affecting leaf pigmentation of the woody subtropical plant Chrysobalanus icaco, referred to as cocoplum. The effects of temperature, UV-light and magnesium treatments were examined at different developmental stages. Shoot growth intensity and chlorophyll concentrations increased while anthocyanin concentration decreased with rise in temperature. UV-a light had a slight effect on shoot growth, but no effect on the pigment concentration of the leaves. Anthocyanin concentration decreased while chlorophyll increased as leaves matured. The change in anthocyanin concentration was due to dilution of the pigment at the early stages of development and its degradation later on. In an attempt to inhibit anthocyanin degradation in maturing leaves, whole plants were treated with magnesium salts. Magnesium increased anthocyanin concentration two fold at the developmental stage at which degradation was detected in control plants. By controlling UV-a light via shading, applying magnesium treatments, growers may manipulate both plant height and colour, thereby increasing the horticultural value of the crops.

Effect of calcium, boron, zinc, magnesium, potassium and pre-storage water dip treatment on firmness of peaches

Experiments were conducted to test the effect of boron, zinc, magnesium, potassium and calcium as post-harvest dips on the firmness of 'Red-Haven' and 'Sun-Crest' peaches during storage. No significant differences were found in peach firmness between fruits treated with any of the mineral elements and non-treated peaches. The effect of pre-storage water dip on peach quality was also determined. It was found that the water dip significantly reduced the retention of fruit firmness compared with non-treated fruits.

Organic matter mobilization as affected by soil-solution composition and prevailing clay minerals

Laboratory experiments were conducted to study organic matter (OM) loss from soil columns with different clay mineral composition and treated with high sodium (Na) and potassium (K) saline solutions (SAR and Removal of organic and inorganic colloids was evaluated by determining organic matter content in the soil at the end of the trial and measuring absorbency of the percolated solutions. Though clay dispersion after magnesium (Mg) treatment was marked in the case of illitic and smectitic soils, little effect was detected in kaolinitic soil. For treatments with solutions containing Na, the highest removal of organic colloids was observed in illitic and kaolinitic soils. In smectitic soil this effect was more pronounced with calcium (Ca) in combination with Na and K. These findings have significance to explain differences in OM mobilization in salt affected depressions of different composition.

Effect of Long-Term, Postasphyxial Administration of Magnesium Sulfate on Immunostaining of Microtubule-Associated Protein-2 and Activated Caspase-3 in 7-Day-Old Rat Brain

To test whether magnesium inhibits apoptosis during hypoxia-ischemia (HI) in the developing brain, we studied the effect of long-term magnesium treatment on an early marker of neuronal damage (loss of microtubule-associated protein-2; MAP-2) and a marker of apoptosis (activated caspase-3) after HI in newborn rats. Seven-day-old rat pups (n = 107) were exposed to unilateral carotid artery ligation and 2 hours of hypoxia (8% oxygen in 92% nitrogen). Magnesium was administered by a micro-osmotic pump implanted in the back, at an infusion rate of 75 mg/kg per hour for 3 days. Neuronal loss in the cerebral cortex and hippocampus was evaluated by loss of MAP-2 at 24 and 48 hours after HI and visually ranked by a semiquantitative, three-point scale (mild, moderate, and severe). Caspase-3 activation was evaluated similarly in an adjacent section. Area and severity of the damaged lesion were compared between the two staining methods and between magnesium and controls, by chi(2) test and Fisher test. Three-day magnesium administration reduced loss of MAP-2 (from 33 of 50 to 21 of 45, P =.06) and activation of caspase-3 (from 34 of 50 to 21 of 45, P =.04) in the cerebral cortex after HI. There was no significant change in these immunostainings in the hippocampal regions. In the hippocampal CA3, the severity ranked by activated caspase-3 staining was significantly less than that of MAP-2 staining. Long-term, post-HI treatment with magnesium inhibited caspase-3 activation and MAP-2 immunostaining, suggesting that magnesium inhibited apoptotic neuronal death of HI in 7-day-old rats.

Increased anthocyanin accumulation in aster flowers at elevated temperatures due to magnesium treatment.

Temperature is one of the main external factors affecting anthocyanin accumulation in plant tissues: low temperatures cause an increase and elevated temperatures cause a decrease in anthocyanin concentration. Several metals have been shown to increase the half-life time of anthocyanins, by forming complexes with them. We studied the combined effect of elevated temperatures and increased metal concentrations on the accumulation of anthocyanins in aster 'Sungal' flowers. It has been found that magnesium treatment of aster plants or detached flower buds, partially prevents colour fading at elevated temperatures. Anthocyanin concentration of aster 'Sungal' flowers grown at 29 degrees C/21 degrees C day/night, respectively, was about half that of flowers grown at 17 degrees C/9 degrees C. The activity of phenylalanine ammonia-lyase (PAL) and chalcone isomerase (CHI) decreased as the temperature increased. Treatment of both whole plants and detached flower buds grown at elevated temperatures in the presence of magnesium salts, increased flower anthocyanin concentration by up to 80%. Measurement of magnesium following these treatments revealed an increased level of the metal in the petals, suggesting a direct effect. Magnesium treatment does not seem to cause increased synthesis of anthocyanin through a stress-related reaction, since the activities of both PAL and CHI did not increase due to this treatment. The results of this study show that increasing magnesium levels in aster petals prevents the deleterious effect of elevated temperatures on anthocyanin accumulation, thus enhancing flower colour.

