Magnesium research最新文献

Addiction is a dysregulation of brain reward systems that progressively increases, resulting in compulsive drug use and loss of control over drug-taking. Addiction is a brain disease. There is evidence that magnesium deficit is involved in addiction to various addictive substances (heroin, morphine, cocaine, nicotine, alcohol, caffeine, and others). Magnesium is involved in all the stages of addiction. Magnesium deficit enhances the vulnerability to psychoactive substance addiction. Stress and trauma reduce the brain magnesium level and at the same time favor addiction development. In experimental studies, administration of magnesium while inducing morphine dependence in rats reduced the dependence intensity. Magnesium reduces the NMDA receptor activity and the glutamatergic activity. Because stress and trauma induce hypomagnesemia with increased vulnerability to addiction, magnesium intake by people who are under prolonged stress could be a way to reduce this vulnerability and the development of addiction to different psychoactive substances. Anxiety and depression appear to be associated with increases in drug-related harm and addictive substance use. Magnesium anxiolytic effect could be important for the antiaddictive action. Addiction is characterized by relapses. Magnesium deficiency may be a contributing factor to these relapses.

Antidepressant therapy exhibits low clinical efficacy and produces a variety of unwanted side effects. Therefore, the search for more effective antidepressants is still in progress. Antidepressant properties of magnesium and zinc have been demonstrated in animal screen tests/models and clinical studies. Moreover, these bio-elements enhance antidepressant activity of conventional antidepressants in these behavioral paradigms. As for magnesium, clinical studies demonstrated equivocal results concerning its supplementary effectiveness in the treatment of depression. Generally, some depressed patients with hypomagnesemia responded very well to such supplementation, whereas response of other patients was weaker. Clinical data on the effectiveness of zinc supplementation in the therapy of depression are much more robust. A number of studies demonstrated enhancement of the efficacy of pharmacotherapy by zinc supplementation in major depression. What is important, recent studies demonstrate that zinc supplementation augments efficacy of antidepressants also in treatment-resistant patients. All the available data indicate the importance of magnesium and zinc in the therapy of depression.

The aims of this study were to determine whether low concentrations of magnesium in vitro exacerbated the human umbilical vein endothelial cell (HUVEC) response to inflammatory challenge, and whether expression of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) through the toll-like receptor 4 (TLR4) played a role in this process. HUVECs were incubated with different concentrations of Mg (low- 0.1mM, control- 1mM, high- 5mM) for 72 h before being stimulated with bacterial lipopolysaccharide (LPS) for 4 h. The response of cells to LPS was greater in cells cultured in low Mg, relative to control cells and suppressed in high Mg. Expression of NF-κB was increased in low-Mg and decreased with high Mg. Low Mg increased the expression of TLR4 mRNA, but only in the presence of LPS. Antibody blockade of TLR4 but not TLR2 blunted the response of cells to LPS in low Mg, such that they were similar to unblocked 1mM Mg cells. Associations of Mg with cardiovascular disease may therefore relate to inflammatory responses mediated through the TLR4/NF-κB pathway.

This study examined the effect of chronic (2 weeks) administration of zinc oxide nanoparticles (NPs-ZnO) and standard zinc oxide (S-ZnO) on the levels of zinc (Zn), magnesium (Mg) and calcium (Ca) in rat serum. S-ZnO and NPs-ZnO were administered either per os (p.o.) or intraperitoneally (i.p.) at doses of 7 mg/kg or 14 mg/kg. Neither form of ZnO administered p.o. altered serum zinc concentration. However, different effects dependent upon either S-ZnO or NPs-ZnO forms were noticed after i.p. administration. Namely, while S-ZnO increased serum zinc concentration (by 136%) only at the higher dose (14 mg/kg), both doses of NPs-ZnO increased zinc concentration (by 97% at 7 mg/kg and by 564% at 14 mg/kg). The form-dependence of the ZnO effect was also demonstrated in the effect on the serum magnesium level. Only the S-ZnO form (at the dose of 14 mg/kg) reduced serum magnesium concentration (by 14% p.o., 6% i.p.). No influence of NPs-ZnO on the serum calcium level was observed. The present study demonstrated effects on the serum Zn and Mg levels, which differed between the standard and nanoparticle forms of ZnO. This may contribute to the different functional effects of these ZnO forms shown previously.

Depression is one of the major causes of disability worldwide. A proportion of adults with major depression fail to achieve remission with first-line treatment. Magnesium influences the neurotransmission involved in emotional processes, such as the serotonergic, noradrenergic, dopaminergic, GABAergic and glutamatergic systems. It has been reported that the mechanism of antidepressants' action is involved in the glutamatergic system. Theories about the role of magnesium ions in pathophysiology of major depressive disorder include blocking the glutamatergic N-methyl-D-aspartate receptor (NMDAR). Ketamine, NMDAR antagonist, was found to promote fast-acting antidepressant and antisuicidal effects. Magnesium and ketamine seem to be involved in key mechanisms of the major depression pathophysiology. The evidence in the paper discussed may indicate the synergistic interaction between magnesium and ketamine pharmacodynamic activity being of particular importance in mood disorders.

Aim: Elevated fractional excretion of magnesium (FEMg) is a noninvasive biomarker of kidney damage, but its association with kidney functional parameters in nondiabetic chronic kidney disease (CKD) patients has not been sufficiently explored thus far.

Methods: We enrolled 111 adult patients with nondiabetic CKD and 30 controls. To precisely investigate kidney function, the following parameters were assessed measured glomerular filtration rate (mGFR), effective renal plasma flow (ERPF), Cystatin C, albuminuria, and fractional excretion of magnesium (FEMg). All the CKD patients were divided into two groups according to the values of mGFR (mL/min/1.73m²): the first group consisted of those with GFR≥ 60 mL/min/1.73m², whereas the second group included those with GFR< 60 mL/min/1.73m².

Results: FEMg (%) was significantly higher in the group of nondiabetic patients with CKD compared to the healthy subjects [6.3 vs. 5.3 %, P=0.013]. There was also significant difference in the value of FEMg between the first and second groups of CKD patients. Increased FEMg was significantly correlated with all the investigated kidney function parameters, mGFR, ERPF, Cystatin C and albuminuria (r=-0.62; r=-0.60; r=0.77; r=0.39; p<0.01 for all). In multiple regression analyses based on observed parameters of kidney function, only cystatin C was independently and significantly associated with FEMg (multiple correlation coefficients: 0.738, p < 0.001)). Nondiabetic CKD patients with GFR< 60 mL/min/1.73m² have increased FEMg above 6.1% with 78.7 % specificity and 83.7% sensitivity.

Conclusion: Highly significant association between kidney functional parameters and FEMg may indicate significance of this parameter in clinical practice.

Given a possible anti-inflammatory role of magnesium in endothelial cells, the aim of this study was to investigate the effects of magnesium on human umbilical vein endothelial cell (HUVEC) viability, gene expression, and the pro-inflammatory response caused by a bacterial endotoxin (LPS). HUVECs were cultured at three different concentrations of magnesium sulphate (0.1 mM; control-1 mM; 5 mM) for 72 hours. Exposing the cells to LPS reduced cell viability in culture with low magnesium, but high magnesium protected the HUVECs from LPS-induced cell death. LPS-treated HUVECs cultured in low magnesium showed up-regulation of mRNA expression for pro-inflammatory factors and the expression of cytokine proteins, including IL-2, IL-3, IL-8, IL-15 and MCP-1. This was associated with greater adhesion of monocytes to the cells. In contrast, high magnesium decreased the expression of inflammatory factors and cytokines. The study found that LPS activation of the expression of many pro-inflammatory factors is exacerbated in the presence of low magnesium concentration whilst a high magnesium concentration partly inhibited the inflammatory response to LPS.

In both types of diabetes mellitus (DM), type 1 and type 2 (T1DM and T2DM), there are both endocrine and exocrine dysfunctions of the pancreas (PED), as well as disturbances in serum magnesium levels. The aim of this study was to examine the frequency of PED according to the level of fecal elastase-1 (FE-1) in patients with T1DM and T2DM, determining the correlation of the level of FE-1 with certain anthropometric parameters, certain indicators of metabolic regulation of diabetes, and certain nutritive markers of PED.

Materials and methods: In the examinees, (56 with T1DM (F = 35 and M = 21), 62 with T2DM (F = 30 and M = 32), and 40 in the control group (F = 19 and M = 21)), we examined anthropometric parameters, and using standard biochemical methods, we measured the level of FE-1, magnesium concentration in blood and erythrocytes, and selected blood parameters.

Results: FE-1 concentration < 200 μg/g was present in 14.2% of the examinees with T1DM, 20.9% with T2DM, and 2.5% in the control group. In all examinees with DM, there was a statistically significant correlation (P < 0.05) between the level of FE-1 and Mg concentration in the erythrocytes (R = 0.40).

Conclusions: Prevalence of pancreatic exocrine insufficiency (PEI), according to the level of FE-1, is significantly higher in patients with DM than in the control group, while it is a bit higher in patients with T2DM than the ones with T1DM. In both types of DM, Mg concentration in erythrocytes is in a significant correlation with the level of FE-1.

Although a magnesium-mediated attenuation of memory deficits was reported in animal models of ageing and traumatic brain injury, a possible memory enhancement in healthy subjects has not been investigated yet. We used novel object recognition test (NORT) to examine the effects of acute (30 mg/kg) and chronic (50 mg/kg, 28 days) Mg-sulfate treatment on the long-term memory (LTM) in healthy adult male rats, and to test the sustainability of magnesium effects in the models of acute and chronic (21 days) ACTH administration (10 μg/animal), mimicking the stress- and depression-like conditions. A single dose of Mg-sulfate enhanced the LTM retrieval in the 24 h inter-trial NORT protocol, in healthy, as well as in rats acutely treated with ACTH. Memory enhancement was also detected after 4-week long Mg-sulfate intake, in both healthy and rats chronically treated with ACTH. While the present findings on procognitive effects of chronic Mg-sulfate treatment corroborate with those from studies on the therapeutic potential of Mg-threonate, the current study is the first to report on memory enhancement induced by a single dose of magnesium.