Effect of cadmium and magnesium on free amino acids, polyamines and peroxidase enzyme activity in wheat seedlings

The effect of cadmium and combined cadmium and magnesium was examined on wheat seedlings (Triticum aestivum L. cv. Alfold-90). The one-week-old hydroponically-grown seedlings of wheat were exposed to Cd 2 + (10 - 7 M, 10 - 3 M) and Cd 2 + (10 - 7 M, 10 - 3 M) + 1 % MgCl2 stresses. The stress effects were followed by changes in free amino acid, polyamine contents and peroxidase enzyme activity in roots and shoots. Free amino acid content was determined by ion-exchange liquid chromatography. Polyamine content was identified by OPLC (overpressured layer chromatography). Peroxidase activity (U/mg protein) was measured by spectrophotometric method. The results showed significant differences between the two organs of the plant (root and shoot) with respect to the biochemical response to the applied stress. The cadmium stress caused the accumulation of proline in both shoots and roots. Magnesium reduced the proline content in the samples treated with cadmium. The magnesium treatment seemed to reduce the negative effects of cadmium in wheat seedlings.

The relation of magnesium treatment and blood magnesium levels with development of atrial fibrillation after coronary artery bypass surgery

The relation of magnesium treatment and blood magnesium levels with development of atrial fibrillation after coronary artery bypass surgery

High-Dose Oral Magnesium Treatment of Chronic, Intractable Erythromelalgia

BACKGROUND:Previous studies with magnesium have shown beneficial effects in pain syndromes and in vascular disorders (hypertension, migraines, Raynaud's phenomenon). However, results have been variable, possibly because of the limited oral doses achievable due to frequent diarrhea.OBJECTIVE:To describe the case of a 53-year-old white man (the author) with disabling erythromelalgia (EM) who achieved modest improvement limited by adverse effects with calcium antagonists and then obtained remission with the use of magnesium. Intolerant of several standard magnesium products, he attained high doses of magnesium by taking intravenous-grade magnesium sulfate diluted in water orally (up to 24 mL/d of MgSO4 50% = 1166 mg/d of magnesium).METHODS:After 12 months of continued improvement, patient 1, a board member of The Erythromelalgia Association, notified other members of the success of this therapy via an Internet communication channel. He encouraged those interested in high-dose magnesium therapy to consult their physicians and to report their results to the Association. Twelve patients responded to this request, describing several standard oral magnesium products.RESULTS:Overall, 8 of 13 patients (61.5%) reported improvement (1, remission; 3, major improvement; 2, moderate improvement; 2, mild improvement). Four patients (30.8%) reported no response to magnesium therapy, and 1 patient's symptoms worsened. Two patients' magnesium dose was limited because of diarrhea.CONCLUSIONS:Despite recent progress in understanding and treating EM, this vascular disorder remains painful and life-altering for many patients. In this informal survey, the use of high oral doses of magnesium produced good and sometimes dramatic results in 8 of 13 patients who had been unresponsive to many other treatments. These results suggest a possible role for high-dose oral magnesium in the treatment of EM and, perhaps, other vascular disorders.

The central role of magnesium deficiency in Tourette's syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette's syndrome and several reported comorbid conditions

Prior studies have suggested a common etiology involved in Tourette's syndrome and several comorbid conditions and symptomatology. Reportedly, current medications used in Tourette's syndrome have intolerable side-effects or are ineffective for many patients. After thoroughly researching the literature, I hypothesize that magnesium deficiency may be the central precipitating event and common pathway for the subsequent biochemical effects on substance P, kynurenine, NMDA receptors, and vitamin B6 that may result in the symptomatology of Tourette's syndrome and several reported comorbid conditions. These comorbid conditions and symptomatology include allergy, asthma, autism, attention deficit hyperactivity disorder, obsessive compulsive disorder, coprolalia, copropraxia, anxiety, depression, restless leg syndrome, migraine, self-injurious behavior, autoimmunity, rage, bruxism, seizure, heart arrhythmia, heightened sensitivity to sensory stimuli, and an exaggerated startle response. Common possible environmental and genetic factors are discussed, as well as biochemical mechanisms. Clinical studies to determine the medical efficacy for a comprehensive magnesium treatment option for Tourette's syndrome need to be conducted to make this relatively safe, low side-effect treatment option available to doctors and their patients.